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.
- So I'd like to thank Dr. Ascher, Dr. Sidawy, Dr. Veith, and the organizers for allowing us to present some data. We have no disclosures. The cephalic arch is defined as two centimeters from the confluence of the cephalic vein to either the auxiliary/subclavian vein. Stenosis in this area occurs about 39%
in brachiocephalic fistulas and about 2% in radiocephalic fistulas. Several pre-existing diseases can lead to the stenosis. High flows have been documented to lead to the stenosis. Acute angles. And also there is a valve within the area.
They're generally short, focal in nature, and they're associated with a high rate of thrombosis after intervention. They have been associated with turbulent flow. Associated with pre-existing thickening.
If you do anatomic analysis, about 20% of all the cephalic veins will have that. This tight anatomical angle linked to the muscle that surrounds it associated with this one particular peculiar valve, about three millimeters from the confluence.
And it's interesting, it's common in non-diabetics. Predictors if you are looking for it, other than ultrasound which may not find it, is calcium-phosphate product, platelet count that's high, and access flow.
If one looks at interventions that have commonly been reported, one will find that both angioplasty and stenting of this area has a relatively low primary patency with no really discrimination between using just the balloon or stent.
The cumulative patency is higher, but really again, deployment of an angioplasty balloon or deployment of a stent makes really no significant difference. This has been associated with residual stenosis
greater than 30% as one reason it fails, and also the presence of diabetes. And so there is this sort of conundrum where it's present in more non-diabetics, but yet diabetics have more of a problem. This has led to people looking to other alternatives,
including stent grafts. And in this particular paper, they did not look at primary stent grafting for a cephalic arch stenosis, but mainly treating the recurrent stenosis. And you can see clearly that the top line in the graph,
the stent graft has a superior outcome. And this is from their paper, showing as all good paper figures should show, a perfect outcome for the intervention. Another paper looked at a randomized trial in this area and also found that stent grafts,
at least in the short period of time, just given the numbers at risk in this study, which was out after months, also had a significant change in the patency. And in their own words, they changed their practice and now stent graft
rather than use either angioplasty or bare-metal stents. I will tell you that cutting balloons have been used. And I will tell you that drug-eluting balloons have been used. The data is too small and inconclusive to make a difference. We chose a different view.
We asked a simple question. Whether or not these stenoses could be best treated with angioplasty, bare-metal stenting, or two other adjuncts that are certainly related, which is either a transposition or a bypass.
And what we found is that the surgical results definitely give greater long-term patency and greater functional results. And you can see that whether you choose either a transposition or a bypass, you will get superior primary results.
And you will also get superior secondary results. And this is gladly also associated with less recurrent interventions in the ongoing period. So in conclusion, cephalic arch remains a significant cause of brachiocephalic AV malfunction.
Angioplasty, across the literature, has poor outcomes. Stent grafting offers the best outcomes rather than bare-metal stenting. We have insufficient data with other modalities, drug-eluting stents, drug-eluting balloons,
cutting balloons. In the correct patient, surgical options will offer superior long-term results and functional results. And thus, in the good, well-selected patient, surgical interventions should be considered
earlier in this treatment rather than moving ahead with angioplasty stent and then stent graft. Thank you so much.
- So this was born out of the idea that there were some patients who come to us with a positive physical exam or problems on dialysis, bleeding after dialysis, high pressures, low flows, that still have normal fistulograms. And as our nephrology colleagues teach us, each time you give a patient some contrast,
you lose some renal function that they maintain, even those patients who are on dialysis have some renal function. And constantly giving them contrasts is generally not a good thing. So we all know that intimal hyperplasia
is the Achilles Heel of dialysis access. We try to do surveillance. Debbie talked about the one minute check and how effective dialysis is. Has good sensitivity on good specificity, but poor sensitivity in determining
dialysis access problems. There are other measured parameters that we can use which have good specificity and a little better sensitivity. But what about ultrasound? What about using ultrasound as a surveillance tool and how do you use it?
Well the DOQI guidelines, the first ones, not the ones that are coming out, I guess, talked about different ways to assess dialysis access. And one of the ways, obviously, was using duplex ultrasound. Access flows that are less than 600
or if they're high flows with greater than 20% decrease, those are things that should stimulate a further look for clinical stenosis. Even the IACAVAL recommendations do, indeed, talk about volume flow and looking at volume flow. So is it volume flow?
Or is it velocity that we want to look at? And in our hands, it's been a very, very challenging subject and those of you who are involved with Vasculef probably have the same thing. Medicare has determined that dialysis shouldn't, dialysis access should not be surveilled with ultrasound.
It's not medically necessary unless you have a specific reason for looking at the dialysis access, you can't simply surveil as much as you do a bypass graft despite the work that's been done with bypass graft showing how intervening on a failing graft
is better than a failed graft. There was a good meta-analysis done a few years ago looking at all these different studies that have come out, looking at velocity versus volume. And in that study, their conclusion, unfortunately, is that it's really difficult to tell you
what you should use as volume versus velocity. The problem with it is this. And it becomes, and I'll show you towards the end, is a simple math problem that calculating volume flows is simply a product of area and velocity. In terms of area, you have to measure the luminal diameter,
and then you take the luminal diameter, and you calculate the area. Well area, we all remember, is pi r squared. So you now divide the diameter in half and then you square it. So I don't know about you,
but whenever I measure something on the ultrasound machine, you know, I could be off by half a millimeter, or even a millimeter. Well when you're talking about a four, five millimeter vessel, that's 10, 20% difference.
