- This is a little bit more detailed explanation of the pathophysiology behind Type IV AVM's. Medical disclosures are none. And this is the Yakes classification and this is Type IV lesion we are going to talk about now. So, this angioarchitecture has not been described before, and was first described in the Yakes classification.
What is so unique? It has multiple arteries, arterioles, but these arterioles form innumerable fistulas that are of a microsize, and they infiltrate the affected tissue. So, this is, this can affect every kind of tissue,
skin involvement and muscle involvement, and other than brain AVM, bleeding occurs if mucosa involvement is present or if an ulcer is present. So, we have to think about the definition of an AVM, which is an artery to vein connection
without an intervening capillary bed. But, what applies in Type IV? As you can see here, very nice example of this infiltrating type is that the tissue where the AVM is located is also viable, so the assumption is that
normal capillary beds are interspersed into these innumerable AVMs existing next to the malformed AVM fistulas, and this is a new definition of AVM. So, how to access this lesion? Of course, transarterial is possible
with a catheter or micro catheter. If anatomy doesn't allow transarterial approach, direct puncture is an option. Also, as you can see, in the direct puncture in the lower video, you can see the venus drainage of these fistulas,
and direct puncture of the vein compressed to reflux ethanol into the fistulas is also an approach. But, what is the challenge here? If you want to treat this lesion, you have to keep in mind
that you don't want to occlude the capillaries that are supplying the tissue. So, to find the right treatment approach, the physiologic concept is often important to understand that the arteriovenous fistulas drain into multiple veins and arterialize these veins
so we have a high pressure on this venus outflow site. The normal capillaries have a normal outflow too but this is of lower pressure, and this comes to competition between the arterialized veins and the normal venus outflow, which is, which is inferior to the normal capillary outflow.
So, what follows is a restriction of normal tissue flow with back-up to the capillaries, and backing up into the arterial inflow. So, we have the situation that the arterial venus fistulas have a lower pressure, lower resistance, and an increased arterial flow
compared to the normal capillaries, and this has to be taken into advantage for treatment. How can this be achieved? Thicken the fluid and dilute the ethanol by creating a mixture of 50/50 contrast and ethanol. So, this mixture will follow the preferential flow
into the arteriovenous fistulas in transarterial injections bearing the normal capillaries. So, if it's possible to puncture into the fistulas, pure ethanol can be used, but especially in transarterial access where normal nutrient vessels can be filled,
50:50 mixture contrast is the key to treat a Type IV AVM, Type IV Yates AVM, and here, you can see, using this approach, how this AVM can partly be treated in many several treatment sessions. And here you can see the clinical result. So, this huge ulcer, after seven treatments, healed
because of the less venus hypertension in the lesion. So the additional benefit of 50/50% ethanol contrast mixture is that your injection is visible on flouroscopy so you can see if which vessels you are including. You can react and adjust the pressure you're injecting. So, it also has to be considered
that the more you give diluted, the more total ethanol can be needed, but it's not efficient in larger vessels. This is also the advantage that you just treat the microfistulas. It's of importance that you use non-ionic contrast
as ionic contrast precipitates in the mixture. So here, you can see again, see the Type IV AVM of the arm and hand, which I already showed in my first talk, and here, you see the cured result after multiple sessions showing good arterial drum without fistulas remaining.
So, the conclusion is that Yakes Type IV is a new entity. It's crucial to understand the hemodynamics and the concept of 50/50 contrast ethanol mixture to treat this lesion with also a curative approach. Thank you very much.
- Thank you so much, Peter. So, after interesting pictures of a clear disease, let's see pictures of a normal subject, and let's see if compression can have a meaning on them. We published these data on JVS. We have no conflict of interest to declare, apart of the fact that the stockings
that were used were donated by MEDI. But I am quite conflicted when I'm looking at these commercials like this one that is stating, for example, that whatever kind of compression you can find in a shop, can actually aid in performance or improve blood circulation, whatever improving
blood circulation means according to this ad. So, let's have a look a little bit at the literature and let's see, for example, that if we have a healthy subject that is running for 10 kilometers wearing 25 to 35 millimeters of mercury, where we know from the literature that this guy
will have lower limb volume control, that there will be no actually benefit in terms of symptoms. So, if you really look at the revision of the literature, what we can see is that the only thing that has been demonstrative with these compression garments is that we have a benefit just
in a delayed muscle soreness onset. They are like other interesting data, or they are like this paper showing that there is a dose-related fact in compression in hundreds, and this is a study done with electromyography, for example, showing that just a 30 millimeter mercury rather than 18
of sham are able to impact on the pressure exertion on the tricep soleus. So, what should we say to our friends when they're asking us if they should go walking eventually with stockings, and eventually with what kind of compression? To answer to this question,
we enrolled 10 physically active, healthy volunteers. They underwent, of course, an ultrasound checkup. We had them come into our university, walking on a treadmill in a standardized way, and I do think that always standardization or reproducibility, that must be in our mind when we are doing these investigation.
We are then walking without stalkings, and the following week, same kind of walk with stockings. To standardize the walk, we use the Tanaka's formula, which means 70% of the maximum heart rate of every single subject so that we were talking about the same values in terms of excursion also,
and we measure the lower limb volume with a Concesa formula or the truncated cone tape measurement. We use the Borg scale to evaluate the excursion which is a scale that is ranging from six to 20, where six is no effort, and 20 is the maximum effort you can get. Very important thing is always to report the interface
pressure measurement so we know that the stockings we were using were performing, in average, 24.6 millimeter of mercury. And what we can say now is that if we have a subject, like a healthy subject that is walking for 30 minutes in a standardized way on a treadmill, the lower limb volume
is not going to significantly change after those 30 minutes, but if he's running at least 24 millimeter of mercury, this lower limb volume will decrease by 5%. Now, the interesting thing is that the perceived exertion with the validated scale of Borg will decrease from 14 to 11, so with a significant decrease
in the perceived exertion. So, now we can say to our friends that, if they will wear at least 24 millimeter of mercury, and they will walk for 30 minutes in a standardized way, they will feel less tired, but what if these friends of ours will say to us
that they want to go walking with a dog, so intermittently, so stopping and going, and stopping and going, what do we really know about the difference in intermittent versus continuous walking for our lower limb venous drainage? The only paper I was able to find was this one about
the performance of multiple sclerosis patients in intermittent versus continuous walk, so it has nothing to do with our own venous ward. So, we did another publication in International Angiology where we used golfers because, if you really think about that, golfers are walking intermittently.
They go to the ball and then they start again, and we used the sham versus 18 versus 23 in placebo, and randomized, and lined the way. Of course, at the hole one, you are not the same as the hole 18 in terms of pressure exertion, so we use the Borg scale, also, in this case,
and, long story short, what you can see is that if you are 18 holes walk, you will have a lower limb volume that will increase by 5% if you are not using ready compression. If you're using 18, your lower limb volume will remain the same.
If you are using 23, your lower limb volume will decrease by 4%. Now, the interesting thing is that also in this study, there was, again, placebo organized in blind, just a group with 23 was reporting a significant decrease in the Borg scale.
So, of course, with the bias of combining the two data, we can see that around 23, 24 millimeter of mercury, unnecessary to impact the perceived exertion. Of course, now, we are literally down on our knees collecting data to explain the basic science behind this. We are under a data embargo with the Italian Ministry
of alpha grant, so I hope that soon we will be able to deliver this data with a team that is involved and that I do thank a lot. We will deliver part of this data the next meeting we will have on the Italian Alps next January, and another data set will be presented at the AVF
next February, and this is a chance to thank, of course, the AVF friends that got us over here, so thank you Lowell and thank you Jose.
- [Narrator] So how can we evaluate flow? I'm going to answer some of that, that when is good and when is it good enough? We don't know the answer yet. These are my disclosures. So, what do we currently do to evaluate flow after say an iliac stenting procedure?
Most of the time we're eyeballing it. We're looking for absence of collaterals and speed of contrast emptying. For example, in this case, this gentlemen with lots of collaterals, we've stented him, the collaterals are gone.
So, really it's good enough when the stent stays open and even more importantly when the patients symptoms improve or resolve. But is there someway we can get a more objective measure while we're doing the procedure of what's good enough? So my training before I went to medical school
was in chemical engineering, and we worked a lot on this sort of thing. Clogging up pipes, oil pipes, and gasoline pipes. Can we apply these flow dynamics to the venous system? Well it's really not as simple as looking at flow in a rigid pipe.
We talk about a lot in vascular surgery about Poiseuille's Law of fluid mechanics, which shows that flow, Q, is related to drop in pressure, radius of the vessel, viscosity, and length. However, this is assuming that the tube is straight and rigid.
So it might work for a trachea, but as we know, veins are curvy and not rigid. It assumes that tube is circular. This is an IVUS image, veins are not circular, that the radius is constant, in veins it changes, that the flow is laminar,
smoked cure laminar at the bottom, turbulent at the top, and sometimes veins have turbulent flow. And then finally, that the flow is Newtonian. So what's the difference between these two? So a Newtonian fluid, is one that has a constant viscosity at a given pressure and temperature.
So gasoline, that is a Newtonian fluid. It's easier to deal with, with chemical engineering than say oil, which is a slurry. Water is Newtonian, and this was my senior project in chemical engineering, very fun, distillation of alcohol, Newtonian fluid.
Non-Newtonian fluids are cool because of viscosity changes with shear. So Rheopectic, is things like printers ink, which becomes more thick with shear, or synovial fluid, or lubricants. Thixotropic, also fun to say,
is something that increases, or decreases with shear. So ketchup, Lahar, so when the mountain turns to liquid when it's flowing, and blood. So bottom line of this physics review is, that the simple physics formulas with tubes and simple fluid, don't work well in veins,
and you would need to make a model for every single patient if the patient was the factory with the pipes going through it, you would need one for everybody. Is there a surrogate marker that we can use like ultrasound, to predict stent failure, given that we can't do
a perfect physics model. Currently we're using flow volumes in dialysis access to predict accuracy, and we should learn how to do, see whether this will work in veins. So right now we're maximizing flow by using appropriately sized stents,
trying to cover all disease, anticoagulation to control viscosity, and knowing that the longer the length, the shorter lesions do better. So duplex scanning volume flow can be calculated with this equation,
I'm just going to leave this up here briefly that you can look it up, on how to calculate flow, and this is slides courtesy of Dr. Zierler, who really should be giving this talk cause he knows a lot more about this than I do. But what you do is, you expand your Doppler sample volume,
to include the entire lumen. You want to find a circular part of the vein that's fairly straight without turbulence, and then your machine can calculate the flow volume. So Dr. Luries group, one of his grad students, did a study in 2002, looking in normal patients
in deriving flow volumes, and showed that it was reproducible. So here's an example of flow through an iliac stent that again avoiding turbulence, branching, curving and irregular shape, that shows a flow volume. And from the University of Washington
they're studying this, and they're finding, unfortunately there's a large range. So what we need to do in the future, is to see whether there's intra and intra related reliability of flow volumes in both normal and stented patients
measure flow volumes before and after intervention, and the prospectively follow these patients to see if we can reliably predict what flow is needed to keep a stent open. Controlling for things like viscosity if we can. And understanding that finding a perfect flow model
is going to be challenging for the reason I told you before. But finding a reliable surrogate marker may be possible. Thank you.
- Thank you chairman, ladies and gentlemen. I have no conflict of interest for this talk. So, basically for vTOS we have the well known treatment options. Either the conservative approach with DOAC or anticoagulation for three months or longer supported by elastic stockings.
And alternatively there's the invasive approach with catheter thrombolysis and decompression surgery and as we've just heard in the talk but Ben Jackson, also in surgeons preference, additional PTA and continuation or not of anticoagulation.
And basically the chosen therapy is very much based on the specific specialist where the patient is referred to. Both treatment approaches have their specific complications. Rethrombosis pulmonary embolism,
but especially the post-thrombotic syndrome which is reported in conservative treatment in 26 up to 66%, but also in the invasive treatment approach up to 25%. And of course there are already well known complications related to surgery.
The problem is, with the current evidence, that it's only small retrospective studies. There is no comparative studies and especially no randomized trials. So basically there's a lack of high quality evidence leading to varying guideline recommendations.
