- 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 very much. Well this is a series that was actually published five years ago. And it outlined 45,000 patients after carotid endarterectomy, as well as open and closed thoracic abdominal procedures and infrainguinal bypasses.
And you can see here, that the VTE rate, and this is emblematic of a lot of studies. If you take everything together in a ball, you get an average result. And as you can see, the peripheral bypasses had a low incidence.
Carotids, very low incidence. But open procedures had a higher incidence than endovascular procedures. But here is the nub. Here is what's really important and why you need to do risk assessment.
Look at what happened to these percentages if the patients had any morbidity during hospitalization, as high as 7.8%. And here's the list after they went home. Again, it's not the .5 tenths of a percent or 1%, and this is what it's all about.
It's about the extra risk factors that the patient has. So now, anybody that's starting to do work with the Caprini Score, you've got to go to the patient-friendly form. Because we don't just do it,
if the patient comes in for surgery, and somebody does a preoperative evaluation in the holding area, stop it! It's ridiculous! Have you ever been in the holding area? What are you worried about?
You're worried about having the operation. Are they going to find cancer? Will the surgeon have a bad day? How much pain am I going to be in? How long am I going to be out of work? They're not going to talk to you
about their family history or their obstetrical misadventures. So you have them fill a form out ahead of time with their family, and then when they come in, you just double-check it. And we've studied this, it's in five languages,
and it's got perfect correlation with trained observers doing the same thing. And remember, if you fail to carefully interrogate your patients regarding the history or family history of venous thromboembolism, vascular surgery or not, sooner or later you may
be faced with a fatal PE. And the idea that you're giving anticoagulants during your procedure that's going to protect them is not valid. The relative risk of thrombosis increases with the number of risk factors identified.
A combination of genetic and acquired risk factors in a person without a history of a thrombosis personally, but with a family history, has a 60-fold higher chance than those that have a negative family history. And a positive family history increased
the risk of venous thrombosis more than 2-fold, regardless of the other risk factors. Don't forget the history of thrombosis. You won't need to look this article up. It's 183,000 patients over 25 years and it shows that both in first, second,
and third-degree relatives, as well as cohabitants in the household, there's an increased risk of venous thromboembolism. Lowering down, getting lower for each degree of a relative.
But a DVT in a cousin, there may also be a thrombopathic condition in that patient. So you better pay attention to that. National Surgical Quality Improvement Program, wonderful program. The database has no information on history
or family history of VTE, use of perioperative VTE prophylaxis, intraoperative anticoagulation, or perioperative use of antiplatelet agents. How are you supposed to make any sense out of DVT-related studies?
Finally, due to the lack of routine screening for VTE, the incidence of VTE may be underestimated in this NSQIP database, which only makes the need for further study more pressing. This is an important consideration because
more recent data indicates that two-thirds of the patients are found to have DVT during screening and after vascular operations, have no signs or symptoms of the problem. And I'd like to remind you, so this is based on the Boston data, which is the best data.
Patients with a low score pneumatic compression during hospitalization. Moderate score, of 7-10 days of anticoagulation. Don't make any difference if they're inpatient or outpatient. And 28 days if their score is over nine.
They lowered their incidence on the surgical services from 2.2% to a tenth of a percent at 30 days. And finally, and I think this is really, really important. Take a look at all these risk assessment scores.
To my knowledge, there's only two scores. It's not the Padua, it's not the IMPROVE that have a history of obstetrical misadventures which can reflect antiphospholipid antibody syndrome, as well as family history
in various degrees of relatives. So with that, thank you very much.
- 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.
- [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.
- 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.
- 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.
- 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.
- Alright-ey, hands put up. Who is for Onyx? Put your arms up. - [Male Audience Member] Who supports the Onyx Motion? - Onyx Motion, that's correct. He should've gone to law school. Who supports the alcohol motion?
Who supports the motion in the ocean? Alright, thank you I think we covered a lot of territory today. We want to have theses things and we are so glad that everybody came. I think this is Tony's first time,
Walter's first time here, Loronze and we really learned a lot today. I'm really glad Pletio Rossi was here because without him and his development of selective catheterization, I mean where would we be
sticking needles in every artery like that, trying to do angiograms, much less advanced sheaths or anything else. Pletio was wonderful having him here, one of my hero's. Anybody like to say anything?