Now you square that and you've got a big difference. So it's important to use the longitudinal view when you're measuring diameter. Always measure it if you can. It peaks distally, and obviously try to measure it in an non-aneurysmal area.
Well, you know, I'm sure your patients are the same as mine. This is what some of our patients look like. Not many, but this is kind of an exaggerated point to make the point. There's tortuosity, there's aneurysms,
and the vein diameter varies along the length of the access that presents challenges. Well what about velocity? Well, I think most of us realize that a velocity between 100 to 300 is probably normal. A velocity that's over 500, in this case is about 600,
is probably abnormal, and probably represents a stenosis, right? Well, wait a minute, not necessarily. You have to look at the fluid dynamic model of this, and look at what we're actually looking at. This flow is very different.
This is not like any, not like a bypass graft. You've got flow taking a 180 degree turn at the anastomosis. Isn't that going to give you increased turbulence? Isn't that going to change your velocity? Some of the flow dynamic principles that are important
to understand when looking at this is that the difference between plug and laminar flow. Plug flow is where every bit is moving at the same velocity, the same point from top to bottom. But we know that's not true. We know that within vessels, for the most part,
we have laminar flow. So flow along the walls tends to be a little bit less than flow in the middle. That presents a problem for us. And then when you get into the aneurysmal section, and you've got turbulent flow,
then all bets are off there. So it's important, when you take your sample volume, you take it across the whole vessel. And then you get into something called the Time-Averaged mean velocity which is a term that's used in the ultrasound literature.
But it basically talks about making sure that your sample volume is as wide as it can be. You have to make sure that your angle is as normal in 60 degrees because once you get above 60 degrees, you start to throw it off.
So again, you've now got angulation of the anastomosis and then the compliance of a vein and a graft differs from the artery. So we use the two, we multiply it, and we come up with the volume flow. Well, people have said you should use a straight segment
of the graft to measure that. Five centimeters away from the anastomosis, or any major branches. Some people have actually suggested just using a brachial artery to assess that. Well the problems in dialysis access
is there are branches and bifurcations, pseudoaneurysms, occlusions, et cetera. I don't know about you, but if I have a AV graft, I can measure the volume flow at different points in the graft to get different numbers. How is that possible?
Absolutely not possible. You've got a tube with no branches that should be the same at the beginning and the end of the graft. But again, it becomes a simple math problem. The area that you're calculating is half the diameter squared.
So there's definitely measurement area with the electronic calipers. The velocity, you've got sampling error, you've got the anatomy, which distorts velocity, and then you've got the angle with which it is taken. So when you start multiplying all this,
you've got a big reason for variations in flow. We looked at 82 patients in our study. We double blinded it. We used a fistulagram as the gold standard. The duplex flow was calculated at three different spots. Duplex velocity at five different spots.
And then the diameters and aneurysmal areas were noted. This is the data. And basically, what it showed, was something totally non-significant. We really couldn't say anything about it. It was a trend toward lower flows,
how the gradients (mumbles) anastomosis, but nothing we could say. So as you all know, you can't really prove the null hypothesis. I'm not here to tell you to use one or use the other, I don't think that volume flow is something that
we can use as a predictor of success or failure, really. So in conclusion, what we found, is that Debbie Brow is right. Clinical examinations probably still the best technique. Look for abnormalities on dialysis. What's the use of duplex ultrasound in dialysis or patients?
And I think we're going to hear that in the next speaker. But probably good for vein mapping. Definitely good for vein mapping, arterial inflow, and maybe predicting maturation. Thank you very much.
- Thank you (mumbles). The purpose of deep venous valve repair is to correct the reflux. And we have different type of reflux. We know we have primary, secondary, the much more frequent and the rear valve agenesia. In primary deep venous incompetence,
valves are usually present but they are malfunctioning and the internal valvuloplasty is undoubtedly the best option. If we have a valve we can repair it and the results are undoubtedly the better of all deep vein surgery reconstruction
but when we are in the congenital absence of valve which is probably the worst situation or we are in post-thrombotic syndrome where cusps are fully destroyed, the situation is totally different. In this situation, we need alternative technique
to provide a reflux correction that may be transposition, new valve or valve transplants. The mono cuspid valve is an option between those and we can obtain it by parietal dissection. We use the fibrotic tissue determined by the
sickening of the PTS event obtaining a kind of flap that we call valve but as you can realize is absolutely something different from a native valve. The morphology may change depending on the wall feature and the wall thickness
but we have to manage the failure of the mono cuspid valve which is mainly due to the readhesion of the flap which is caused by the fact that if we have only a mono cuspid valve, we need a deeper pocket to reach the contralateral wall so bicuspid valve we have
smaller cusps in mono cuspid we have a larger one. And how can we prevent readhesion? In our first moment we can apply a technical element which is to stabilize the valve in the semi-open position in order not to have the collapse of the valve with itself and then we had decide to apply an hemodynamic element.