And I'm not going through them in detail 'cause it's a rather busy slide. But if you take a quick look then you can see some disparencies between the different guidelines and at some aspects there is no recommendation at all,
or the guidelines refer to selected patients, but they define how they should be selected. So again, the current evidence is insufficient to determine the most clinically and cost effective treatment approach, and we believe that a randomized trial is warranted.
And this is the UTOPIA trial. And I'm going to take you a bit through the design. So the research question underline this trial is, does surgical treatment, consisting of catheter directed thrombolysis and first rib section, significantly reduce post-thrombotic syndrome
occurrence, as compared to conservative therapy with DOAC anticoagulation, in adults with primary upper extremity deep vein thrombosis? The design is multicenter randomized and the population is all adults with first case of primary Upper Extremity
Deep Venous Thrombosis. And our primary outcome is occurrence of post-thrombotic syndrome, and this the find according the modified Villalta score. And there are several secondary outcomes, which of course we will take into account,
such as procedural complications, but also quality of life. This is the trial design. Inclusion informed consent and randomization are performed at first presentation either with the emergency department or outpatient clinic.
When we look at patients 18 years or older and the symptoms should be there for less than 14 days. Exclusion criteria are relevant when there's a secondary upper extremity deep vein thrombosis or any contra-indication for DOACs or catheter directed thrombolysis.
We do perform imaging at baseline with a CT venography. We require this to compare baseline characteristics of both groups to mainly determine what the underlying cause of the thrombosis being either vTOS or idiopathic.
And then a patient follows the course of the trial either the invasive treatment with decompression surgery and thrombolysis and whether or not PTA is required or not, or conservative treatment and we have to prefer DOAC Rivaroxaban or apixaban to be used.
Further down the patient is checked for one month and the Villalta score is adapted for use in the upper extremity and we also apply quality of life scores and scores for cost effectiveness analysis. And this is the complete flowchart of the whole trial.
Again, very busy slide, but just to show you that the patient is followed up at several time points, one, three, six, and 12 months and the 12 months control is actually the endpoint of the trial
And then again, a control CT venography is performed. Sample size and power calculation. We believe that there's an effect size of 20% reduction in post-thrombotic syndrome in favor of the invasive treatment and there's a two-side p-value of 0.05
and at 80% power, we consider that there will be some loss to follow up, and therefore we need just over 150 patients to perform this trial. So, in short, this slide more or less summarize it. It shows the several treatment options
that are available for these patients with Upper Extremity Venous Thrombosis. And in the trial we want to see, make this comparison to see if anticoagulation alone is as best as invasive therapy. I thank for your attention.
- Thanks Bill and I thank Dr. Veith and the organizers of the session for the invitation to speak on histology of in-stent stenosis. These are my disclosures. Question, why bother with biopsy? It's kind of a hassle. What I want to do is present at first
before I show some of our classification of this in data, is start with this case where the biopsy becomes relevant in managing the patient. This is a 41 year old woman who was referred to us after symptom recurrence two months following left iliac vein stenting for post-thrombotic syndrome.
We performed a venogram and you can see this overlapping nitinol stents extending from the..., close to the Iliocaval Confluence down into Common Femoral and perhaps Deep Femoral vein. You can see on the venogram, that it is large displacement of the contrast column
from the edge of the stent on both sides. So we would call this sort of diffuse severe in-stent stenosis. We biopsy this material, you can see it's quite cellular. And in the classification, Doctor Gordon, our pathologist, applies to all these.
Consisted of fresh thrombus, about 15% of the sample, organizing thrombus about zero percent, old thrombus, which is basically a cellular fibrin, zero percent and diffuse intimal thickening - 85%. And you can see there is some evidence of a vascularisation here, as well as some hemosiderin deposit,
which, sort of, implies a red blood cell thrombus, histology or ancestry of this tissue. So, because the biopsy was grossly and histolo..., primarily grossly, we didn't have the histology to time, we judged that thrombolysis had little to offer this patient The stents were angioplastied
and re-lined with Wallstents this time. So, this is the AP view, showing two layers of stents. You can see the original nitinol stent on the outside, and a Wallstent extending from here. Followed venogram, venogram at the end of the procedure, shows that this displacement, and this is the maximal
amount we could inflate the Wallstent, following placement through this in-stent stenosis. And this is, you know, would be nice to have a biological or drug solution for this kind of in-stent stenosis. We brought her back about four months later, usually I bring them back at six months,
but because of the in-stent stenosis and suspecting something going on, we brought her back four months later, and here you can see that the gap between the nitinol stent and the outside the wall stent here. Now, in the contrast column, you can see that again, the contrast column is displaced
from the edge of the Wallstent, so we have recurrent in-stent stenosis here. The gross appearance of this clot was red, red-black, which suggests recent thrombus despite anticoagulation and the platelet. And, sure enough, the biopsy of fresh thrombus was 20%,
organizing thrombus-75%. Again, the old thrombus, zero percent, and, this time, diffuse intimal thickening of five percent. This closeup of some of that showing the cells, sort of invading this thrombus and starting organization. So, medical compliance and outflow in this patient into IVC
seemed acceptable, so we proceeded to doing ascending venogram to see what the outflow is like and to see, if she was an atomic candidate for recanalization. You can see these post-thrombotic changes in the popliteal vein, occlusion of the femoral vein.
You can see great stuffiness approaching these overlapping stents, but then you can see that the superficial system has been sequestered from the deep system, and now the superficial system is draining across midline. So, we planned to bring her back for recanalization.
So biopsy one with diffuse intimal thickening was used to forego thrombolysis and proceed with PTA and lining. Biopsy two was used to justify the ascending venogram. We find biopsy as a useful tool, making practical decisions. And Doctor Gordon at our place has been classifying these
biopsies in therms of: Fresh Thrombus, Organizing Thrombus, Old Thrombus and Diffuse Intimal thickening. These are panels on the side showing the samples of each of these classifications and timelines. Here is a timeline of ...
Organizing Thrombus here. To see it's pretty uniform series of followup period For Diffuse Intimal thickening, beginning shortly after the procedure, You won't see very much at all, increases with time. So, Fresh Thrombus appears to be
most prevalent in early days. Organizing Thrombus can be seen at early time points sample, as well as throughout the in-stent stenosis. Old Thrombus, which is a sort of a mystery to me why one pathway would be Old Thrombus and the other Diffuse Intimal thickening.
We have to work that out, I hope. Calcification is generally a very late feature in this process. Thank you very much.
- Good morning, I would like to thank Dr. Veith, and the co-chairs for inviting me to talk. I have nothing to disclose. Some background on this information, patients with Inflammatory Bowel Disease are at least three times more likely to suffer a thrombo-embolic event, when compared to the general population.
The incidence is 0.1 - 0.5% per year. Overall mortality associated with these events can be as high as 25%, and postmortem exams reveal an incidence of 39-41% indicating that systemic thrombo-embolism is probably underdiagnosed. Thrombosis mainly occurs during disease exacerbation,
however proctocolectomy has not been shown to be preventative. Etiology behind this is not well known, but it's thought to be multifactorial. Including decrease in fibrinolytic activity, increase in platelet activation,
defects in the protein C pathway. Dyslipidemia and long term inflammation also puts patients at risk for an increase in atherosclerosis. In addition, these patients lack vitamins, are often dehydrated, anemic, and at times immobilized. Traditionally, the venous thrombosis is thought
to be more common, however recent retrospective review of the Health Care Utilization Project nationwide inpatient sample database, reported not only an increase in the incidence but that arterial complications may happen more frequently than venous.
I was going to present four patients over the course of one year, that were treated at my institution. The first patient is 25 year old female with Crohn's disease, who had a transverse colectomy one year prior to presentation. Presented with right flank pain, she was found to have
right sided PE, a right sided pulmonary vein thrombosis and a left atrial thrombosis. She was admitted for IV heparin, four days later she had developed abdominal pains, underwent an abdominal CTA significant for SMA occlusion prompting an SMA thrombectomy.
This is a picture of her CAT scan showing the right PE, the right pulmonary vein thrombosis extending into the left atrium. The SMA defect. She returned to the OR for second and third looks, underwent a subtotal colectomy,
small bowel resection with end ileostomy during the third operation. She had her heparin held post-operatively due to significant post-op bleeding, and over the next three to five days she got significantly worse, developed progressive fevers increase found to have
SMA re-thrombosis, which you can see here on her CAT scan. She ended up going back to the operating room and having the majority of her small bowel removed, and went on to be transferred to an outside facility for bowel transplant. Our second patient is a 59 year old female who presented
five days a recent flare of ulcerative colitis. She presented with right lower extremity pain and numbness times one day. She was found to have acute limb ischemia, category three. An attempt was made at open revascularization with thrombectomy, however the pedal vessels were occluded.
The leg was significantly ischemic and flow could not be re-established despite multiple attempts at cut-downs at different levels. You can see her angiogram here at the end of the case. She subsequently went on to have a below knee amputation, and her hospital course was complicated by
a colonic perforation due to the colitis not responding to conservative measures. She underwent a subtotal colectomy and end ileostomy. Just in the interest of time we'll skip past the second, third, and fourth patients here. These patients represent catastrophic complications of
atypical thrombo-embolic events occurring in IBD flares. Patients with inflammatory disease are at an increased risk for both arterial and venous thrombotic complications. So the questions to be answered: are the current recommendations adequate? Currently heparin prophylaxis is recommended for
inpatients hospitalized for severe disease. And, if this is not adequate, what treatments should we recommend, the medication choice, and the duration of treatment? These arterial and venous complications occurring in the visceral and peripheral arteries
are likely underappreciated clinically as a risk for patients with IBD flares and they demonstrate a need to look at further indications for thrombo-prophylaxis. Thank you.
- Thank you very much again. Thank you very much for the kind invitation. The answer to the question is, yes or no. Well, basically when we're talking about pelvic reflux, we're talking really, about, possibly thinking about two separate entities. One symptoms relate to the pelvis
and issues with lower limb varicose veins. Really some time ago, we highlighted in a review, various symptoms that may be associated with the pelvic congestion syndrome. This is often, either misdiagnosed or undiagnosed. The patients we see have had multiple investigations
prior to treatment. I'm not really going to dwell on the anatomy but, just really highlight to you it is incompetence in either the renal pelvic and ovarian veins. What about the patterns of reflux we've heard from both Mark and Nicos what the pattern are
but, basically if you look a little more closely you can see that not only the left ovarian vein is probably effected in a round-about 60%. But, there is incompetence in many of the other veins. What does this actually have implication for with respect to treatment.
Implications are that you probably, if you only treat an isolated vein. There is a suggestion, that the long term outcomes are not actually as good. Now this is some work from Mark Whiteley's group because, we've heard about the diagnosis
but, there is some discussion as to whether just looking at ovarian vein diameter is efficient and certainly the Whiteley group suggests that actually diameter is relatively irrelevant in deciding as to whether there is incompetence in the actual vein itself.
That diameter should not be used as a single indicator. You may all well be aware, that there are reporting standards for the treatment of pelvic venous insufficiency and this has been high-lighted in this paper. What of the resuts, of pelvic embolization and coiling? The main standard is used, is a visual analog scale
when you're looking at pelvic symptoms to decide what the outcome may be. This is a very nice example of an article that was... A review that was done in Niel Khilnani's group and you can see if you look at the pre
and post procedural visual analog scales there is some significant improvement. You can see that this is out at one year in the whole. Now, this is a further table from the paper. Showing you their either, there's a mixture
of glue, coils, scleroses and foam. The comments are that, there are significant relief and some papers suggest its after 100% and others up to 80%. If you look at this very nice review that Mark Meissner did with Kathy Gibson,
you will see that actually no improvement in worse. There's quite a range there for those patients 53% of patients in one study, had no improvement or the symptoms were potentially worse. We know that those patients who have coil embolization will have reoccurrence of symptomatology
and incompetence up to about a quarter of the patients. What about varicose veins? The answer is there is undoubtedly evidence to suggest that there is physiological/anatomical incompetence in some of the pelvic veins in patients
who have recurrent varicose veins. Whether this is actually a direct cause or an association, I think it's something we need to have some further consideration of. As you know, there are many people who now would advicate actually treating
the pelvic veins prior to treating the leg veins. You can maybe discuss that in the question time. If we then look at a comparative trial. Comparing coils and plugs, you can see over all there really isn't no particular difference. If we then look again to highlight this,
which comes again from the Whiteley group. You can see that 20% of patients will have some primary incompetence but, it'll go up to around 30% if they are re-current. There is no randomized control data looking at this. What are the problems with coils?