Anybody got any questions or anything? - [Female Audience Member] The HHT scientific meeting's in June in Puerto Rico if you want some more good-- - Do they have electricity there yet? - [Female Audience Member] I hope so, I knew it looked nice before.
- Oh, okay, okay. Alright, well thank ya'll so much and we'll see you next year. (Clapping)
- 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.
- 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.
- 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 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.
- 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 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.
- 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.
- First of all I'd like to thank the organizers for inviting me to give this presentation. These are my disclosures. I'm going to divide this presentation into three main parts. I will initially make the case that at the present time we are providing relatively poor value in ESRD and Vascular Access Care.
I'll then submit to you that one way to address this issue is through Patient Centered Device Innovation and then I'll tell you a little bit about some regulatory initiatives in this area. If you define value as being outcomes over cost
then I would argue that in vascular access we actually provide very poor value in that we have pretty bad outcomes and in order to achieve these bad outcomes we actually spend a huge amount of money at about 1.5 billion dollars per year and these is no talk at all
in the construct before you about quality of life. How can we break this cycle of a lack of innovation resulting in poor quality and outcomes and a high cost burden? I would submit to you that one way that we may be able to break the cycle
is through patient centered innovations. Patient centered innovation, whether it's discovery or process of care innovation, is basically innovation that targets the issues that are important to patients, not necessarily the issues that are important to physicians,
or payors, or regulators, or to industry. The reason that this is important is that the things that are relevant and critical to patients are often very different from the things that are important to the other stakeholder groups that I mention. If you look at hemodialysis for example
the things that are important to a patient on hemodialysis are ability to travel, and dialysis free time, and not feeling washed out post dialysis. On the other hand, if you're an nephrologist as I am, the things that are important to me are survival, and hospitalization, and being a nephrologist
I completely obsess about blood pressure which is really not something that patients are that worried or bother about. The next question is, of course, how do we develop therapies that address the issues that are important to patients? I got this slide from Frank Hurst at the FDA.
It basically makes the point that we need to have patient input at every point in the product development process, from initial ideation, to clinical trial design, to patient preferences, to patient centered outcomes. The FDA actually has a number of programs
in this area, one example is their Patient Focused Drug Development Initiative which allows the FDA to speak with patients and patient groups in different therapeutic areas. Closer to home, the Medical Device Innovation Consortium is extremely interested in Patient Preferences
and in a Risk-Benefit analysis. Within the kidney health initiative, which is a public-private partnership between the American Society of Nephrology and the FDA, we are also very interested in patient preferences for renal devices, and the background for this is
that an individual patient's tolerance for risk actually varies tremendously. Patients on home hemodialysis, for example, may be happy to sacrifice some degree of safety with regard to, say, vascular access, in order for an improved
or a more independent quality of life. But if you're a regulator there needs to be a way that you can get insight in to how patients perceive the risk/benefit ratio so that it can be incorporated into the regulatory pathway, and at least at the present time
the tools for this do not exist. The Kidney Health Initiative hosted an extremely successful patient preference workshop in the Baltimore area a couple of years ago. We asked three main questions: how can patients assist in the development
of a new medical device? How can they ensure the success of future clinical trials? And how can they help with the decision to make a new device available? The proceedings of this workshop have been published, and I'm really not going to go into details there.
I'm going to share with you a video that was made to try and attract patients to this webinar, and I think it really epitomizes the importance of patient centered innovation. - Hello, I'm CeCe, a fellow kidney disease patient. For 33 years I've done dialysis, both hemo and PD.
I had a transplant for 10 years and as you can imagine too many pills, shots, and accesses to mention. As kidney patients you and I both know that a few things in life are not optional. Strength, courage,
persistence, and determination. No matter what life throws at us, we try to stay balanced, maintain our routine, and remain positive. But let's face it, we are often in a holding pattern. Kidney disease treatments have not
changed much over the years. The options for patients like us have largely remained the same for many years. You want to help change that? We need you. Each day we're asked to share our lives with our treatment. But now, let's share our voice, ideas, opinions.