Whenever possible, the valve is created in front of a vein confluence. In this way we can obtain a kind of competing flow, a better washout and a more mobile flap. This is undoubtedly a situation that is not present in nature but helps in providing non-collapse
and non-thrombotic events in the cusp itself. In fact, if we look at the mathematical modeling in the flow on valve you can see how it does work in a bicuspid but when we are in a mono cuspid, you see that in the bottom of the flap
we have no flow and here there is the risk of thrombosis and here there is the risk of collapse. If we go to a competing flow pattern, the flap is washed out alternatively from one side to the other side and this suggest us the idea to go through a mono cuspid
valve which is not just opens forward during but is endovascular and in fact that's what we are working on. Undoubtedly open surgery at the present is the only available solution but we realized that obviously to have the possibility
to have an endovascular approach may be totally different. As you can understand we move out from the concept to mimic nature. We are not able to provide the same anatomy, the same structure of a valve and we have to put
in the field the possibility to have no thrombosis and much more mobile flap. This is the lesson we learn from many years of surgery. The problem is the mobile flap and the thrombosis inside the flap itself. The final result of a valve reconstruction
disregarding the type of method we apply is to obtain an anti-reflux mechanism. It is not a valve, it is just an anti-reflux mechanism but it can be a great opportunity for patient presenting a deep vein reflux that strongly affected their quality of life.
- 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.
- Great thank you very much. It's great to be here at Veith and talk to you about optimally deploying the Supera interwoven stent. This is a stent which is very unique and different from other stents. Slotted-tube stents are laser
cut from nitinol tubes with an open cell geometry compared to Supera which incorporates six pairs of elastic nitinol wires into an interwoven helical closed cell geometry.
This design gives it vascular-mimetic like properties in the dynamic vessel that we treat. And it has four times the radial strength of slotted-tube stents so it is resistant to compression from outside. That said its physiologically conformable
and essentially fracture-proof and it has by far the lowest chronic outward force of any of the nitinol-like stents. This just shows the off the-chart radial strength of Supera compared to nitinol and it is this
outward radial force which may generate some of the neoplastic hyperplasia. This gives the clinical advantages. You can use it in flexion points, calcified lesions with no recoil, long lesions with its conformability
and lack of fractures and if you want to convince yourself I encourage you do either intervascular ultrasound or bent-knee angiograms and compare them in this type of stent to the slotted-tube stents.
It's a unique stent so it has unique deployment. It's a ratchet delivery rather than a conventional mechanisms. The stent length is not at exact and depends on who well you implant it. It's not oversized.
You must aggressively pre-treat all segments that you're going to implant the stent. It is a slower deployment, a two-handed which is kind of an art-from if you will. It's a great stent but you have
more potential for trouble if you don't do it correctly. Here are the three important easy steps you must have documented. Aggressive pre-dilation to all of the segments where you're
going to put the stent. It's got to be one-to-one sizing. And you have to deploy it slowly on high magnification after that pre-treatment. That's it, those three steps. The pre-treatment we usually do
on Roadmap with focal force or regular balloons at least one-to-one what we're going to implant and usually a little bit higher. After that, the stent deployment, we use a Roadmap for the distal edge only.
Once we have the distal edge released, we take the Roadmap off, mag up and go slowly. The right hand throws the ratchet system, the left hand adjusts the tension. If the stent elongates a little bit, you slow down and push forward.
If it packs too much slow down, pull backwards. Here's a typical but illustrative case long disease, CTO, calcified disease in the adductor canal and the popliteal. Here's the pre-treatment with a 6 O ballon before a 5 5 superium
to make sure that it's well-expanded. Here is the mag-ed up slow deployment but you can see how beautiful it looks immediately on delivery and how well it stands up without post-dilation in this heavy calcium in the adductor canal.
Now here's the final AP angiogram. We're used to seeing good angiograms in the AP view but here's a bent-knee angiogram just showing the conformability of this stent and its strength in calcified lesions. It has great data.
Eighty-six point three primary patency in the superb trial with no fractures. Furthermore if you deploy it properly and nominally the primary patency was more than ninety percent. Extremely durable at three years
if you nominally deploy the stent, ninety-four percent freedom from TLR. Some things to remember. Again, pre-treat every vessel segment where you're going to put the stent, not just the tight part.
If you don't get pre-dilation with a longer balloon go to a shorter more aggressive focal force or non-compliant balloon. After you pre-medicate the patient don't use the small Superas.
And I can summarize mag up and slow down when you deploy the stent. We don't post dilate unless there's issues but if it does elongate or pack that's when we post dilate. What not to do with a Supera stent.
Don't use it if precision is needed at the back end for example an ostial SFA lesion from above. Again it's not an exact stent length. If there's a lot of mismatch it's not your stent.
You must adequately pre-treat, if you can't pre-treat it, don't put a Supera or in my opinion and stent. And of course you would never primary stent with this type of stent. So in conclusion the Supera stent
is a unique interwoven design giving it vascular mimetic qualities uniquely suited for the femora-popliteal lesion. Has excellent clinical results that seem to be independent of the stent length. All that said proper lesion preparation
and stent deployment techniques are essential to the success of this device. And I thank you very much for your attention.
- Thank you, Larry, thank you, Tony. Nice to be known as a fixture. I have no relevant disclosures, except that I have a trophy. And that's important, but also that Prabir Roy-Chaudhury, who's in this picture, was the genesis of some of the thoughts that I'm going to deliver here about predicting renal failure,
so I do want to credit him with bringing that to the vascular access space. You know, following on Soren's talk about access guidelines, we're dealing with pretty old guidelines, but if you look at the 2006 version, you know, just the height--
The things that a surgeon might read in his office. CKD four, patients there, you want a timely referral, you want them evaluated for placement of permanent access. The term "if necessary" is included in those guidelines, that's sometimes forgotten about.