Actually, a bit like (mumbling) you can find them anywhere. You can find them in the chest and also you can find that there are patients now who are allergic to nickel and the very bottom corner is a patient who's coils I took out by open laparotomy because they were allergic to nickel.
So, ladies and gentlemen I would suggest to you certainly, for continuing with pelvic embolization when doubtedly it needs some more RCT data and some much better registry data to look where we're going. Thank you very much.
- Hello, thank you again for the invitation. I have the disclosure here is kind of funny because I'm going to talk about CLaCS but I don't profit on that. Those are the most frustrating result on sclerotherapy and obviously death. These are very frustrating result. Sorry.
And this is not like funny but it's unfortunately the worst part is that all those cases are not published and that's less change from frustrating to devastating, the death cases. Let's talk about the less common, sorry,
the most common problems, skin ulcer. Like skin ulcer. Skin ulcer may be also terrible. Those are slides from my father's collection from the 60s probably. And I suggest you to read this paper.
It took me 20 years to get published with the help of Ted King of this hypothesis from the 70s and he studied on rabbit ears and I cannot have time to explain all that but he simulated the skin ulcer and showed that the causes the reflux to the arterial venous system
and how to avoid it, CLaCS is a great solution and by using the extra 75% due to its high viscosity, you avoid 100% of reflux to the arterial system. Matting is another problem.
Those are theories of my father as well. He said divided in two types of angiogenic where you inject on the telangiectasia and you destroy veins that you wanted to close or you didn't want to touch. And then you have reflux a new reflux and
a lot of telangiectasia. There would be occlusive, where you destroy too much, you destroy the drainage of those telangiectasias. And then how to avoid? Is to be less aggressive or to be more focal. That means treat only the feeder vein
and the telangiectasia and avoid injecting a lot of volume and because those sclerotic agents will reach another vein that you don't want to touch. Pigmentation is another problem. And to control pigmentation of course
you have to have less thrombus and once again ClaCS would be very nice idea because the transdermal lazer causes vein wall edema and contraction and then you inject the Dextrose 75%. And then you have less internal diameter
in the vein, that means you have less outflow, the Dextrose will stay there it's a synergy, and you have less clot, less pigmentation. Also Dextrose is a medium power sclerosing agent that doesn't cause too much pigmentation as the other agents.
Well once again my father, and my father is at the hospital right now, and he probably will not survive, but here is a tribute for him. And he developed this surgical treatment of the telangiectasia by removing
the feeder veins. And, sorry. Here a study with phlebography showing a double perforant insufficient vein, and these telangiectasia wouldn't respond. And that's a complex telangiectasia, not a simple telangiectasia.
Like here another example, the phlebectomy showing the result of the treatment of telangiectasia. Well, diagnosis is very important if you are a skipper of a boat, if you have a special device to diagnose you certainly will have a better result.
And here are very tricky, looks simple to treat but as you compress you see there is a reflux, and this reflux is going have five feeder veins and one is going to the reflux in saphenous vein and patient the patient is CEAP1. Well, I also.
Sorry. Next slide. If you are a painter and you want to paint this wall, it's not easy you need to find a feeder vein and that's why I've developed this classification where you have three, two questions
and you look for varicosities and telangiectasias and here you have, lets go fast, the ultrasound showing reflux and the augmented reality showing if there is feeder vein or not. And here a good example of a patient that was,
the examination would lead to a CEAP 1, but as we exam, we noticed that she's score nine, where she had a long reflux asymptomatic that was treated with endovenous lazer phlebectomy and CLaCS, and that's how we got the result. Then treatment failure is also can be avoided
by a good classification and then CLaCS. If you want to learn more about that, we have a congress, it's going to be the ninth in IMAP in Saul Paulo next year, and I kindly invite you to participate. Thank you.
- Thank you very much both. It was a great pleasure to see you. I continue to be grateful for the guidance you have given me over the years. Thank you to the organizers for advising me to speak. These are my disclosures. So really there are two questions posed by this topic.
One is, is the patent popliteal vein necessary? I would assume from this is it necessary for patency and symptom relief to be achieved in treating patients with both acute DVT and potentially chronic. And has the evolution formic mechanical therapy
led to over stenting. Which means we have to ask the question what is an appropriate rate for stenting. I am not sure we know the answer to that. So being able to answer over stenting requires us to know how many patients
actually need the stent in the first place in acute DVT treatments. The problem is essentially this. Is that when we form lithic therapies and this is a classic case of treatment formed with formic and mechanical device
but without a follow up using lithic in the patient for whom lithic was not feasible. You end up opening up a vessel but you can see from the image on the left hand side that there is a degree still of luminol contrast deficit suggesting some cult left behind
in the external iliac vein. Well there is obviously a May-Thurner legion at the top. The question of over stenting is one of do we just stent the May-Thruner and extend it down into the external iliac vein to trap that thrombus
or would a period of time of lithic have resulted in this clot resolving and not needed a stent at the end of it. To get to the question of how many people should be stented. The only way we can really do this
is try and exstipulate from the literature to some extent. This is the short and long term outcome from the Kevin study. Where there is ultrasound follow up of patients underwent standard treatment only.
And a additional group in the patients had catheter-directed thrombolysis. We can see there that the patients did six months in catheter-directed thrombolysis group is around 60%. And the patency seen with the non treated group
is around 40%. If we kind of use these numbers as a guide we probably expect therefore that the stent rate would be somewhere between 40 and 60 percent. To account for treating the outflow structure that presumably patients see at six months.
But this is clearly not a very rebost method of being absolutely clear on who needs stents. Additional method is we don't really have and answer for who should be stented at the end of a procedure. So if you look at the massive variability
in the other studies. We see that attract stent rate is approximately 28% for the study. Which is obviously a operative discretion and has been criticized for that reason. But there is no comment on the Popliteal vein
or Popliteal vein patency. Cavent did an stent rate of 15% again with no real comment on whether the Popliteal vein was open and it wasn't a prerequisite for treatment in the study. This contrast with the Ansberg Aspirex Registry.
Which is a registry of a purely mechanical device to aspirex clot and the stent rate is 100%. Baekgaard Copenhagen used a catered-directed thrombolysis with a mandated open popliteal vein for purpose to be in the study. He has a stent rate of 60%.
My own personal experience of 160 odd patients is that were stenting around 80% of patients with outflow legion at the end of treatment. And were not really bothered by whether the popliteal vein is clear or not. But that doesn't necessarily answer the question
whether it makes a difference in the long run. So its very difficult even looking at the data we have because there is no standard definition of what a outflow stenosis is. There is no objective measure for an outflow stenosis. So stenting becomes and operative discretion decision.
But you would have to say that if your taking purely mechanical devices and the stent rates are going up to 100% that the inclination would be that there is potential for formic mechanical therapy to lead to overstenting and increase use
for stents for sure. In our experience then we had 81 patients who had CDT alone verse 70 patients who had AngioJet Thrombectomy. The basic characteristics of the group are pretty much identical.
With similar ages and no difference between whether the thrombus with left side or right side of body or so on. And these are the patency curves for the different groups with equivalent primary, primary assisted and secondary patency over two yeas.
We had no difference in stent rates with the median stenting of 80% in both groups with two stents used in average for each of those patients. However in our practice AngioJet is rarely used alone. So we had 70 patients for whom AngioJet was used. 24 of those where AngioJet was used up front
as the first line of treatment followed by some CDT. We have tended find that if we wanted full clock clearance. We have always had omit to some extent. And single stage therapy is quite difficult to achieve unless you spent a lot of time in it.
Patency in the popliteal vein is clearly affected by some extent. These are our follow up results if we don't have a patent popliteal vein at the end. It does drop off in stent patency. So the conclusions then I think.
Is that patent popliteal vein is necessary for long term results. But you can still treat patients that have acute popliteal vein for larsons that is not a contraindication. Pure mechanical therapies may well lead to higher stent rate.
But is this a bad thing or a good thing? We don't really know this at this stage as to what the long term outcomes will be. Thank you very much.
- Ladies and gentlemen, I thank Frank Veith and the organizing committee for the invitation. I have no disclosures for this presentation. Dialysis is the life line of patients with end-stage renal failure. Hemodialysis can be done by constructing an A-V fistula, utilizing a graft or through a central venous catheter.
Controversy as to the location of A-V fistula, size of adequate vein and priority of A-V fistula versus A-V graft exists among different societies. Our aims were to present our single center experience with A-V fistulas and grafts. Compare their patency rates,
compare different surgical sites, and come up with preferences to allow better and longer utilization. We collected all patients who underwent A-V fistula or A-V graft between the years 2008 through 2014. We included all patients who had preoperative
duplex scanning or those deemed to have good vessels on clinical examination. Arteries larger than two point five millimeter and veins larger than three millimeter were considered fit. Dialysis was performed three times per week. Follow up included check for a thrill,
distal pulse in the arter non-increased venous pressure or visible effective dialysis and no prolonged bleeding. Any change of one of the above would led to obtaining
fistulogram resulting in either endovascular or open repair of the fistula. We started with 503 patients, 32 of which were excluded due to primary failure within 24 hours. We considered this, of course, the surgeon's blame. So we left with 471 patients with a mean age of 58 years,
51 were older than 60, there was a male predominance of 63%, and over half were diabetics. The type of fistula was 41% brachio-cephalic fistula, 30% radio-cephalic fistula, 16% A-V Graft, and 13% brachio-basilic fistula.
Overall, we had 84% fistulas and 16% grafts. The time to first dialysis and maturation of fistula was approximately six weeks. First use of grafts was after two weeks. 11 patients with A-V fistula needed early intervention prior to or after the first dialysis session.
In sharp contrast, none of the A-V grafts needed early intervention. 68 patients were operated for their first ever fistula without duplex scanning due to clinically good vessels. Their patency was comparable to those who underwent a preoperative scanning.
Looking at complications, A-V grafts needed more reintervention than fistulas. All of them were late. Infection was more prominent in the graft group and pseudoaneurysms were more prominent in the A-V fistula group, some of them occluded
or invaded the skin and resulted in bleeding. Here's a central vein occlusion and you can see this lady is after a brachio-basilic A-V shunt. You can see the swollen arm, the collaterals. Here are multiple venous aneurysms. Here's an ulcer.
When we looked at primary patency of A-V fistulas versus graft, A-V fistulas fared better than grafts for as long as five years. When you looked at 50% patency in grafts, it was approximately 18 months, in Fistula, 13. Here's an assisted primary patency by endovascular technique
and when we looked at the secondary patency for the first 24, two years, months, there was no difference between A-V fistulas and A-V grafts, but there's a large difference afterwards. Comparing radio-cephalic fistula to brachio-cephalic fistula there was really no big difference in maturation.
The time was approximately six weeks. As for primary patency there is a trend towards better patency with brachio-cephalic fistula after six months, one year, and two years, but it didn't reach statistical significance. For patients with diabetes,
differences were statistically significant. Brachio-cephalic fistula showed a trend toward shorter maturation time, needed less reintervention, and had a longer patency rate. In conclusions then, ladies and gentlemen, A-V fistula require a longer maturation time
and have higher pseudoaneurysm formation rate, but better patency rates compared to A-V grafts. A-V grafts have a faster maturation time, but more late interventions are required and infection is more common. Finally, diabetic patients have a better result
with proximal A-V fistulas. Thank you for the opportunity to present our data.
- Ladies and gentlemen, I have no disclosures. I'm in the robot for the first rib resection, but mostly for the veinous thrombosis, so it's going to be more about the vitals than general, the first rib resections, for arterial and neurogenic those. So, as you all know, we're treating the Paget-Schroetter Disease, which is a
effort thrombosis of the subclavian vein, it's a type of the Thoracic Outlet Syndrome and it's an excessive arm activity combined with a compressive element at the thoracic inlet. Here we see the compressive elements, which are the clavicle, first rib,
the anterior scalene, and the subclavius muscle. This is the clinical find, you see the swollen arm, and how do we manage this? With the thrombolytic therapy, anticoagulation, then the first rib resection, if necessary, subclavian venoplasty.