From patients like us, they matter. Key people are realizing our voices matter too. Here's what I found out. The Food and Drug Administration, often known as the FDA, is looking for patients living with kidney disease like you and me, to provide input
on how potential treatments of the future could look. Picture a big table. Around it are dialysis caregivers, researchers, doctors, nurses, and companies providing new products and treatments. They want us and our families to sit beside them
and have a seat at this table. We'll work together to bring potential new treatment options, safe and effective ones, and ones that patients like you and me want and need. Imagine the future of your treatment. What does it look like?
How does it improve your day-to-day life? This future doesn't have to remain just a dream. Join me and other patients to contribute our thoughts and make our ideas a possible reality. - The driving force and also the voice behind that video was the lady on the right, Celeste Lee.
She was a dialysis patient for over 30 years, she was a member of the KHI board of directors, and Celeste died a year and a half ago, she basically withdrew from dialysis because of bone disease from the 30 years of dialysis. I really think that her death
should be a charge for all of us really to try and develop therapies that target the things that are important to patients. Thank you very much for your attention.
- 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.
- Thank you for introduction. Thanks to Frank Veith for the kind invitation to present here our really primarily single-center experience on this new technique. This is my disclosure. So what you really want
in the thromboembolic acute events is a quick flow restoration, avoid lytic therapies, and reduce the risk of bleeding. And this can be achieved by surgery. However, causal directed local thrombolysis
is much less invasive and also give us a panoramic view and topographic view that is very useful in these cases. But it takes time and is statistically implied
and increases risk of bleeding. So theoretically percutaneous thrombectomy can accomplish all these tasks including a shorter hospital stay. So among the percutaneous thrombectomy devices the Indigo System is based on a really simple
aspiration mechanism and it has shown high success in ischemic stroke. This is one of my first cases with the Indigo System using a 5 MAX needle intervention
adapted to this condition. And it's very easy to understand how is fast and effective this approach to treat intraprocedural distal embolization avoiding potential dramatic clinical consequences, especially in cases like this,
the only one foot vessel. This is also confirmed by this technical note published in 2015 from an Italian group. More recently, other papers came up. This, for example, tell us that
there has been 85% below-the-knee primary endpoint achievement and 54% in above-the-knee lesions. The TIMI score after VAT significantly higher for BTK lesions and for ATK lesions
a necessity of a concomitant endovascular therapy. And James Benenati has already told us the results of the PRISM trials. Looking into our case data very quickly and very superficially we can summarize that we had 78% full revascularization.
In 42% of cases, we did not perform any lytic therapy or very short lytic therapy within three hours. And in 36% a long lytic therapy was necessary, however within 24 hours. We had also 22% failure
with three surgery necessary and one amputation. I must say that among this group of patients, twenty patients, there were also patients like this with extended thrombosis from the groin to the ankle
and through an antegrade approach, that I strongly recommend whenever possible, we were able to lower the aspiration of the clots also in the vessel, in the tibial vessels, leaving only this region, thrombosis
needed for additional three hour infusion of TPA achieving at the end a beautiful result and the patient was discharged a day after. However not every case had similar brilliant result. This patient went to surgery and he went eventually to amputation.
Why this? And why VAT perform better in BTK than in ATK? Just hypotheses. For ATK we can have unknown underlying chronic pathology. And the mismatch between the vessel and the catheter can be a problem.
In BTK, the thrombus is usually soft and short because it is an acute iatrogenic event. Most importantly is the thrombotic load. If it is light, no short, no lytic or short lytic therapy is necessary. Say if heavy, a longer lytic therapy and a failure,
regardless of the location of the thrombosis, must be expected. So moving to the other topic, venous occlusive thrombosis. This is a paper from a German group. The most exciting, a high success rate
without any adjunctive therapy and nine vessels half of them prosthetic branch. The only caution is about the excessive blood loss as a main potential complication to be checked during and after the procedure. This is a case at my cath lab.