And, of course, veins should be protected. We already heard a little bit about that, and so out our hospital, with our new dialysis patients, we usually try to butcher both antecubital veins at the same time. And then, before we send them to surgery
after they've been vein-marked, we use that vein to put in their preoperative IV, so that's our vascular access management program at Christiana Care. - [Male Speaker] That's why we mark it for you, Teddy. (laughing)
- So, you know, the other guideline is patients should have a functional permanent access at the initiation of dialysis therapy, and that means we need a crystal ball. How do we know this? A fistula should be placed at least six months
before anticipated start of dialysis, or a graft three to six weeks. Anybody who tells you they actually know that is lying, you can't tell, there's no validated means of predicting this. You hear clinical judgment, you can look at
all sorts of things. You cannot really make that projection. Now there is one interesting study by Tangri, and this is what Premier brought to our attention last year at CIDA, where this Canadian researcher and his team developed a model for predicting
progression of chronic kidney disease, not specifically for access purposes, but for others. They looked at a large number of patients in Canada, followed them through chronic kidney disease to ESRD, and they came up with a model. If you look at a simple model that uses age, sex,
estimated GFR from MDRD equation and albuminuria to predict when that patient might develop end stage renal disease, and there's now nice calculators. This is a wonderful thing, I keep it on my phone, this Qx Calculate, I would recommend you do the same,
and you can put those answers to the questions, in this app, and it'll give you the answer you're looking for. So for instance, here's a case, a 75-year-old woman, CKD stage four, her creatinine's 2.7, not very impressive,
eGFR's 18. Her urine protein is 1200 milligrams per gram, that's important, this is kind of one of the major variables that impacts on this. So she's referred appropriately at that stage to a surgeon for arteriovenous access,
and he finds that she really has no veins that he feels are suitable for a fistula, so an appropriate referral was made. Now at that time, if you'd put her into this equation with those variables, 1200, female, 75-year-old, 18 GFR, at two years, her risk of ESRD is about 30%,
and at five years about 66%, 67%. So, you know, how do you use those numbers in deciding if she needs an access? Well, you might say... A rational person might say perhaps that patient should get a fistula,
or at least be put in line for it. Well, this well-intentioned surgeon providing customer service put in a graft, which then ended up with some steal requiring a DRIL, which then still had steal, required banding, and then a few months, a year later
was thrombosed and abandoned because she didn't need it. And I saw her for the first time in October 2018, at which time her creatinine is up to 3.6, her eGFR's down to 12, her protein is a little higher, 2600, so now she has a two-year risk of 62%, and a five-year risk of 95%,
considerably more than when this ill-advised craft was created. So what do you do with this patient now? I don't have the answer to that, but you can use this information at least to help flavor your thought process,
and what if you could bend the curve? What if you treated this patient appropriately with ACE inhibitors and other methods to get the protein down? Well, you can almost half her two-year risk of renal failure with medical management.
So these considerations I think are important to the team, surgeon, nurses, nephrologists, etc., who are planning that vascular access with the patient. When to do and what to do. And then, you know, it's kind of old-fashioned to look at the trajectory.
We used to look at one over creatinine, we can look at eGFR now, and she's on a trajectory that looks suspicious for progression, so you can factor that into your thought process as well. And then I think this is the other very important concept, I think I've spoken about this here before,
is that there's no absolute need for dialysis unless you do bilateral nephrectomies. Patients can be managed medically for quite a while, and the manifestations of uremia dealt with quite safely and effectively, and you can see that over the years, the number of patients
in this top brown pattern that have been started on dialysis with a GFR of greater than 15 has fallen, or at least, stopped rising because we've recognized that there's no advantage, and there may be disadvantages to starting patients too early.
So if your nephrologist is telling I've got to start this patient now because he or she needs dialysis, unless they had bilateral nephrectomies that may or may not be true. Another case,
64-year-old male, CKD stage four, creatinine about four, eGFR 15, 800 milligrams of proteinuria, referred to a vascular access surgeon for AV access. Interesting note, previous central lines, or AICD, healthy guy otherwise.
So in April 2017 he had a left wrist fistula done, I think that was a very appropriate referral and a very appropriate operation by this surgeon. At that time his two-year risk was 49, 50%, his five-year risk 88%. It's a pretty good idea, I think, to get a wrist fistula
in that patient. Once again, this is not validated for that purpose. I can't point you to a study that says by using this you can make well-informed predictions about when to do vascular access, but I do think it helps to flavor the judgment on this.
Also, I saw him for the first time last month, and his left arm is like this. Amazing, that has never had a catheter or anything, so I did his central venogram, and this is his anatomy. I could find absolutely no evidence of a connection between the left subclavian and the superior vena cava,
I couldn't cross it. Incidentally, this was done with less than 20 CCs of dye of trying to open this occlusion or find a way through, which was unsuccessful. You can see all the edema in his arm. So what do you do with this guy now?
Well, up, go back. Here's his trajectory of CKD four from the time his fistula is done to the time I'm seeing him now, he's been pretty flat. And his proteinuria's actually dropped
with medical management. He's only got 103 milligrams per gram of proteinuria now, and his two-year risk is now 23%, his five-year risk is 56%, so I said back to the surgeon we ligate this damn thing, because we can't really do much to fix it,
and we're going to wait and see when it's closer to time to needing dialysis. I'm not going to subject this guy to a right-arm fistula with that trajectory of renal disease over the past two years. So combining that trajectory with these predictive numbers,
and improved medical care for proteinuria I think is a good strategy. So what do you do, you're weighing factors for timing too early, you've got a burden of fistula failure, interventions you need to use to maintain costs, morbidity, complications,
steal, neuropathy that you could avoid versus too late and disadvantages of initiating hemodialysis without a permanent access. And lastly, I'm going to just finish with some blasphemy. I think the risk of starting dialysis with a catheter is vastly overstated.