We think that at this time, there's not enough evidence of we think there's no role for anticoagulation alone, and we have the best long-term results with prompt thrombolytic therapy followed by first rib resection and short term anticoagulation. Although there are many controversies staying, which is:
A true pathophysiologic mechanism, the bilaterality of the disease, what is the ideal surgical approach, the extent of the first rib resections, need for scalenectomy, and an appropriate management of patients with prolonged subclavian vein occlusion.
Different surgical approaches are: The posterolateral thoracotomy, hardly used anymore, anterior thoracotomy, transaxillary, supraclavicular and infraclavicular approach, and then thoracoscopy. But all those surgical approaches have their shortcomings.
They're all "key hole surgery" with all surgical approaches, there's poor visualization of the medial aspect of the first rib, long thoracic nerve injury, possibility of it, injury of superficial cervical nerves, brachial plexus injury, and inadequate rib resection.
So here, you see the transthoracic approach, what we are doing with the Da Vinci robot, and we can visualize the medial aspect very well of the first rib. So it's a direct, minimally invasive, transthoracic approach to the resection of the first rib,
and we also perform scalenectomy. So how do we do it? First we've done the general anesthesia, single lung ventilation. It's four phases. First is the thoracic access, right lateral decubitus.
And here you see the incisions for the camera, the robotic endograsper, and the hook. Then very important is, this is your sight and you see the orientation where the cranial aspect is downwards, so here it's all happening here and this is the intercostal space.
That's in the beginning, you have to get used to that a bit. And then we create a floating rib. Sorry. And here, we would do a partial scalenectomy, and then in the third phase is the VATS transsection of the rib.
The fourth phase is a robotic assisted venolysis, where here we have freed the vein of all the scar tissue. Postoperative care, patient goes to regular ward, gets a chest tube, 10 or 15 cm water, a chest x-ray, and stays a mean hospital stay of two days. Here I can show you some footage.
So, we're entering the thoracic cavity. Here you see the trocar. This is still the old Da Vinci. The newer ones, we put the trocars more into a line and not in a V shape. The first rib is identified, it's here we go.
We open the pleura, then we perform scalenectomy and we create the floating rib. A lot of coagulation, as you see, cause everything's done with the cauterization hook. And then we cut the costo-sternal joint,
so we really have that medial aspect and that we can cut with the cauterization, then we have the VATS, you see it's moving a bit because the robot is installed and we do this via VATS, the cutting of the lateral part of the first rib. Okay.
I think I have to hurry in time, like this. Then the venolysis, just want to skip it a bit, where we remove all the tissue around the vein. Okay, the advantages is we have a complete visualization and resection of the anteromedial/costosternal region. We, of course, have the advantages of the Da Vinci system,
the 3D vision, the agility of the endowrist, additional venolysis that we can perform, and there is less nerve injury. Limitations is also the visualization of the posterior-lateral region, and can we perform a complete resection, especially in the cases of
a neurological task. The cost, of course, of the Da Vinci system, and the limitations is that you need the Da Vinci robot to perform the procedure. We are not able to perform an extensive neurolysis through the thoracic cavity, the transthoracic approach.
If we have a cervical rib it will be very hard to resect that rib, so we haven't done that yet, and of course if the patient had some paralysis of strength, or if we have problems with the transthoracic access. And then, the cost of course is the cost of your platform,
although that's not really the cost for the surgeon but for the hospital and institution, and the cost for the additional trocars and materials and disposal is a very low because we only use the cauterization. Thank you very much, and sorry that I exceeded my time.
- [Peter] Thanks, again. Let's stay right on track here, hopefully. So as this audience knows, and Joanne reviewed very nicely, deep vein thrombosis, it's common. It's a big problem, we all know that in this audience. Importantly, it really hasn't decreased
in terms of incidence over the last 20 years or more. The treatment, as you heard and know, is anticoagulation, but this confers a bleeding risk, and of course post-thrombotic syndrome is a big area of morbidity for patients. But certainly, the mainstays of therapy
to prevent PTS are rapid and therapeutic anticoagulation. That's really not argued. Leg elevation may help. Compression, controversial, may have little effect based on the Sox Trial. I know there's problems with that,
but, again, that's what the evidence shows. And even more so, the invasive techniques to clear the thrombus, CaVENT and ATTRACT, really is unlikely to be a game-changer, except maybe an iliofemoral DVT. So a couple things just to focus on is three main papers,
and these are a couple old agents, quinacrine and MTX, that may have some benefit in the venous thrombosis resolution in PTS. And lymphocytes are typically a cell not considered with DVT. Just a quick review of the models.
This is put out by Jose Diaz. This is, you can either ligate the IVC and produce thrombus that way to analyze, or narrow the IVC, and you get a stenosis and flow-related DVT. So this paper from Dr. Sarkar's group from Maryland looked
at Myeloid p53 in terms of venous thrombosis resolution. And quinacrine is a p53 agonist and shows some data that that may accelerate thrombus resolution. So looking here, these first graphs at day four and eight show no difference
if you genetically delete p53 in the mouse, but you do see bigger clots at Day 12, suggesting a resolution impact here. If you just knock out the p53 and the myeloid cells, again, the same effect is seen, with an increased thrombus weight at Day 12.
And these just show the pink staining is fibrosis, and it's greater when you knock out p53. And that's characterized and shown in the graph to your right. If you give quinacrine, the p53 agonist, no difference at day four,
smaller clots at Day 12, correlating, again, with a lesser amount of fibrosis in the clot, again the pink staining, compared to the control. And again, the percent fibrosis area is reduced. So whether you can use quinacrine to accelerate DVT resolution, I think, is of interest
and maybe on the forefront in the future, not that far away because it's a pretty safe agent. How 'about the lymphocyte? This's a little more basic biology. This was a nice paper put out and researched by a German group who looked
at the T effector memory cells, CD8 cells, and their role in thrombus resolution in thrombosis. And this is just a number of graphs showing flow cytometry, but the important is that the T effector memory cells were highest in the vein wall after experimental stenosis DVT model.
Now if you inhibit or genetically deplete those T effector memory cells, it increases or improves resolution with smaller clots area at four and 12 days, and that's graphically shown here. They looked at some factors
that are associated with thrombus resolution, and MMP-9 may have some effect in resolving the clot. But MMP-2 is not, nor was tPA, which is typical for plasmin activation. So it may not be through thos
however, you can see that the Mac2, which marks macrophages, were significantly greater in the control, compared to the T effector cell memory depleted mice, and there's increased amount of CD31 staining, suggesting it made more channels through that clot. And that's just shown in the graphs shown over here as well.
So, this is farther out, of course, and using anti-gamma interferon, which stimulates T effector memory cells to inhibit this function to accelerate DVT, would probably have to be given locally. You wouldn't want to give this systemically.
But this was an accompanying editorial to that paper that suggested this as a potential mechanism. OK, lastly, methotrexate and its effect on vein wall scarring in experimental deep vein thrombosis from Dr. Jaffer's group at Mass General, for who we collaborate with.
And this study had two hypotheses: one, that methotrexate may inhibit VT-induced inflammation and attenuate subsequent vein wall injury and may or may not impair thrombus resolution, based on its anti-inflammatory properties. So this was a stenosis model, total ligation.
And the dosing was given after the clot was created, which is clinically, I think, quite relevant. And you can see the amount that was given there, I think a clinically relevant dose. But looking at just the vein wall thickness, this is a circle staining again,
or sirius red staining rather. And you can see that the methotrexate had a thinner vein wall at the later time points characteristic in the mouse when post-thrombotic syndrome is likely, or what we characterize is that timeframe.
So it was reduced significantly. Concurrently, we saw a decrease in Collagen I and Collagen III, which are profibrotic genes, as well as FSP-1, which is a fibroblast-specific protein. But interestingly, no difference in TGF beta, which is also a profibrotic pathway.
So how 'about the translation here? Well, I think this one may be closest. Methotrexate is already being tested in arterial inflammation with the group
- 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 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 so much for having me here discussing about the results of one of our latest applications dealing with perforating veins. I have no conflicts of interest to declare. In this investigation we did about perforating veins that we could define as vessels that are draining blood from the surface
toward the deeper compartments of the leg. But are we sure it's really so? Because if we really go back in the literature and in time, and we look, for example, at this investigation by Johensgard done in the fifties what we see is that actually the posterior tibial vein
and the great saphenous vein are behaving like conjoined vessels. Let me get a little bit deeper in this. What you're looking at over here is the Hojensgard tracing of the pressures inside the venous system. The upper tracing is the posterior tibial vein.
The lower tracing is the great saphenous vein. So if you measure this pressure when we are walking what you see is that at the first step there is a steep increase inside the pressure inside the posterior tibial vein
that is not followed by an increase in pressure in the great saphenous vein. Like if there is a wall that is keeping the two systems separated. But, already at the second step, you see that these two vessels
are behaving exactly in the same way in terms of pressure, like if they are conjoined vessels indeed. And this is happening both in chronic venous disease, and in healthy controls as is stated most recently by Raceck. So, we try to focus in this investigation
on how we are defining incompetence of the perforating veins. That as we know, it's a diastolic flow in an outward direction, lasting 0.5 or 0.35 second. And we tried to assess these incompetence
with a brand new software called QDP. Because indeed, if you really think about how we are assessing these perforating veins, we are having, of course, the color, that is a qualitative measurement, and then we have the spectral analysis.
But remember that the spectral analysis is dependent on the tortuosity of the vessel. So, it really depends on where we are putting that simple volumes, and on how we are seering. QDP, as I was saying before, is a new software
that is giving you 256 simple volumes at the same time, independently by the tortuosity of the vessels, telling you the net direction of the flow. So, is this investigation, we enrolled 193 chronic venous disease patients. And what we did was,
looking at the redirection of perforating veins, as you can see in the study population was 443. And we look at the ones that were showing a traditional definition of incompetence, which means again that diastolic outward flow lasting more than 0.5, and the one that we are showing less than 0.5.
And then assessed them with a QDP. And what we saw is, that if we take into consideration the perforating vein with an outward diastolic flow lasting 0.5 second, just 84% of them in the thigh, and 20.6% of them in the leg
are actually having a net outward flow. This is pretty big if you really look at the data, because it means that we have a sensitivity in terms of the current definition of incompetence of the perforating vein of just 13.9%. This means that just 13.9% of time,
when we are seeing or manding our patients, an outward diastolic flow in the perforating vein, just in 13.9% of cases, the net flow direction is actually outward. Because the net direction is actually inward. To the contrary, for manding we will see our patients
with an outward diastolic flow lasting less than 0.5, while the specificity of that is good because it is 96.4%, so it's good to know that in this case we are pretty confident that the net flow direction will be inward. So we conclude the talk quoting Aristotle,
was saying that, "The aim of art is to represent not just the outward appearance of things, but also their inward significance." Just to go back to the concept of not just the outward diastolic flowing perforating veins, but also of the net flow direction.
This is a topic we'll discuss at the next meeting we'll be having in January in the Italian Alps, where I hope you will be there with us brainstorming about the guidelines involving also this one on perforating veins. Thank you so much.