An acute aortic renal thrombosis after a open repair. We were able to find the proximate thrombosis in this flush occlusion to aspirate close to fix the distal stenosis
and the distal stenosis here and to obtain two-thirds of the kidney parenchyma on both sides. And this is another patient presenting with acute mesenteric ischemia from vein thrombosis.
This device can be used also transsympatically. We were able to aspirate thrombi but after initial improvement, the patient condition worsened overnight. And the CT scan showed us a re-thrombosis of the vein. Probably we need to learn more
in the management of these patients especially under the pharmacology point of view. And this is a rapid overview on our out-of-lower-limb case series. We had good results in reimplanted renal artery, renal artery, and the pulmonary artery as well.
But poor results in brachial artery, fistula, and superior mesenteric vein. So in conclusion, this technology is an option for quick thromboembolic treatment. It's very effective for BTK intraprocedural embolic events.
The main advantage is a speeding up the blood flow and reestablishing without prolonged thrombolysis or reducing the dosage of the thrombolysis. Completely cleaning up extensive thromobosed vessels is impossible without local lytic therapies. This must be said very clearly.
Indigo technology is promising and effective for treatment of acute renovisceral artery occlusion and sub massive pulmonary embolism. Thank you for your attention. I apologize for not being able to stay for the discussion
because I have a flight in a few hours. Thank you very much.
- We are talking about the current management of bleeding hemodialysis fistulas. I have no relevant disclosures. And as we can see there with bleeding fistulas, they can occur, you can imagine that the patient is getting access three times a week so ulcerations can't develop
and if they are not checked, the scab falls out and you get subsequent bleeding that can be fatal and lead to some significant morbidity. So fatal vascular access hemorrhage. What are the causes? So number one is thinking about
the excessive anticoagulation during dialysis, specifically Heparin during the dialysis circuit as well as with cumin and Xarelto. Intentional patient manipulati we always think of that when they move,
the needles can come out and then you get subsequent bleeding. But more specifically for us, we look at more the compromising integrity of the vascular access. Looking at stenosis, thrombosis, ulceration and infection. Ellingson and others in 2012 looked at the experience
in the US specifically in Maryland. Between the years of 2000/2006, they had a total of sixteen hundred roughly dialysis death, due to fatal vascular access hemorrhage, which only accounted for about .4% of all HD or hemodialysis death but the majority did come
from AV grafts less so from central venous catheters. But interestingly that around 78% really had this hemorrhage at home so it wasn't really done or they had experienced this at the dialysis centers. At the New Zealand experience and Australia, they had over a 14 year period which
they reviewed their fatal vascular access hemorrhage and what was interesting to see that around four weeks there was an inciting infection preceding the actual event. That was more than half the patients there. There was some other patients who had decoags and revisional surgery prior to the inciting event.
So can the access be salvaged. Well, the first thing obviously is direct pressure. Try to avoid tourniquet specifically for the patients at home. If they are in the emergency department, there is obviously something that can be done.
Just to decrease the morbidity that might be associated with potential limb loss. Suture repairs is kind of the main stay when you have a patient in the emergency department. And then depending on that, you decide to go to the operating room.
Perera and others 2013 and this is an emergency department review and emergency medicine, they use cyanoacrylate to control the bleeding for very small ulcerations. They had around 10 patients and they said that they had pretty good results.
But they did not look at the long term patency of these fistulas or recurrence. An interesting way to kind of manage an ulcerated bleeding fistula is the Limberg skin flap by Pirozzi and others in 2013 where they used an adjacent skin flap, a rhomboid skin flap
and they would get that approximal distal vascular control, rotate the flap over the ulcerated lesion after excising and repairing the venotomy and doing the closure. This was limited to only ulcerations that were less than 20mm.
When you look at the results, they have around 25 AV fistulas, around 15 AV grafts. The majority of the patients were treated with percutaneous angioplasty at least within a week of surgery. Within a month, their primary patency was running 96% for those fistulas and around 80% for AV grafts.