If you look at old data and patient selection issues, and catheter maintenance issues, I think... It's not such an unreasonable thing to start a patient with a catheter. We do it all the time and they usually live.
And even CMS gives us a 90-day grace period on our QIP penalties, so... If you establish a surgeon and access plan, I think you're good to go. So who monitors access maturation? I don't know, somebody who knows what they're doing.
If you look at all the people involved, I know some of these individuals who are absolute crackerjack experts, and some are clueless. It has nothing to do with their age, their gender, their training, their field. It's just a matter of whether they understand
what makes a good fistula. You don't have to be a genius, you just can't be clueless. This is not a mature usable fistula, I know that when I see it. Thank you.
- Thank you 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.
- We are talking about the current management of bleeding hemodialysis fistulas. I have no relevant disclosures. And as we can see there with bleeding fistulas, they can occur, you can imagine that the patient is getting access three times a week so ulcerations can't develop
and if they are not checked, the scab falls out and you get subsequent bleeding that can be fatal and lead to some significant morbidity. So fatal vascular access hemorrhage. What are the causes? So number one is thinking about
the excessive anticoagulation during dialysis, specifically Heparin during the dialysis circuit as well as with cumin and Xarelto. Intentional patient manipulati we always think of that when they move,
the needles can come out and then you get subsequent bleeding. But more specifically for us, we look at more the compromising integrity of the vascular access. Looking at stenosis, thrombosis, ulceration and infection. Ellingson and others in 2012 looked at the experience
in the US specifically in Maryland. Between the years of 2000/2006, they had a total of sixteen hundred roughly dialysis death, due to fatal vascular access hemorrhage, which only accounted for about .4% of all HD or hemodialysis death but the majority did come
from AV grafts less so from central venous catheters. But interestingly that around 78% really had this hemorrhage at home so it wasn't really done or they had experienced this at the dialysis centers. At the New Zealand experience and Australia, they had over a 14 year period which
they reviewed their fatal vascular access hemorrhage and what was interesting to see that around four weeks there was an inciting infection preceding the actual event. That was more than half the patients there. There was some other patients who had decoags and revisional surgery prior to the inciting event.
So can the access be salvaged. Well, the first thing obviously is direct pressure. Try to avoid tourniquet specifically for the patients at home. If they are in the emergency department, there is obviously something that can be done.
Just to decrease the morbidity that might be associated with potential limb loss. Suture repairs is kind of the main stay when you have a patient in the emergency department. And then depending on that, you decide to go to the operating room.
Perera and others 2013 and this is an emergency department review and emergency medicine, they use cyanoacrylate to control the bleeding for very small ulcerations. They had around 10 patients and they said that they had pretty good results.
But they did not look at the long term patency of these fistulas or recurrence. An interesting way to kind of manage an ulcerated bleeding fistula is the Limberg skin flap by Pirozzi and others in 2013 where they used an adjacent skin flap, a rhomboid skin flap
and they would get that approximal distal vascular control, rotate the flap over the ulcerated lesion after excising and repairing the venotomy and doing the closure. This was limited to only ulcerations that were less than 20mm.
When you look at the results, they have around 25 AV fistulas, around 15 AV grafts. The majority of the patients were treated with percutaneous angioplasty at least within a week of surgery. Within a month, their primary patency was running 96% for those fistulas and around 80% for AV grafts.
If you look at the six months patency, 76% were still opened and the fistula group and around 40% in the AV grafts. But interesting, you would think that rotating an adjacent skin flap may lead to necrosis but they had very little necrosis
of those flaps. Inui and others at the UC San Diego looked at their experience at dialysis access hemorrhage, they had a total 26 patients, interesting the majority of those patients were AV grafts patients that had either bovine graft
or PTFE and then aneurysmal fistulas being the rest. 18 were actually seen in the ED with active bleeding and were suture control. A minor amount of patients that did require tourniquet for a shock. This is kind of the algorithm when they look at
how they approach it, you know, obviously secure your proximal di they would do a Duplex ultrasound in the OR to assess hat type of procedure
they were going to do. You know, there were inciting events were always infection so they were very concerned by that. And they would obviously excise out the skin lesion and if they needed interposition graft replacement they would use a Rifampin soak PTFE
as well as Acuseal for immediate cannulation. Irrigation of the infected site were also done and using an impregnated antibiotic Vitagel was also done for the PTFE grafts. They were really successful in salvaging these fistulas and grafts at 85% success rate with 19 interposition
a patency was around 14 months for these patients. At UCS, my kind of approach to dealing with these ulcerated fistulas. Specifically if they bleed is to use
the bovine carotid artery graft. There's a paper that'll be coming out next month in JVS, but we looked at just in general our experience with aneurysmal and primary fistula creation with an AV with the carotid graft and we tried to approach these with early access so imagine with
a bleeding patient, you try to avoid using catheter if possible and placing the Artegraft gives us an opportunity to do that and with our data, there was no significant difference in the patency between early access and the standardized view of ten days on the Artegraft.