- Thank you again Lowell, Josee, Ed for inviting me. Technical first approach is patient positions. You could ask your patient to move and to feel yourself as comfortable as possible. So you have to ask your patient to move. In this position again, you have to ask your patient,
you have to be as comfortable as possible for injection. For example, for small saphenous veins, this position, I do not like this position. I prefer this one. You have to ask your patient to put this foot
on the achilles tendon of their leg and this, you can see, this position allows us to relax the muscles and thus, have a bit of vision of the small saphenous vein to inject. It's quite easy,
it's not so complicated as the previous position. First of all, you have also to identify the vein and to see all the arteries around the vein. So you couldn't predict which of the arteries, because in this case, you have two arteries, but in this case, you have more than two,
you have possibly four arteries. I have to move them. So I have to teach you a trick. So when you identify your vein in a safe area, you put your probe and you have to draw a line
with a pastel pencil and like this, and this pastel pencil can mark in the gel. Like this, you're dealing with two zones. One zone, the examination area, so you could put your probe just above the line
and to the puncture area, where you will disinfect and you will puncture after the vein. So it's just to show you, with this pencil you can mark into the gel, so you identify the vein,
check you have no artery, like this is the perforator, so you can see small arteries... Not so small. Or like this, as I was showing you in the previous slides. So you mark the line
and like this, you have not to find again where to put your probe. It's quite easy. So you have time to prepare your foam, because you have not to check again
where is a safe area. Because the time elapse after preparing the foam and the injection of the foam, should be as short as possible. So with this small trick,
it's quite easy to put your probe and you will inject quite quickly. From production, so you could use a triple weight, but I do not like the triple weight, because in the previous slides,
with the previous speakers, you can see you can turn your hub more or less and the foam will be more or less dense. That's why I prefer a female-female connector. So I do not say that the foam is better quality, but you have always the same quality of foam
and with this, your foam could be dense, less dense, more dense and with this exact same quality of foam. So, ratio is 1 part liquid + 4 parts of air, according to the European guidelines.
So procedure must be entirely done under Duplex control, during the four stages. Vein to be treated, identified, detection of the possible nearby arteries. Vein puncture, check needle position. Injection.
Post-injection assessment, you have to control the filling of the vein by the foam. Doses. So you have to adapt your concentration according to the size of a vessel. For example, the vein's inferred to 4mm,
you have to inject 0.5 Polidocanol, also 0.2 to 0.5 STS. So per 4 and for 6, 1% Polidocanol, 0.5 to 1% of STS. So per 6 and for 8, 2% Polidocanol, 1% STS.
So per 8, 3% Polidocanol, 3% STS. It's a (mumbles) today in Europe. But you have also to measure your vein. So you can measure Intima-Intima in a border. So for example, in this case, it's 4.5,
so you will inject foam 1% Polidocanol. But if you measure your vein at the Dist outside border, it's 6.2mm, so we will inject 2%. So I prefer this measure, Adventice-Adventice. Always more than less.
Longitudinal or cross-section, it's equivalent, so there's no better technique. Duplex scan, 14 at the minimum, your probe, you must be 14 or 18 Mhz. So you puncture your vein and you check during all the procedure,
where the foam is going, so you keep seeing your screen. All the time, you can see sometimes some foam going like this. And after, to check, after the procedure, where I insert the foam.
And you could have a segment spasm filled with foam and this, nothing of foam, so a second injection is recommended. In conclusion, procedure must be entirely done under Duplex, check before injection the proximity of small arteries
and respect doses and volumes. Thank you for your attention.
- [Constantino] Thank you, Mark, thanks for the organizers for having me. I'm really going to summarize a lot of what you've heard already, all these different devices, and how they come together in treating these patients without lytics.
Obviously when we're treating in terms of percutaneous techniques in thrombectomy, we know about catheter-direct thrombolysis, but how we put together all these different mechanical techniques you've heard about today?
I like to think about them as fragmentation. The Rheolytic Thrombectomy device, then different types of vacuum assisted and suction devices and then extraction devices. And then is how I like to consider them, as we start making our choice of what to use.
And why do we have these devices? Because sometimes the patient's contraindicated for thrombolysis or there's failure of thrombolysis, or maybe we just need a kickstarter, a rapid response, and we want it, get flow established and we do this as we continue
with some type of combination therapy. What's the ideal device, and we start considering, I think it's something that's simple, easy to use, low profile, minimal blood loss, which is really important to consider when we're
in the venous system, especially when you're looking at suction devices, that can be done with moderate sedation, percutaneously, and does not traumatize the vessel that we're working on. So let's go through these and wrap it all together.
Fragmentation, initially we had just bending the catheter, like a pigtail catheter in, and then most of the time we got our early, our early experience in the pulmonary artery. Patient's with massive pulmonary embolism, and of course, these had very high mortality rate
in these patients, but we saw that we could break up clot, and could break down the pressure. When you look at studies, they found that this to be clinically, was, say, helpful, in about 86% of patients. What about having mechanical type of device
that can do this? So you're looking at devices predominantly used in the venous system in really dialysis type work, but we applied them in other types of veins, atrial tola device, six French device, or a cleaner type of device.
Again, a mechanical agitates create fragmentation, usually battery operated, and again, something you can use in that venous system, to try to get up, get some clot out. Macerate it, and create flow. I think the limitation is is how much thrombus
are we dealing with, and how quickly can you establish flow? Rheolytic systems, you already heard talks abut this, I think the take home message with this type of device is that when you look at PEARL Registry, we can see that you can get a one in done type
of scenario with this, but most of those are done with combination lytics. We see that we can use this type of device in a single setting. I think it's difficult, there's a new device now,
there's Alanta device from this type of, which is a bigger device, gets you a lot more rheolytic action, and I think this has really helped us in the venous system. Particularly to get things going, and now we're seeing even more success
with a single type of a treatment option. Again, you know, there is an FDA in terms of looking at it in the pulmonary artery. We look at bradycardia and brady arrhythmias, it's important to have that in mind. And other speakers already spoke of,
a little bit about other things to look at. Hydrating the patient and what have you. What about the suction devices? I like to think to them as a suction assisted thrombectomy, you can have a system where it's a circuit with a canula, or just basically a manual aspiration.
And I think this kind of goes to how much thrombus, how big is the vein that we're dealing with, and how we can get through this. So you can go something as simple as a guide catheter to atherate a small amount of thrombus, and this is something we learned
from the arterial treatment, to something that's a little bit bigger. So it's a 16 French catheter, but it's very limited by the amount of suction that you can actually create. 'Cause really you're using a syringe.
Other types of devices, this is a pretty simple device. It basically, you can create suction, with your hand by hitting that gadget at the end, and you can create a certain amount of aspiration. Again, helps, maybe limited by the amount of thrombus
and the size of the vein that you're using. This is the other extreme. We've already had a talk this session about the AngioVac. When you have a lot of thrombus, this is something that can be used, but this is definitely the other extreme.
A larger canula requires extra corporeal circulation to go on pump. Again, you need to anti coagulate the patient, so a lot of time you're looking at patient that can't relieve lytics. They may be the same patient population that can't undergo
this type of anticoagulation, with these large devices. Vacuum assisted devices, and we've already heard a little bit about that, using this type of an Indigo Suctions System, a maintained aspiration of 29 millimeters of, of vacuum.
Being able to use these flexible catheters with a torque to help us in these large veins, and start looking at a CAT-8, an eight French device. Really, I think this is when we started seeing, again, in a single setting, being able to clear veins and thrombus,
and you can see the aspiration volume that is achievable with these larger eight French devices. Quickly, the pulmonary artery, and the amount of clot we can go on, running out of amount of time, so here's a focal area in the iliac vein.
You can see here a Gianturco Stent and then a stent in the iliac vein that's occluded. And again, being able to use this kind of focal aspiration to aspirate the clot and here you see some clot in the, some contrast in the clot,
and as you can aspirate with these type of suction devices. And then treatment. I'm just going to go to my conclusion.
- Thank you very much. I'd like to thank the organizers for inviting me. When I started working on this talk, I felt like I was coming to defend that climate change isn't occurring, despite increasing data that suggests it's occurring. - [Woman] (laughing)
- I wasn't quite sure where to take it and I actually wanted to just change the title a little bit, and say DOAC's, I feel, are not indicated for all cancer patients with VTE. I'm going to argue that Low Molecular Weight Heparins are still indicated for substantial
subset of patients with cancer and VTE. These are my disclosures, none of which are relevant to this session. Let's talk about these studies, because these studies give us some insights as we look at them.
This was the Hokusai VTE cancer trial, and showed that Dalteparin and Dioxeapan were the same essentially. But this was a combined outcome of thromboembolism and major bleeding. As Dr. Murley showed you, the patients did better
with the Edoxaban arm as far as preventing recurrent VTE, but there was an increase risk of bleeding in patients who received Edoxaban compared to Dalteparin. The important question then becomes are there subsets of patients that we can identify who we may not want to give Edoxaban to.
They had to go to the supplemental material in the paper to figure this out, and the group subsequently published it... Oops, sorry. Group has subsequently published this, which shows you that if those patients
who had Gastrointestinal cancers had a markedly increased risk of a major bleed, compared to those who received Dalteparin. In contrast, non-gastrointestinal cancers really had no difference. Suggesting that those patients with gastrointestinal cancers
should be looked at as people who probably would benefit more from being on a Low Molecular Weight Heparin. Now, is this specific to Edoxoban? No, the SELECT-D trial also was run. Rivaroxoban for Cancer-Associated VTE,
and as you have already seen, the primary outcome for recurrent VTE was better for Rivaroxoban compared to Dalteparin. However, again, we see this safety signal of increased bleeding in the group that received the Rivaroxoban compared to Dalteparin.
Now if you look as this group as far as which patients had cancers or where did they bleed, the sites of major bleeding, Gastrointestinal was twofold higher in the Riveroxaban arm compared to Dalteparin. Again, a GI cancer related issue.
If you look at clinically relevant non-major bleeding, you also see a threefold increase risk of bleeding in the Riveroxaban arm with GI type bleeding, genital urinary you don't see, genital urinary also had a markedly increased risk of bleeding with Riveroxaban.
However, genital urinary cancers as a whole, were not necessarily associated with the increased risk of bleeding. In contrast, esophagogastric cancers were associated with an increased risk of bleeding. There's also a lot of subsets of patients
with cancer and VTE who are treated. This was an interesting study that just came out looking at Rivaroxoban for central venous catheter associated venous thromboembolism. The enrolled patients greater than 18 years of age, active malignancy and symptomatic proximal,
upper extremity DVT, treated them with Rivaroxoban, this was a prospect of single arm trial, 15mg twice a day for three weeks, and 20mg daily for nine weeks. Primary outcome was achieved,
all of these folks had line preservation at 12 weeks. Interestingly, there was one recurrent event, it was a fatal PE at six weeks, but again the bleeding signal is what stood out. This is the risk of bleeding, you can see by 40 days, slightly more than one month.
About 13% of people had sustained a major bleed or clinically relevant non-major bleed. Again this bleeding issue pops up. Importantly, it wasn't bleeding around the catheter, it was bleeding from GI, GU, and GY insights. Okay?
Again, the bleeding issue becomes important. Gastrointestinal tumors become important. Now if bleeding is an issue, what about Thrombocytopenia? Should we be using this in patients who have Thrombocytopenia,
which is a common problem in the cancer patient population. Now patients with platelet counts less than 50 times 10 to the 9th per liter were excluded from participation in Hokusai VTE Cancer, and SELECT-D required adequate hematologic function.
Both of these trials did have protocols in place for what to do if the platelet count dropped. Never the less, what's come out from the SSC group from the International Society on Thrombosis and Hemostasis is that the data on the use of the DOAC's in cancer associated thrombosis patients with severe thrombocytopenia
that less than 50,000 is lacking. The DOAC's may therefore may not be appropriate for most patients with cancer associated thrombosis and platelet counts less than 50,000. Now the last group, and the last thing that you need to think about
which was also just briefly mentioned in one of Dr. Murley's slides was this drug-drug interaction with the DOAC's. This is important because certain drugs do interact with the DOAC's and these are some of the chemotherapy agents.
In fact, certain classes of chemotherapeutic agents interact with CYP3A4, P-glycoprotein, or both. Drugs that interact with these mechanisms can interfere with the effect of the direct oral anticoagulants and potentially cause it to be cleared faster or accumulate.
These included the antimitotic microtubule inhibitors. The taxanes, it included the TKI's which are used in CML and it included a series of immune-modulating agents, including steroids. So in conclusion, who to favor for a Low Molecular Weight Heparin, gastrointestinal malignancy,
severe thrombocytopenia, selected chemotherapies, and then some considerations for following scenarios. Thank you very much.