If you look at the six months patency, 76% were still opened and the fistula group and around 40% in the AV grafts. But interesting, you would think that rotating an adjacent skin flap may lead to necrosis but they had very little necrosis
of those flaps. Inui and others at the UC San Diego looked at their experience at dialysis access hemorrhage, they had a total 26 patients, interesting the majority of those patients were AV grafts patients that had either bovine graft
or PTFE and then aneurysmal fistulas being the rest. 18 were actually seen in the ED with active bleeding and were suture control. A minor amount of patients that did require tourniquet for a shock. This is kind of the algorithm when they look at
how they approach it, you know, obviously secure your proximal di they would do a Duplex ultrasound in the OR to assess hat type of procedure
they were going to do. You know, there were inciting events were always infection so they were very concerned by that. And they would obviously excise out the skin lesion and if they needed interposition graft replacement they would use a Rifampin soak PTFE
as well as Acuseal for immediate cannulation. Irrigation of the infected site were also done and using an impregnated antibiotic Vitagel was also done for the PTFE grafts. They were really successful in salvaging these fistulas and grafts at 85% success rate with 19 interposition
a patency was around 14 months for these patients. At UCS, my kind of approach to dealing with these ulcerated fistulas. Specifically if they bleed is to use
the bovine carotid artery graft. There's a paper that'll be coming out next month in JVS, but we looked at just in general our experience with aneurysmal and primary fistula creation with an AV with the carotid graft and we tried to approach these with early access so imagine with
a bleeding patient, you try to avoid using catheter if possible and placing the Artegraft gives us an opportunity to do that and with our data, there was no significant difference in the patency between early access and the standardized view of ten days on the Artegraft.
Prevention of the Fatal Vascular Access Hemorrhages. Important physical exam on a routine basis by the dialysis centers is imperative. If there is any scabbing or frank infection they should notify the surgeon immediately. Button Hole technique should be abandoned
even though it might be easier for the patient and decreased pain, it does increase infection because of that tract The rope ladder technique is more preferred way to avoid this. In the KDOQI guidelines of how else can we prevent this,
well, we know that aneurysmal fistulas can ulcerate so we look for any skin that might be compromised, we look for any risk of rupture of these aneurysms which rarely occur but it still needs to taken care of. Pseudoaneurysms we look at the diameter if it's twice the area of the graft.
If there is any difficulty in achieving hemostasis and then any obviously spontaneous bleeding from the sites. And the endovascular approach would be to put a stent graft across the pseudoaneurysms. Shah and others in 2012 had 100% immediate technical success They were able to have immediate access to the fistula
but they did have around 18.5% failure rate due to infection and thrombosis. So in conclusion, bleeding to hemodialysis access is rarely fatal but there are various ways to salvage this and we tried to keep the access viable for these patients.
Prevention is vital and educating our patients and dialysis centers is key. Thank you.
- Thank you very much. Let's see, no disclosures related to this issue. I think, we are, now, talking about a lot of physical measurements, and trying to figure out what's best for the patient but, in fact, the evaluation of the quality of care has changed, and we are now more related
to value-based healthcare. And that relates to the fact that you measure the outcome of your treatment, and you divide it by the costs. This is me in the old days that I thought, what's outcome? Well, I have a perfect technical result.
I have no complications and a 99% success rate. Unfortunately, that idea doesn't stand anymore. We have to do other things to prove that we're doing well. We need patient-reported outcomes, we need clinical-reported outcomes.
That value comes to outcome, and that you divide to the cost of the treatment. These are the arrows are the patient-reported outcomes. First, of course, you have the quality of care. That's the patient mentions how he evaluates the quality of the care that he had got.
The other thing is the quality of life. Those are the patient-reported outcomes. On the other side are the clinical-reported outcomes. That's the clinical opinion, which is the VCSS, the CF, and the other classification that we have, are clinical measurements, of course,
which are duplex outcomes, MRVs, CTVs, etc. So, as said Patient Reported Experience Measurements PREMs as called, is something which you collect alongside with the PROMs, Patient Reported Outcome Measures and that tells you something about how the patient evaluates the care that he got.