Prevention of the Fatal Vascular Access Hemorrhages. Important physical exam on a routine basis by the dialysis centers is imperative. If there is any scabbing or frank infection they should notify the surgeon immediately. Button Hole technique should be abandoned
even though it might be easier for the patient and decreased pain, it does increase infection because of that tract The rope ladder technique is more preferred way to avoid this. In the KDOQI guidelines of how else can we prevent this,
well, we know that aneurysmal fistulas can ulcerate so we look for any skin that might be compromised, we look for any risk of rupture of these aneurysms which rarely occur but it still needs to taken care of. Pseudoaneurysms we look at the diameter if it's twice the area of the graft.
If there is any difficulty in achieving hemostasis and then any obviously spontaneous bleeding from the sites. And the endovascular approach would be to put a stent graft across the pseudoaneurysms. Shah and others in 2012 had 100% immediate technical success They were able to have immediate access to the fistula
but they did have around 18.5% failure rate due to infection and thrombosis. So in conclusion, bleeding to hemodialysis access is rarely fatal but there are various ways to salvage this and we tried to keep the access viable for these patients.
Prevention is vital and educating our patients and dialysis centers is key. Thank you.
- Now I want to talk about, as Chrissy mentioned AVM Classification System and it's treatment implication to achieve cure. How do I put forward? Okay, no disclosures. So there are already AVM Classification Systems. One is the well-known Houdart classification
for CNS lesions, and the other one is quite similar to the description to the Houdart lesion, the Cho Do classification of peripheral AVM's. But what do we expect from a good classification system? We expect that it gives us also a guide how to treat with a high rate of cure,
also for complex lesions. So the Yakes Classification System was introduced in 2014, and it's basically a further refinement of the previous classification systems, but it adds other features. As for example, a new description of
a new entity, Type IV AVM's with a new angioarchitecture, it defines the nidus, and especially a value is that it shows you the treatment strategy that should be applied according to angioarchitecture to treat the lesion. It's based on the use of ethanol and coils,
and it's also based on the long experience of his describer, Wayne Yakes. So the Yakes Classification System is also applicable to the very complex lesions, and we start with the Type I AVM, which is the most simple, direct
arterial to venous connection without nidus. So Type I is the simplest lesion and it's very common in the lung or in the kidney. Here we have a Type I AVM come from the aortic bifurcation draining into the paralumbar venous plexus,
and to get access, selective cauterization of the AVM is needed to define the transition point from the arterial side to the venous side, and to treat. So what is the approach to treat this? It's basically a mechanical approach, occluding
the lesion and the transition point, using mechanical devices, which can be coils or also other devices. For example, plugs or balloons. In small lesions, it can also be occluded using ethanol, but to mainly in larger lesions,
mechanical devices are needed for cure. Type II is the common and typical AVM which describes nidus, which comes from
multiple in-flow arteries and is drained by multiple veins. So this structure, as you can see here, can be, very, very dense, with multiple tangled fistulaes. And the way to break this AVM down is mainly that you get more selective views, so you want to get selective views
on the separate compartments to treat. So what are the treatment options? As you can see here, this is a very selective view of one compartment, and this can be treated using ethanol, which can be applied
by a superselective transcatheter arterial approach, where you try to get as far as possible to the nidus. Or if tangled vessels are not allowing transcatheter access, direct puncture of the feeding arteries immediately proximal to the nidus can be done to apply ethanol. What is the difference between Type IIa and IIb?
IIb has the same in-flow pattern as Type a, but it has a different out-flow pattern, with a large vein aneurysm. It's crucial to distinguish that the nidus precedes this venous aneurysm. So here you can see a nice example for Type IIb AVM.
This is a preview of the pelvis, we can here now see, in a lateral view, that the nidus fills the vein aneurysm and precedes this venous aneurysm. So how can this lesion be accessed? Of course, direct puncture is a safe way
to detect the lesion from the venous side. So blocking the outflow with coils, and possibly also ethanol after the flow is reduced to reflux into the fistulaes. It's a safe approach from the venous side for these large vein aneurysm lesions,
but also superselective transcatheter arterial approach to the nidus is able to achieve cure by placing ethanol into the nidus, but has to be directly in front of the nidus to spare nutrient arteries.
Type IIIa has also multiple in-flow arteries, but the nidus is inside the vein aneurysm wall. So the nidus doesn't precede the lesion, but it's in the vein wall. So where should this AVM be treated?
And you can see a very nice example here. This is a Type IIIa with a single out-flow vein, of the aneurysm vein, and this is a direct puncture of the vein, and you can see quite well that this vein aneurysm has just one single out-flow. So by blocking this out-flow vein,
the nidus is blocked too. Also ethanol can be applied after the flow was reduced again to reflux into the fistulas inside the vein aneurysm wall. And here you can see that by packing a dense packing with coils, the lesion is cured.
So direct puncture again from the venous side in this venous aneurysm venous predominant lesion. Type IIIb, the difference here is again, the out-flow pattern. So we have multiple in-flow arteries, the fistulaes are again in the vein aneurysm.
Which makes it even more difficult to treat this lesion, is that it has multiple out-flow veins and the nidus can also precede into these or move into these out-flow veins. So the dense packing of the aneurysm might have to be extended into the out-flow veins.