- Thank you very much, so my disclosures, I'm one of the co-PIs for national registry for ANARI. And clearly venous clot is different, requires different solutions for the arterial system. So this is a device that was built ground up to work in the venous system. And here's a case presentation of a 53 year old male,
with a history of spondylolisthesis had a lumbar inner body fusion, he had an anterior approach and corpectomy with application of an inner body cage. And you can see these devices here. And notably he had application of local bone graft and bone powder
and this is part of what happened to this patient. About seven days later he came in with significant left leg swelling and venous duplex showed clot right here, and this extended all the way down to the tibial vessels. And if you look at the CT
you can see extravasation of that bone powder and material obstructing the left iliac vein. And had severe leg swelling so the orthopedic people didn't want us to use TPA in this patient so we considered a mechanical solution. And so at this day and age I think goals of intervention
should be to maximize clot removal of course and minimize bleeding risk and reduce the treatment or infusion time and go to single session therapy whenever possible. Our ICUs are full all the time and so putting a lytic patient in there
reduces our ability to get other patients in. (mouse clicks So this is the ClotTriever thrombectomy device. It has a sheath that is a 13 French sheath and they're developing a 16 French, that opens up with a funnel
after it's inserted into the poplitiel. So the funnel is in the lower femoral vein and this helps funnel clot in when it's pulled down. The catheter has this coring element that abuts the vein wall and carves the thrombus off in a collecting bag
that extends up above to allow the thrombus to go into the bag as you pull it down. So you access the popliteal vein, cross the thrombosed segments with standard techniques and you need to then put an exchange length wire up into the SVC
or even out into the subclavian vein for stability. And then the catheter's inserted above the clot and is gradually pulled down, sort of milking that stuff off of the wall and into the bag that is then taken down to the funnel and out of the leg.
So this is the patient we had, we had thrombus in the femoral and up into the IVC. Extensive, you can see the hardware here. And it was very obstructed right at that segment where it was, had the bone material pushing on the vein it was quite difficult to get through there
but finally we did and we ballooned that to open a channel up large enough to accommodate ClotTriever catheter. We then did multiple passes and we extracted a large amount of thrombus. Some looking like typically acute stuff
and then some more dense material that may have been a few days worth of build up on the wall there. We then stinted with an 18 by 90 across the obstructed segment and this was our completion run.
It's not perfect but it looks like a pretty good channel going through. This is the hardware not obstruction at that level. Hospital course, the patient had significant improvement in their swelling by post-op day one. Was discharged on compression and anti-coagulation.
He returned about two months ago for his three month follow-up and really had very minimal symptoms in the left leg. Venous duplex showed that the left common femoral was partially compressible but did have phasic flow and the stent appeared to be open through it's course.
So of course this is an anecdote, this is early in the experience with this catheter. There have been numerous improvements made to ease the use of it and do it in fewer steps. And so we're starting a ClotTriever outcomes registry
to enroll up to 500 patients to begin to define outcomes with this device. It does offer the promise of single session therapy without lytic administration and we'll see how it performs and which patients it works best in through the registry.
Thank you very 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.
- [Speaker] Okay, a little on femoral vein stenting. So the idea here is, as we've heard earlier, inflow can be a problem in post-thrombotic patients which influences stent patency. Anticoagulation is key, landing stents, but how can we improve inflow? Usually, as we've heard, the profunda femoris vein
is a good collateral or conduit if the femoral vein is closed. And this is what we like to see after a post-thrombotic occlusion is axal transformation of the profunda, with good flow and that will usually maintain a proximal stint
and good symptom relief. However, 20% of post-thrombotic limbs, the profunda is involved. If it's the profunda origin, sometimes you can access the profunda and land the stint through the profunda origin.
That's difficult especially in obese patients. But if the profunda femoris involvement is more extensive now you've got no inflow from the profunda and no inflow from the femoral vein. Of course the saphenous is a poor inflow source and now these are the stents that have problems.
So can we improve inflow when the profunda and the femoral vein are post-thrombotic? This is a case. This guy has been in the practice for over 10 years, a UPS worker who is on his feet and running around a lot,
thrombophilic, and he had an iliac stent that did well for a long time, on Warfarin. And he got sub therapeutic, occluded iliac stent which we re-opened and then let him recanalize. I thought he would do well from that
because he did have good profunda inflow here. The femoral vein's post-thrombotic and poor inflow but he had good profunda inflow and a patent stent. And a couple of years later he just came into the office and said look I'm happy my thigh is decompressed but it's the calf, the calf still bothers me when I work,
carrying boxes around. So I said let me try this, see if we can improve this, this femoral vein. So the key here is, his popliteal vein looks decent, he had good axial transformation of the profunda, which surprised me,
but we went ahead and dealt with this segment right here, the femoral vein, to see if we could improve his symptoms. So with IVUS you see that the femoral vein was occluded but his popliteal vein looked pretty good. And we went ahead and stented him a little. So he had a proximal iliac and we stented his femoral vein,
taking care not to jail the profunda inflow now. And this one did well and is still open a few years later. This is a different case. A young kid, thrombophilic, multiple DVTs at this age, with recurrent ulceration.
We looked hard for a iliac lesion but it was normal and we placed a common femoral stent which was abnormal, and he did okay for a couple of years with this. And then he came back with recurrent ulceration asking if something can be done. And in this case
we got sucked in to looking at his thigh. He does not have good axial transformation of the profunda, a very stringy post-thrombotic femoral vein, and a saphenous vein over here. I had to access the gastroc vein because I couldn't get into the popliteal
and that's the key to the case, as you're going to hear. So I did get him stented, pretty decent looking venogram afterwards. I landed above this important collateral, taking care not to knock it out. You see that the profunda is open,
he's got a trifurcation down there. But he got sub therapeutic with his INR, and thrombosed. So, before I went through the popliteal, now he's supined through the posterior tibial and here's his venogram. Occluded his popliteal and his stent.
We got him open with an AngioJet but a very poor popliteal, when he came back later, he's occluded. And that's really going to be the lesson here, that you need, so if you're dealing with an iliac stent you need inflow from the thigh. If you're considering something in the thigh
you need inflow from the calf. So if you're going to do something with femoral vein stenting, what I'm learning is, you need to pay a lot of attention to the posterior tibial veins and the popliteal vein. This case is a little different. Iliac stent did well for a while
and she comes back with new symptoms. And with venogram she had a proximal femoral vein lesion that I thought was segmental, and again this should be a short femoral vein stent, lets see if I get away with this. And you can see a tight lesion that we angioplastied.
Not a good post-angioplasty result so we stented it.
- So I'm just going to talk a little bit about what's new in our practice with regard to first rib resection. In particular, we've instituted the use of a 30 degree laparoscopic camera at times to better visualize the structures. I will give you a little bit of a update
about our results and then I'll address very briefly some controversies. Dr. Gelbart and Chan from Hong Kong and UCLA have proposed and popularized the use of a 30 degree laparoscopic camera for a better visualization of the structures
and I'll show you some of those pictures. From 2007 on, we've done 125 of these procedures. We always do venography first including intervascular intervention to open up the vein, and then a transaxillary first rib resection, and only do post-operative venography if the vein reclots.
So this is a 19 year old woman who's case I'm going to use to illustrate our approach. She developed acute onset left arm swelling, duplex and venogram demonstrated a collusion of the subclavian axillary veins. Percutaneous mechanical thrombectomy
and then balloon angioplasty were performed with persistent narrowing at the thoracic outlet. So a day later, she was taken to the operating room, a small incision made in the axilla, we air interiorly to avoid injury to the long thoracic nerve.
As soon as you dissect down to the chest wall, you can identify and protect the vein very easily. I start with electrocautery on the peripheral margin of the rib, and use that to start both digital and Matson elevator dissection of the periosteum pleura
off the first rib, and then get around the anterior scalene muscle under direct visualization with a right angle and you can see that the vein and the artery are identified and easily protected. Here's the 30 degree laparoscopic image
of getting around the anterior scalene muscle and performing the electrocautery and you can see the pulsatile vein up here anterior and superficial to the anterior scalene muscle. Here is a right angle around the first rib to make sure there are no structures
including the pleura still attached to it. I always divide, or try to divide, the posterior aspect of the rib first because I feel like then I can manipulate the ribs superiorly and inferiorly, and get the rib shears more anterior for the anterior cut
because that's most important for decompressing the vein. Again, here's the 30 degree laparoscopic view of the rib shears performing first the posterior cut, there and then the anterior cut here. The portion of rib is removed, and you can see both the artery and the vein
are identified and you can confirm that their decompressed. We insufflate with water or saline, and then perform valsalva to make sure that they're hasn't been any pneumothorax, and then after putting a drain in,
I actually also turn the patient supine before extirpating them to make sure that there isn't a pneumothorax on chest x-ray. You can see the Jackson-Pratt drain in the left axilla. One month later, duplex shows a patent vein. So we've had pretty good success with this approach.
23 patients have requires post operative reintervention, but no operative venous reconstruction or bypass has been performed, and 123 out of 125 axillosubclavian veins have been patent by duplex at last follow-up. A brief comment on controversies,
first of all, the surgical approach we continue to believe that a transaxillary approach is cosmetically preferable and just as effective as a paraclavicular or anterior approach, and we have started being more cautious
about postoperative anticoagulation. So we've had three patients in that series that had to go back to the operating room for washout of hematoma, one patient who actually needed a VATS to treat a hemathorax,
and so in recent times we've been more cautious. In fact 39 patients have been discharged only with oral antiplatelet therapy without any plan for definitive therapeutic anticoagulation and those patients have all done very well. Obviously that's contraindicated in some cases
of a preoperative PE, or hematology insistence, or documented hypercoagulability and we've also kind of included that, the incidence of postop thrombosis of the vein requiring reintervention, but a lot of patients we think can be discharged
on just antiplatelets. So again, our approach to this is a transaxillary first rib resection after a venogram and a vascular intervention. We think this cosmetically advantageous. Surgical venous reconstruction has not been required
in any case, and we've incorporated the use of a 30 degree laparoscopic camera for better intraoperative visualization, thanks.
- You already heard about different devices which can finish the treatment of acute DVT in the lab and I would like to add one of the devices which is quite widespread in Europe. And share the first study on this device. This is called the Aspirex device. So what is the objective?
Post traumatic syndrome after proximal DVT, I think that's clear. 25% of the patient are at risk for developing post traumatic syndrome. I think that is clear and some of these patient even expect severe post traumatic syndrome.
We already saw this ATTRACT trial outcome and we learned that especially patient with Iliofemoral DVT might benefit from treatment, invasive treatment of Iliofemoral DVT but of course, we need to know that is catheter-directed thrombolysis causes issues
and therefore our way should be to go away from thrombolytic therapy to a pure mechanical thrombectomy approach. This is a typical case example of a patient, 20 year old female patient who came to the emergency room with that leg on the left side in the morning,
back pain in the evening and this is clear that it is a descending Iliofemoral DVT in that patient caused by May-Thurner syndrome. So, with modern devices like this Aspirex, mechanical thrombectomy device, the 10 French device is able to aspirate up to 130 millimeter,
ml per minute of clots. You see that this can be effectively treated and then stinted within the May-Thurner syndrome within one session approach. So, but, what is clear of course that we need to get data
for these modern Mechanical Thrombectomy devices and therefore, we conducted clinical follow-up study to evaluate safety and efficiency of that Aspirex Mechanical Thrombectomy device. This device is based on the Archimedic principle which you can see here it comes with six up
to 10 French systems and with that you are able, as I already showed to sac 130ml of thrombus per minute. So these are the study details I want to show you. We treated 50 psychs, 56 patients with acute, subacute and acute on chronic which means up to 3 months of symptoms patients with Iliofermal DVT.
We performed IVIS on all these patients. We found May-Thurner syndrome in at least half of these patients as a reason for the Iliofermal DVT. You see the patient demographics. Some of the patients had even malignancy condition. A lot of patients were on oral contraceptives.
Here are the clinical symptoms within our cohort. Most of the patients came with swelling and rest pain. The rVCSS at the beginning was 4.5 within this cohort. Most of the traumatic lesions were on the left side involving even the profunda and the common femoral vein in this cohort.
You see here the excess which we used for treating these Iliofermal DVT, we used in the main part of the cohort, the left popliteal vein access or left femoral vein access. 84% were treated with 10 French system, the Aspirex device. As I mentioned we used IVIS
to analyze underlying pathologies. We found in most of the patients underlying pathologies and this explains why we implanted stents in 100% of the patients. You see the treatment duration which was in mean 94 minutes within this treatment cohort.