Then of course, quality of life, there's a huge amount of things out there. We analyzed the overview of the most commonly used. We came in fact to the conclusion that VEINES-QOL/Sym is the only quality of life, disease-specific quality of life score,
which, let's say quantifies the disease from varicose veins up to ulcer disease. All the specific scores and the others which are out there unfortunately only do it, going to quantify the quality of life in a segment of the venous disease, which you can see here.
So we have C(EAP) for clinical, Villalta, VCSS, AVVQ, CIVIQ and VEINES-QOL/Sym. And the VEINES-QOL/Sym is something which is around there in lot of languages and tells you something about the disease of the patient. Of course you need to take generic quality of life,
a lot of people use the SF-36 but unfortunately, that's not the value that you can use to quantify the care you need. The EQ-5D-5L to economically evaluate and calculate for qualities. And that said if we do the VEINES-QOL/Sym.
Well, clinical outcomes, C(EAP), VCSS, Villalta scale, venous claudication, which are all there, venous claudication is not in the other three. So we need, at least, a quantification of venous claudication in a new one. And we know that aspects of venous claudication,
pain during exercise, pain subsides at rest, leg-elevation decreases the pain, and it correlated with a pain-free walking distance. And as Gerry O'Sullivan just mentioned, that there is no arterial brachial pressure index, or whatever physically to measure this.
Of course we have clinical measurements like the duplex and the MRVs, etc., and so in fact what we are used to and we are aware of is that you have quality of care, quality of life, clinical opinion, and clinical measures. But we need something else.
There is also a case-mix variable, which is not in these systems, and it influences the outcome significantly. If you look at these two patients, which are not shown yet, but they have the same VEINES-QOL/Sym, they have the same CF, they have the same VCSS, and same Villalta,
but unfortunately they can be very, very different. So this relates to the fact that you also have to look at age, gender, and the co-morbidity. And that altogether influences the measures that you need to quantify the outcome of your treatment. So, as said, we have patient-reported experience measures,
you have quality of life, clinical opinion, clinical measures, and the case-mix variables. That should be the venous outcome set. And we are working now closely with ICHOM, which is the International Consortium for Heath Outcomes Measurement
with Michael Porter and try to come up with a data set for all venous disease, which we can use in the future to measure the outcome of the patients that we treat. Thank you very much.
- Thank you so much. We have no disclosures. So I think everybody would agree that the transposed basilic vein fistula is one of the most important fistulas that we currently operate with. There are many technical considerations
related to the fistula. One is whether to do one or two stage. Your local criteria may define how you do this, but, and some may do it arbitrarily. But some people would suggest that anything less than 4 mm would be a two stage,
and any one greater than 4 mm may be a one stage. The option of harvesting can be open or endovascular. The option of gaining a suitable access site can be transposition or superficialization. And the final arterial anastomosis, if you're not superficializing can either be
a new arterial anastomosis or a venovenous anastomosis. For the purposes of this talk, transposition is the dissection, transection and re tunneling of the basilic vein to the superior aspect of the arm, either as a primary or staged procedure. Superficialization is the dissection and elevation
of the basilic vein to the superior aspect of the upper arm, which may be done primarily, but most commonly is done as a staged procedure. The natural history of basilic veins with regard to nontransposed veins is very successful. And this more recent article would suggest
as you can see from the upper bands in both grafts that either transposed or non-transposed is superior to grafts in current environment. When one looks at two-stage basilic veins, they appear to be more durable and cost-effective than one-stage procedures with significantly higher
patency rates and lower rates of failure along comparable risk stratified groups from an article from the Journal of Vascular Surgery. Meta-ana, there are several meta-analysis and this one shows that between one and two stages there is really no difference in the failure and the patency rates.