So what you can see here is an example. Again you need a more selective view, but you can already see the vein aneurysm, which can be targeted by direct puncture. And again here, the system applies. Placing coils and dense packing of the vein aneurysm,
and possibly also of the out-flow veins, can cure the lesion. This is the angiogram showing cure of this complex AVM IIIb. Type IV is a very new entity which was not described
in any other classification system as of yet. So what is so special about this Type IV AVM is it has multiple arteries and arterioles that form innumerable AV fistulaes, but these fistulaes infiltrate the tissue. And I'm going to specify this entity in a separate talk,
so I'm not going too much into details here. But treatment strategy of course, is also direct puncture here, and in case possible to achieve transarterial access very close to the nidus transarterial approach is also possible. But there are specific considerations, for example
50/50 mixture of alcohol, I'm going to specify this in a later talk. And here you can see some examples of this micro-fistulae in Type IV AVM infiltrative type. This is a new entity described. So the conclusion is that the Yakes Classification System
is based on the angioarchitecture of AVM's and on hemodynamic features. So it offers you a clear definition here the nidus is located, and where to deliver alcohol in a safe way to cure even complex AVM's.
Thank you very much.
- These are my disclosures, as it pertains to this talk. FEVAR has become increasingly common treatment for juxtarenal aneurysm in the United States since it's commercial release in 2012. Controversy remains, however, with regard to stenting the SMA when it is treated with a single-wide, 10 mm scallop in the device.
You see here, things can look very similar. You see SMA treated with an unstented scallop on the left and one treated with the stented SMA on the right. It has been previously reported by Jason Lee that shuttering can happen with single-wide scallops of the SMA and in their experience
the SMA shuttering happens to different degree in patients, but is there in approximately 50% of the patients. But in his experience, the learning curve suggests that it decreases over time. At UNC, we use a selective criteria for stenting in the SMA. We will do a balloon test in the SMA,
as you see in the indication, and if the graft is not moved, then our SMA scallop is appropriate in line. If we have one scallop and one renal stent, its a high likelihood that SMA scallop will shift and change over time. So all those patients get stented.
If there is presence of pre-existing visceral stenosis we will stent the SMA through that scallop and in all of our plans, we generally place a 2 mm buffer, between the bottom edge of the scallop and the SMA. We looked over our results and 61 Zenith fenestrated devices performed over a short period of time.
We looked at the follow-up out up to 240 days and 40 patients in this group had at least one single wide scallop, which represented 2/3 of the group. Our most common configuration as in most practices is too small renal fenestrations and one SMA scallop.
Technically, devices were implanted in all patients. There were 27 patients that had scallops that were unstented. And 13 of the patients received stented scallops. Hospital mortality was one out of 40, from a ruptured hepatic artery aneurysm post-op.
No patients had aneurysm-related mortality to the intended treated aneurysm. If you look at this group, complications happen in one of the patients with stented SMA from a dissection which was treated with a bare metal stent extension at the time
of the initial procedure. And in the unstented patients, we had one patient with post-op nausea, elevated velocities, found to have shuttering of the graft and underwent subsequent stenting. The second patient had elevated velocities
and 20-pound weight loss at a year after his treatment, but was otherwise asymptomatic. There is no significant difference between these two groups with respect to complication risk. Dr. Veith in the group asked me to talk about stenting choice
In general, we use the atrium stent and a self-expanding stent for extension when needed and a fenestrated component. But, we have no data on how we treat the scallops. Most of those in our group are treated with atrium. We do not use VBX in our fenestrated cases
due to some concern about the seal around the supported fenestration. So Tips, we generally calculate the distance to the first branch of the SMA if we're going to stent it. We need to know the SMA diameter, generally its origin where its the largest.
We need to position the imaging intensifier orthogonal position. And we placed the stent 5-6 mm into the aortic lumen. And subsequently flare it to a 10-12 mm balloon. Many times if its a longer stent than 22, we will extend that SMA stent with a self-expanding stent.
So in conclusion, selective stenting of visceral vessels in single wide scallops is safe in fenestrated cases during this short and midterm follow-up if patients are carefully monitored. Stenting all single wide scallops is not without risk and further validation is needed
with multi-institution trial and longer follow-up
- I think there'll be a little bit of duplication here cuz he talked about a lot of things that I put in here. I've no disclosures. The Goals of Sclerotherapy is damage of the endothelium with vascular fibrosis and obliteration. The idea is to use the minimal dose of sclerosant and minimal concentration and avoid injury
to the surrounding normal vessels and tissue. Of course, I won't go into a lot of detail about the history and physical, but what is very important is trying to get some realistic expectations. I saw some incredible results just now.
I don't know if I get that all the time, and so I do want my patients to be aware that perfection is I usually don't seem to really get that. So the consent's very important and photographic documentation is extremely important
because you really do want to show em what it looked like beforehand cuz many times they forget where they started. Just like Dr. Miyake said determine the source of the spider vein's very important. If there's axial vein problems,
I'm not suggesting you have to do a duplex on everybody, but if you have evidence of varicosities, venous insufficiency you might you're not going to get very good results if you have axial vein reflux particularly in line with where
the spider veins and telangiectases are. Same with perforator veins, you may have an issue there, and if you're just treatin' the spiders and not gettin' the source. Dr. Dillavou is going to talk about reticular veins next, but I do emphasize the importance of treating
the feeding veins that are feeding into the spider complex. The equipment, well these are now absolutely required for me and use to be I may not have had to have em, but now I do. I have to have magnification, course you need sclerosants, syringes, needles, and cotton balls.