These are the patency analysis within one year. You see patency at 12 months, 87% percent in these patients, which we could follow up after 12 months. Here you see the Post-thrombotic syndrome analysis after 12 months so only low PTS
and some kind of moderate PTS were seen in these patients. There were no severe Post-thrombotic syndrome. Most of the patients just had a little bit of swelling after that procedure. Of course, it's important to mention safety and those end points.
There were just some small punctures associated, site being complicationS. Of course re-hospitalization is a severe adverse event which you can see here. But there were of course no bleeding events in this cohort. And to follow up
on this much more multicentric perspective trial, we just started a multicenter trial on this and we'll follow up patients up to five years within this just initiated multicenter registry. And I think we can show some preliminary data next year. Thank you very much.
So I think when it comes to distal bypasses and ultra-distal bypasses it's all about how we make our decision. We know now that early intervention these patients have better outcome. We use waveform analysis to make our decision about how critical their skin is
we use different topical anesthesia depending the patient's fitness. I think this is just one important point that patient's with dark skin did not show all the full range of skin changes and patients get this dark foot sign
even before they start necrosing their skin. It's very important how we give our anesthetics we use vascular anesthesia with special interest prevascular disease because these patients are quite labile. We use even sometimes inotropes during the procedure
and post operative to maintain a good blood pressure. We believe that short bypasses have got better outcomes. Dr. Veith, have already published in the 80s about short bypasses also doing now the Tibiotibial bypasses on the look anesthetic. Some patients with very high risk for general anesthesia.
And our study we showed that the majority of our patients, who had ultra-distal bypasses had the bypasses from either popliteal or SFA artery. We use different techniques to improve on how to take our bypasses from the proximal anastomosis distally. So we use hybrid revascularization, we use drug-eluting
balloons, and stenting of the SFA and popliteal artery, so we can perform our bypass from the popliteal level. We even use Remote Endarterectomy to improve on our length of the inflow. So by doing remote endarterectomy of the SFA
and popliteal artery, we can take the bypass quite distally from the popliteal artery to the foot level. This is a patient who got critical leg ischaemia on the right side limited, venous conduit. We did remote endarterectomy of her SFA and popliteal artery. And then we can
easily take the bypass from the popliteal artery down to the foot level. On the left side, she had hybrid revascularization with SFA stenting and ultra-distal bypass. We use venous conduit in almost all our patients with ultra-distal bypass.
In distal bypasses we can PTFE but the majority of our patients have long saphenous veins or even arm veins. We started using Omniflow in our infected patients for distal bypasses with quite good results. We scan all our veins prior to the procedure
to make sure that we got good quality vein and amount to perform the procedure. We have published in our small veins series less than 3mm, we still have a very good outcome in distal bypasses. Especially when we do tibial bypasses
or dorsalis pedis bypasses we turn the grafts anatomically. You can see in this angiogram the graft going through the interosseous membrane down to the foot level. We put our incision a bit immediately on the foot level so if there is necrosis of the wound on the foot level that we don't expose the graft, especially when we
knew the patient was coming from the lateral aspect through the interosseous membrane. We select our bypasses especially in the foot level using the duplic scanogram, angiogram or CT angiogram. During the procedure we don't clamp our arteries we use the Flo-Rester and Flo-Through prothesis
to stop patients from bleeding while we're doing it. And we've never used tourniquet before all this has been published. Hand held doppler is the only quality control that we do we don't do on-table angiograms and we find this quite useful for our patients.
We can do the debridement and at the same time while we're doing the bypass at the ankle level. As for anticoagulation and antiplatelet therapy We do antiplatelet therapy for all patient with distal and ultra-distal bypass. And we use heparin and warfarin for patients
who have got redo surgery. Graft surveillance for all our patients Unfortunately, we can only afford it in the NHS for one year, but if the patient get an intervention they go for another full year. Salvage angioplasty is essential for these patients
and we treat these patients as quite as a emergency when they present. So, conclusion, Mr. Sherman, ladies and gentlemen, distal and ultra-distal bypasses require good planning. We use veins for all our bypasses when it comes to the foot level and ultra-distal bypasses,
and of course selecting the target vessel in the foot is very important. Graft Surveillance is essential to maintain quality and outcome for these patients. Thank you very much.
- [B.B] Thank you very much Mr. Chairman. Good afternoon, ladies and gentlemen. I will present some topic you are not much familiar here in this side of the Atlantic, especially right after the good lunch hour here. I have nothing to disclose. The venous and lymphatic systems are
mutually dependent dual outflow system. We all know that. Venous capillary can handle about 80% of ultra filtered liquid portion only. We also know that. While the lymphatic capillary absorb the leftover 20%
of the total liquid and and all the protein micromolecules filtered out from arterial capillary, by the lymphatic system as a one single integral part phlebolymphatic unit. Venous and lymphatic circulation systems are therefore two mutually interdependent systems,
but entirely different rheodynamic condition. Normal lymphodynamic is based on self-propelled peristalsis by each unit of lymphangion with positive pressure to 50-60 millimeter of mercury, while venodynamics is purely a passive low-pressure system of 10 millimeter of mercury, you are all familiar with.
Venous and lymphatic systems are such one inseparable system so that insufficiency or overloading to one of two system allow the other to play auxiliary role of fluid return, which is indeed good, but both systems are mutually complimentary only only when they are in normal function.
When one of the two systems should lose its normal function, such mutual interdependence generates a new problem. That's what I'm going to talk to you. When one of the two mutually interdependent systems should fail, it gives additional burdening to the other system.
When this additional loading should exceed, by the way there's a time limit here. I don't see any time clocks here. You didn't force it here. Anyhow, such condition would lead the failure of other system as well, resulting in a total failure
of this inseparable dual system altogether, so called Phlebolymphedema. Another word, Phlebolymphedema is the inevitable outcome of inseparable venous and lymphatic system when both system should fail together. When the venous system exceeds this
maximum lymphatic capacity, the insufficiency become phlebolymphatic. Phlebolymphedema is therefore outcome of this dual outflow veno-lymphatic system failure, as chronic venous insufficiency and chronic lymphatic insuf combined.
This chronic lymphatic insuf appears to become more prominent especially among the compromised lymphatic drainage condition of various etiologies. Then clinical manifestation become extremely variable depending upon the etiology and the degree and extent of the CVI and the CLI.
Primary phlebolymphedema represent a combined condition of chronic venous insuff by the venous malformation and chronic lymphatic insufficiency by the lymphatic malformation. The most common VM to cause a CVI is a
marginal vein with venous hypertension. CLI's are mostly due to primary lymphedema. Primary phlebolymphedema generated by malformation component of Klippel Syndrome is the ultimate challenge. CVI of a secondary phlebolymphedema
is also mostly sequellae of post-thrombotic syndrome following deep vein thrombosis. And the chronic lymphatic insufficiency of secondary phlebolymphedema is generally secondary outcome of regional local lymphedema. Secondary phlebolymphedema developed
along the end stage of CVI is much complicated. Proper assessment for the phlebolymphedema should start with the diagnosis of etiology and then separate CVI and CLI assessment for each condition should be followed. Primary phlebolymphedema is mandated
for the full investigation on the VM and the LM before individual assessment of CVI and the CLI.
- Thank you very much. So these are the disclosures. Venous stents obviously. Can we fix that please? That always happens to me. So the application of venous stents, thank you, have increased and there are certain issues with venous stents, or all the stents,
that we need to be cognizant of. Predisposing factors to stent fracture from the arterial site, obviously biomechanical forces. This is well, sort of understood in a study on the arterial site,
bending during activity, axial compression and elongation, elongation during stent deployment, radial compression. Of course, the stent material design has a lot to do with it.
And then the length and degree of overlap on the arterial site and the surface finish. These are all worked out. So to what degree are these applicable to the venous site? So the stress factors, as you can see on the fem-pop segment
versus carotid, renals or brachiocephalic arteries are different on the arterial site. So we expect the same on the venous site. What is common among all of them is repetitive bending and change in axial dimension. So if you look at this patient here,
we have sort of a May-Thurner here, and there's another compression right there. And if you look at the end of, that's the contralateral flow. And if you look at this so the balloon in there, no impression whatsoever on it.
Obviously there's no scar tissue in there. This was stented. And this is post stenting, and you can see that. Now this is interesting, because if you look at the IVUS, this is that May-Thurner higher up,
this is lower down. As you can see there's no synechiae, no scar tissue in there. So this is one of those issues that it has to do with the stent rather than with balloons. If you look at the MRI,
you can see that's the artery, that's the vein, severely compressed. And now look at the post stent IVUS. So, this is the kind of stress that we have to deal with on the venous site in this location, as opposed to the common femoral vein, alright?
So, and let's look what happens in finite element analysis in these situations. So if you look at the acute bends, so these are around the iliacs, I'm sorry, around the common femoral, you can see the sharper the bend is
the harder the stress on the elements, on the material. This is interesting because this is probably somewhat unique to the veins, and that is the cyclic focal compression. So if you have cyclic focal compression, a stent that is more narrow,
same stent, same material, same diameter, this configuration has more stress on it than this. So what's the lesson for us? So the lesson for us is that if you're doing the common femoral and there's a lesion in there, and you put a stent in there,
you can see this stent is fractured, but you can see that there was a residual narrowing in there. If you're going to do these, you want to left no waste behind. As we saw from an engineering analysis, that in this area under the inguinal ligament
and where the compression is and the cyclic bending is, if the stents look straight there's less stress on the material than if there's residual narrowing. We're also studying the gap between the common femoral and the os pubis.
If there's a layer of fat in here that's somewhat protective, therefore less stress. But this is a theoretical element. So what is the acceptable rate of fracture? It really depends on whether the fracture is consequential or not.
If it's not consequential, it really doesn't matter a whole lot. So this will likely depend on the stent platform. And so, what is the likely or acceptable rate of thrombosis? This comes from that meta-analysis that's been published. You know, basically single digit percentage
thrombosis rate is acceptable. In conclusion, obviously we need more data points to confirm the risk factors in a stent fracture in the veins. The finite element analysis shows us and sort of guide us in a certain direction
that the consequences of a fracture need to be better identified in the veins. We really don't know that at this time. Thank you.
- These are my disclosures. So central venous access is frequently employed throughout the world for a variety of purposes. These catheters range anywhere between seven and 11 French sheaths. And it's recognized, even in the best case scenario, that there are iatrogenic arterial injuries
that can occur, ranging between three to 5%. And even a smaller proportion of patients will present after complications from access with either a pseudoaneurysm, fistula formation, dissection, or distal embolization. In thinking about these, as you see these as consultations
on your service, our thoughts are to think about it in four primary things. Number one is the anatomic location, and I think imaging is very helpful. This is a vas cath in the carotid artery. The second is th
how long the device has been dwelling in the carotid or the subclavian circulation. Assessment for thrombus around the catheter, and then obviously the size of the hole and the size of the catheter.
Several years ago we undertook a retrospective review and looked at this, and we looked at all carotid, subclavian, and innominate iatrogenic injuries, and we excluded all the injuries that were treated, that were manifest early and treated with just manual compression.
It's a small cohort of patients, we had 12 cases. Eight were treated with a variety of endovascular techniques and four were treated with open surgery. So, to illustrate our approach, I thought what I would do is just show you four cases on how we treated some of these types of problems.
The first one is a 75 year-old gentleman who's three days status post a coronary bypass graft with a LIMA graft to his LAD. He had a cordis catheter in his chest on the left side, which was discovered to be in the left subclavian artery as opposed to the vein.
So this nine French sheath, this is the imaging showing where the entry site is, just underneath the clavicle. You can see the vertebral and the IMA are both patent. And this is an angiogram from a catheter with which was placed in the femoral artery at the time that we were going to take care of this
with a four French catheter. For this case, we had duel access, so we had access from the groin with a sheath and a wire in place in case we needed to treat this from below. Then from above, we rewired the cordis catheter,
placed a suture-mediated closure device, sutured it down, left the wire in place, and shot this angiogram, which you can see very clearly has now taken care of the bleeding site. There's some pinching here after the wire was removed,
this abated without any difficulty. Second case is a 26 year-old woman with a diagnosis of vascular EDS. She presented to the operating room for a small bowel obstruction. Anesthesia has tried to attempt to put a central venous
catheter access in there. There unfortunately was an injury to the right subclavian vein. After she recovered from her operation, on cross sectional imaging you can see that she has this large pseudoaneurysm
coming from the subclavian artery on this axial cut and also on the sagittal view. Because she's a vascular EDS patient, we did this open brachial approach. We placed a stent graft across the area of injury to exclude the aneurism.