The second one would suggest there is no overall difference in maturation rate, or in postoperative complication rates. With the patency rates primary assisted or secondary comparable in the majority of the papers published. And the very last one, again based on the data from the first two, also suggests there is evidence
that two stage basilic vein fistulas have higher maturation rates compared to the single stage. But I think that's probably true if one really realizes that the first stage may eliminate a lot of the poor biology that may have interfered with the one stage. But what we're really talking about is superficialization
versus transposition, which is the most favorite method. Or is there a favorite method? The early data has always suggested that transposition was superior, both in primary and in secondary patency, compared to superficialization. However, the data is contrary, as one can see,
in this paper, which showed the reverse, which is that superficialization is much superior to transposition, and in the primary patency range quite significantly. This paper reverses that theme again. So for each year that you go to the Journal of Vascular Surgery,
one gets a different data set that comes out. The final paper that was published recently at the Eastern Vascular suggested strongly that the second stage does consume more resources, when one does transposition versus superficialization. But more interestingly also found that these patients
who had the transposition had a greater high-grade re-stenosis problem at the venovenous or the veno-arterial anastomosis. Another point that they did make was that superficialization appeared to lead to faster maturation, compared to the transposition and thus they favored
superficialization over transposition. If one was to do a very rough meta-analysis and take the range of primary patencies and accumulative patencies from those papers that compare the two techniques that I've just described. Superficialization at about 12 months
for its primary patency will run about 57% range, 50-60 and transposition 53%, with a range of 49-80. So in the range of transposition area, there is a lot of people that may not be a well matched population, which may make meta-analysis in this area somewhat questionable.
But, if you get good results, you get good results. The cumulative patency, however, comes out to be closer in both groups at 78% for superficialization and 80% for transposition. So basilic vein transposition is a successful configuration. One or two stage procedures appear
to carry equally successful outcomes when appropriate selection criteria are used and the one the surgeon is most favored to use and is comfortable with. Primary patency of superficialization despite some papers, if one looks across the entire literature is equivalent to transposition.
Cumulative patency of superficialization is equivalent to transposition. And there is, appears to be no apparent difference in complications, maturation, or access duration. Thank you so 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.
- This one is an easier publication we did, but I do think it's interesting because there are no data for real in the use of the aquatic environment for our lymphedema patients. I have no conflicts of interest to declare, but I declare that I'm really interested in this topic because if you look at the Global Spa & Wellness Summit report,
every single year this is the amount of money that are spent in the business of the aquatic environment and of the spa centers. And we are not behaving so well as vascular specialists because what you're looking at over here is a vision of the literature showing that muscle skeleton system data
are out there in the literature for the benefits of the effects of the aquatic environment, but we as vascular specialists are not producing so much data. Before the publication we put on Phlebology on this topic, just these six papers were dealing with the use
of the aquatic environment for lymphedema patients, and all of them are basically on quality of life measurements, not really on objective data of drainage, so every single day in nice hotels also like this one, you have people going inside the pool
and doing all of these activities, not really knowing what's going on inside their venous system, and something cool could actually happen because if you really think about that every single centimeter of water is performing 0.7 millimeters of mercury in terms of standing load,
so when I have a patient standing up inside the pool at 120 centimeters of depth, his feet is actually over one by 88 millimeters of mercury, so four times the stockings we are usually prescribing. We also know that, of course, activating the muscle pump is fundamental, so what we did was activating
the muscle pump inside the aquatic environment, creating a standardized protocol of exercises that we tested on 32 lower limbs of 16 patients affected by bilateral lymphedema. These patients went inside the pool for doing the standardized protocol:
50 minutes per session, twice per week, for a total of five sessions. The protocol is published on Phlebology, so you can download that for free. Basically it's an activation of all the joints of the lower limb.
What you can have after five sessions of this protocol is a significant reduction of the lower limb volume, that by more than 300 mils. The circumferences of the leg and the subcutaneous thickness measured by ultrasound is significantly decreasing, but the interesting part is this one, I think.
You see over there Michael Jackson with the Moonwalk because we were having patients walking backward because you have the biggest activation of the ankle at that point, and it was interesting to notice that the range of motion of the ankle was increase of up to four degrees, and if you put that into statistics,
it's really interesting to notice that the volume reduction was directly related with a 0.4 correlation to the increase in the ankle motion. The evidence of feeling of the leg was decreased from 7.3 to 5.5 out of ten as a score. The functional ambulation classification,
which is a score for debility of walking, was not significantly changed. Again, everything is on Phlebology if you want to download it, and now we are doing other investigations because of course we could bring some about not just the physical property
of the aquatic environment, but also the chemical properties of the kind of water we are using and on the temperature that we want to use over that. So at the current moment I cannot discuss that. We are under a grant of investigation, but for sure I do think this is a way to go
because it's like killing two birds with one stone because indeed you can have patients that are hypomobile or that are, for example, obese that can perform exercises inside the aquatic environment that they could not perform outside the pool, but I have to say that we didn't find anything new because the guy you see
over there is Conrad Jobst. There is a nice quote by van der Stricht. He was saying we should know the history so to avoid wasting our time trying to open doors that were already opened by others, and the door was already opened by Jobst
because as you know he was an engineer. He was affected by an ulcer and in reality he noticed that when he was standing inside his pool, his ulcers was getting better. Being an engineer he understood that it was related to the standing though and so he created the concept
of the graduated pressure that you have inside the water in the stockings we are now prescribing that are then son of the aquatic environment.
- 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.
- So I'd like to thank Dr. Ascher, Dr. Sidawy, Dr. Veith, and the organizers for allowing us to present some data. We have no disclosures. The cephalic arch is defined as two centimeters from the confluence of the cephalic vein to either the auxiliary/subclavian vein. Stenosis in this area occurs about 39%
in brachiocephalic fistulas and about 2% in radiocephalic fistulas. Several pre-existing diseases can lead to the stenosis. High flows have been documented to lead to the stenosis. Acute angles. And also there is a valve within the area.
They're generally short, focal in nature, and they're associated with a high rate of thrombosis after intervention. They have been associated with turbulent flow. Associated with pre-existing thickening.
If you do anatomic analysis, about 20% of all the cephalic veins will have that. This tight anatomical angle linked to the muscle that surrounds it associated with this one particular peculiar valve, about three millimeters from the confluence.
And it's interesting, it's common in non-diabetics. Predictors if you are looking for it, other than ultrasound which may not find it, is calcium-phosphate product, platelet count that's high, and access flow.
If one looks at interventions that have commonly been reported, one will find that both angioplasty and stenting of this area has a relatively low primary patency with no really discrimination between using just the balloon or stent.
The cumulative patency is higher, but really again, deployment of an angioplasty balloon or deployment of a stent makes really no significant difference. This has been associated with residual stenosis
greater than 30% as one reason it fails, and also the presence of diabetes. And so there is this sort of conundrum where it's present in more non-diabetics, but yet diabetics have more of a problem. This has led to people looking to other alternatives,
including stent grafts. And in this particular paper, they did not look at primary stent grafting for a cephalic arch stenosis, but mainly treating the recurrent stenosis. And you can see clearly that the top line in the graph,
the stent graft has a superior outcome. And this is from their paper, showing as all good paper figures should show, a perfect outcome for the intervention. Another paper looked at a randomized trial in this area and also found that stent grafts,
at least in the short period of time, just given the numbers at risk in this study, which was out after months, also had a significant change in the patency. And in their own words, they changed their practice and now stent graft
rather than use either angioplasty or bare-metal stents. I will tell you that cutting balloons have been used. And I will tell you that drug-eluting balloons have been used. The data is too small and inconclusive to make a difference. We chose a different view.
We asked a simple question. Whether or not these stenoses could be best treated with angioplasty, bare-metal stenting, or two other adjuncts that are certainly related, which is either a transposition or a bypass.
And what we found is that the surgical results definitely give greater long-term patency and greater functional results. And you can see that whether you choose either a transposition or a bypass, you will get superior primary results.
And you will also get superior secondary results. And this is gladly also associated with less recurrent interventions in the ongoing period. So in conclusion, cephalic arch remains a significant cause of brachiocephalic AV malfunction.
Angioplasty, across the literature, has poor outcomes. Stent grafting offers the best outcomes rather than bare-metal stenting. We have insufficient data with other modalities, drug-eluting stents, drug-eluting balloons,
cutting balloons. In the correct patient, surgical options will offer superior long-term results and functional results. And thus, in the good, well-selected patient, surgical interventions should be considered
earlier in this treatment rather than moving ahead with angioplasty stent and then stent graft. Thank you so much.
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.
- [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.
- 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.
- 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.
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