And you can see that there's still some filling in this region here. And it appeared to be coming from the internal mammary artery. We gave her a few days, it still was patent. Cross-sectional imaging confirmed this,
and so this was eventually treated with thoracoscopic clipping and resolved flow into the aneurism. The next case is a little bit more complicated. This is an 80 year-old woman with polycythemia vera who had a plasmapheresis catheter,
nine French sheath placed on the left subclavian artery which was diagnosed five days post procedure when she presented with a posterior circulation stroke. As you can see on the imaging, her vertebral's open, her mammary's open, she has this catheter in the significant clot
in this region. To manage this, again, we did duel access. So right femoral approach, left brachial approach. We placed the filter element in the vertebral artery. Balloon occlusion of the subclavian, and then a stent graft coverage of the area
and took the plasmapheresis catheter out and then suction embolectomy. And then the last case is a 47 year-old woman who had an attempted right subclavian vein access and it was known that she had a pulsatile mass in the supraclavicular fossa.
Was noted to have a 3cm subclavian artery pseudoaneurysm. Very broad base, short neck, and we elected to treat this with open surgical technique. So I think as you see these consults, the things to factor in to your management decision are: number one, the location.
Number two, the complication of whether it's thrombus, pseudoaneurysm, or fistula. It's very important to identify whether there is pericatheter thrombus. There's a variety of techniques available for treatment, ranging from manual compression,
endovascular techniques, and open repair. I think the primary point here is the prevention with ultrasound guidance is very important when placing these catheters. Thank you. (clapping)
- This talk is a brief one about what I think is an entity that we need to be aware of because we see some. They're not AVMs obviously, they're acquired, but it nevertheless represents an entity which we've seen. We know the transvenous treatment of AVMs is a major advance in safety and efficacy.
And we know that the venous approach is indeed very, very favorable. This talk relates to some lesions, which we are successful in treating as a venous approach, but ultimately proved to be,
as I will show you in considerable experience now, I think that venous thrombosis and venous inflammatory disease result in acquired arteriovenous connections, we call them AVMs, but they're not. This patient, for example,
presented with extensive lower extremity swelling after an episode of DVT. And you can see the shunting there in the left lower extremity. Here we go in a later arterial phase. This lesion we found,
as others, is best treated. By the way, that was his original episode of DVT with occlusion. Was treated with stenting and restoration of flow and the elimination of the AVM.
So, compression of the lesion in the venous wall, which is actually interesting because in the type perivenous predominant lesions, those are actually lesions in the vein wall. So these in a form, or in a way, assimilate the AVMs that occur in the venous wall.
Another man, a 53-year-old gentleman with leg swelling after an episode of DVT, we can see the extensive filling via these collaterals, and these are inflammatory collaterals in the vein wall. This is another man with a prior episode of DVT. See his extensive anterior pelvic collaterals,
and he was treated with stenting and success. A recent case, that Dr. Resnick and I had, I was called with a gentleman said he had an AVM. And we can see that the arteriogram sent to me showed arterial venous shunting.
Well, what was interesting here was that the history had not been obtained of a prior total knee replacement. And he gave a very clear an unequivocal history of a DVT of sudden onset. And you can see the collaterals there
in the adjacent femoral popliteal vein. And there it is filling. So treatment here was venous stenting of the lesion and of the underlying stenosis. We tried an episode of angioplasty,
but ultimately successful. Swelling went down and so what you have is really a post-inflammatory DVT. Our other vast experience, I would say, are the so-called uterine AVMs. These are referred to as AVMs,
but these are clearly understood to be acquired, related to placental persistence and the connections between artery and veins in the uterus, which occurs, a part of normal pregnancy. These are best treated either with arterial embolization, which has been less successful,
but in some cases, with venous injection in venous thrombosis with coils or alcohol. There's a subset I believe of some of our pelvic AVMs, that have histories of DVT. I believe they're silent. I think the consistency of this lesion
that I'm showing you here, that if we all know, can be treated by coil embolization indicates to me that at least some, especially in patients in advanced stage are related to DVT. This is a 56-year-old, who had a known history of prostate cancer
and post-operative DVT and a very classic looking AVM, which we then treated with coil embolization. And we're able to cure, but no question in my mind at least based on the history and on the age, that this was post-phlebitic.
And I think some of these, and I think Wayne would agree with me, some of these are probably silent internal iliac venous thromboses, which we know can occur, which we know can produce pulmonary embolism.
And that's the curative final arteriogram. Other lesions such as this, I believe are related, at least some, although we don't have an antecedent history to the development of DVT, and again of course,
treated by the venous approach with cure. And then finally, some of the more problematic ones, another 56-year-old man with a history of prior iliofemoral DVT. Suddenly was fine, had been treated with heparin and anticoagulation.
And suddenly appeared with rapid onset of right lower extremity swelling and pain. So you see here that on an arteriogram of the right femoral, as well as, the super selective catheterization of some of these collaterals.
We can see the lesion itself. I think it's a nice demonstration of lesion. Under any other circumstance, this is an AVM. It is an AVM, but we know it to be acquired because he had no such swelling. This was treated in the only way I knew how to treat
with stenting of the vein. We placed a stent. That's a ballon expanded in the angiogram on your right is after with ballon inflation. And you can see the effect that the stenting pressure, and therefore subsequently occlusion of the compression,
and occlusion of the collaterals, and connections in the vein wall. He subsequently became asymptomatic. We had unfortunately had to stent extensively in the common femoral vein but he had an excellent result.
So I think pelvic AVMs are very similar in location and appearance. We've had 13 cases. Some with a positive history of DVT. I believe many are acquired post-DVT, and the treatment is the same venous coiling and or stent.
Wayne has seen some that are remarkable. Remember Wayne we saw at your place? A guy was in massive heart failure and clearly a DVT-related. So these are some of the cases we've seen
and I think it's noteworthy to keep in mind, that we still don't know everything there is to know about AVMs. Some AVMs are acquired, for example, pelvic post-DVT, and of course all uterine AVMs. Thanks very much.
(audience applause) - [Narrator] That's a very interesting hypothesis with a pelvic AVMs which are consistently looking similar. - [Robert] In the same place right? - [Narrator] All of them are appearing at an older age. - [Robert] Yep.
Yep. - This would be a very, very good explanation for that. I've never thought about that. - Yeah I think-- - I think this is very interesting. - [Robert] And remember, exactly.
And I remember that internal iliac DVT is always a silent process, and that you have this consistency, that I find very striking. - [Woman] So what do you think the mechanism is? The hypervascularity looked like it was primarily
arterial fluffy vessels. - [Robert] No, no, no it's in the vein wall. If you look closely, the arteriovenous connections and the hypervascularity, it's in the vein wall. The lesion is the vein wall,
it's the inflammatory vein. You remember Tony, that the thing that I always think of is how we used to do plain old ballon angioplasty in the SFA. And afterwards we'd get this
florid venous filling sometimes, not every case. And that's the very tight anatomic connection between those two. That's what I think is happening. Wayne? - [Wayne] This amount is almost always been here.
We just haven't recognized it. What has been recognized is dural fistula-- - Yep. - That we know and that's been documented. Chuck Kerber, wrote the first paper in '73 about the microvascular circulation
in the dural surface of the dural fistula, and it's related to venous thrombosis and mastoiditis and trauma. And then as the healing process occurs, you have neovascular stimulation and fistulization in that dural reflection,
which is a vein wall. And the same process happens here with a DVT with the healing, the recanalization, inflammation, neovascular stimulation, and the development of fistulas. increased vascular flow into the lumen
of the thrombosed area. So it's a neovascular stimulation phenomenon, that results in the vein wall developing fistula very identical to what happens in the head with dural fistula had nothing described of in the periphery.
- [Narrator] Okay, very interesting hypothesis.
- Thank you Dr. Veith for this opportunity again, and, like to show you that I have no disclosures relevant to this talk. The objective is to report the management and outcome of five cases of brachial artery injury in children with supracondylar humerus fractures at our institution over the last few years,
and then emphasize the importance of close observation and low threshold for surgical exploration in these cases. The classification of supracondylar fractures is on the Gartland system, and typically the vascular injuries are associated with Type 3, although there are some reported cases with Type 2.
Supracondylar humerus fractures make up about 70% of elbow fractures in children. Displacement and deformity can injure the median nerve, as well as the brachial artery. And up to 20% of children will present with an abnormal vascular exam, on initial evaluation.
There is no doubt what you do for the ischemic hand, is the exploration of the brachial artery. However, for the perfused, pulseless hand, there is considerable controversy as to what one should do. If this is not recognized, and not appropriately treated, there can be significant complications,
which can affect the child for the rest of his life. Physical examination, including neurovascular examination is crucial. These are high-litigation cases, and just writing on your record that neurovascular status is intact, is totally inadequate.
With reference to this particular fracture, evaluation for median nerve intactness, and function of the anterior interosseous nerve in particular, is very important, as I'll show you in just a slide, where they can be associated with arterial injuries. Ladies and gentlemen, this is why
you have the pink pulseless hand, despite obstruction or interruption of the brachial artery, going to these rich collaterals around the elbow. The hand can still be pink, and pulseless. This is a demonstration of the coexisting injury when you have median nerve and brachial artery
damaged by the anteromedial location. This location of the proximal fracture fragment. And many have suggested routine vascular exploration for this sort of injury. The most common finding that we find when we explore the brachial artery
with supracondylar fractures of the humerus, is the artery is tethered between the fracture fragments. This is yet another example, this is the brachialis sign, where the proximal fragment can buttonhole through the brachialis muscle. Most open fractures will need brachial artery exploration
at the time of reduction of the fracture. So, now I would like to share with you these five cases that I mentioned, at Inova Fairfax Hospital. The average age was 5.4 years, and four of them were male, one was a female, and I described to you my personal experience
in taking care of these patients at the hospital, and then following them closely afterwards. Case one was a perfused hand, a pink perfused hand, without a pulse. And this gentleman, this patient presented the next day with compartment syndrome.
On exploration we found a tethered artery, we released it, patient has normal function at two years. Case two, had a positive pulse, positive Doppler signal, nothing was done, other than reducing the fracture, patient sent home, he represented with severe pain, and was found to have compartment syndrome on day three.
On exploration, the artery was tethered. It was released, no thrombectomy was necessary. Patient has been left with slight deficit in two fingers. Third case, perfused pulse, with no pulse was observed, and the last pulse the next day duplex showed that the brachial artery was obstructed.
It was transected, had a vein interposition, I used the basilic vein, and did thrombectomy, and normal function at four months. Fourth case, there was no pulse, no Doppler signal, immediate exploration, tethered artery, no thrombectomy, normal function restored.
Case five had a normal exam, but lost signal the next day, was found to have a massive hematoma. We evacuated the hematoma, normal function. Based on this, the treatment algorithm is when the patient has a positive pulse, has a palpable pulse,
we obviously would do nothing. When it's pulseless and ischemic, immediate surgical exploration. When it's perfused and there's no radial signal, diminished flow, on duplex ultrasound, we explore surgically,
and when there's a positive radial pulse, we observe for 24 to 48 hours before discharge. I have found pulse oximetry, in addition with duplex ultrasound, to be very helpful in this regard. And ladies and gentlemen, in conclusion,
immediate surgical exploration is mandated for the ischemic hand. We recommend close observation after reduction, despite return of palpable pulse or Doppler signal, due to risk of delayed ischemia or compartment syndrome, especially in young children.
Based on our experience, perfused pulseless hand is a consequence of arterial injury or spasm. And, if you use duplex ultrasound, as if we had done, we may have been able to avoid delayed care in three out of the five cases. We recommend immediate exploration, obviously for,
for absent pulse and ischemic hand. And we do recommend that early recognition of ischemia and compartment syndrome is paramount, and patient should be closely observed, even if they have a normal perfusion on reduction of the fracture site. Thank you so much.
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