I like the butterfly needle for the larger veins and 30 gauge for the spiders. There are these polarized lights or vein lights which sometimes come in handy. You've seen the infrared imaging now in the last two talks. I'll show you a little bit of that.
I personally don't use it, but I do think there are probably some cases where it come in very handy, and of course compression stockings and cotton balls and tape even though I don't compress routinely for just spider veins.
Basic Principles, treat the large to small, proximal to distal which you do with varicose veins. The most important though is what Dr. Miyake just mentioned. You want the lowest effective concentration, but in particular, you want to minimize the plunger pressure.
Sometimes you can get a little frustrated when you're trying to get into a vein, you don't want to really inject hard at all or you will get an ulceration. And post-op compression, again is somewhat controversial, at least in my mind, but ambulation of course
is very, very helpful. Contraindications, course allergies, acute DVT, PAD, acute SVT, most of the things you would an active infection in the extremity, you're not going to treat that. The Sclerosants are divided into detergents,
osmotics, and chemical irritants. The main detergents are sodium tetradecyl sulfate and polidocanol. These are primarily what I use in my practice cuz they're FDA-approved and I tend to like to have that when I'm treating patients,
and the concentrations listed here which are in line with what you just saw. There is this study of Sclerotherapy of Telangiectases comparing tetradecyl and polidocanol to a control of isotonic saline and of course there was a significant difference
between the sclerosants and isotonic saline thank goodness. The only thing I'm not real think this study's that helpful cuz it compared one percent STS to .5 polidocanol. I don't think that's a fair comparison
usually I use .1 to .2, and I think STS and tetradecyl are fairly equivalent. The osmotic agents you just heard about, but you know about saline probably, hypertonic saline but also hypertonic dextrose, or there's the combination of saline and dextrose which is a sclerodex.
Again, not really available here. Chemical irritants are glycerin and chromate glycerin. Again, very viscous, low ulcerative capabilities, but again not FDA-approved for this. I don't really use it routinely. There are other sclerosants out there,
but I don't know of anybody using them for telangiectases. Technique, lowest effective concentration again, results determined by the concentration and contact time so that's why I'll say use a low concentration but when you inject, let it sit there a second as you're injecting, just for a few seconds,
maybe 10 seconds even. That contact time helps a lot. I'm already out of time, and I still have quite a bit here, but here's some videos. That's me using a polarized light source. We'll skip through all that.
Here's treating the reticular vein that feeds the spider veins, lower cartoon to kind of show you what I was talking about there. I think you'll probably got the concept but again, if you don't treat the feeder vein,
you're probably not going to get very good results. Here's that infrared technology. Now, I can't seem to skip, okay Complications, well you just actually heard a very good talk on that, so I'll probably stop here since I'm already out of time.
So, I was going to run through that but basically you've already seen it well covered, so I'll stop here.
- (Speaker) Thank you very much So we're going to try to tackle all of these issues. I do have some disclosures. The indigo system that we're going to talk about does have FDA approval in the vascular system. It is contraindicated for neurovascular and coronary use although there are specific catheters made by this company
for use in those areas, so we're going to talk about the use strictly in the periphery. So we know that Acute Limb Ischemia requires revascularization and we use this Power Aspiration system, we call it XTRACT, using the Indigo system for a number of different therapeutic options.
The device we're talking about, these are reinforced catheters so there's no collapsing of the tip during aspiration. They're atraumatic, this technology was developed and really pirated in some way from stroke work, where we were putting these catheters in the
middle cerebral artery, so these catheters track, it's exceptionally rare to see any vessel damage. We have not dissected any vessels in over 120 cases. The catheters are hooked up to direct tubing to a small handheld pump,
which is easy to use, which sucks, an essentially true vacuum, so that you get maximal aspiration. And, they come in different sizes: 3, 5, 6, and 8 French and you can see there's a large increase in aspiration power as we go up
in size. So this would be a typical case where we have an SFA occlusion, in the distal SFA. There's also a TP trunk occlusion. There's an anterior tib. which is a stump distally. And we don't see any real flow below the TP trunk.
Here we can take a CAT6, we place it in the clot. It's very simple to use. The learning curve here is extremely low. You turn the vacuum on, you just be patient and wait. You don't run this through the clot, and if you suck this way and be patient,
embolization is extremely rare, and I'll show you some of that data. We clean that up as I showed you, then we advance down into this tibioperoneal trunk, and after two or three minutes of aspiration with some gentle catheter moving,
we're able to clear up the TP trunk, we can come back and balloon the underlying lesions and leave this patient who had no runoff, essentially with two vessel runoff. In Press right now, we're actually online, published, and in print, are the results of the PRISM trial,
which is using this system as a retrospective registry, and this is used in 79 patients after failed thrombolysis, as a primary device for acute limb ischemia, for distal emboli caused by other interventional procedures such as angioplasty stem placement.
We looked at patients who had little flow or no flow, TIMI 0-1, and basically we evaluated the flow before. We use this system after we use the system and after any other adjunctive intervention. And along the bottom you can see that we restored flow,
excellent flow, TIMI 2 or 3 flow, and 87% percent of the patients, after the final intervention, so treating the underlying lesion, 96% of patients had essentially normal flow. So, 87% as I say success
just with the device alone, and then using adjunct devices. There were no serious adverse events. The complications from this include vasospasm. We did not have any vessel dissections, or vascular injuries, and
no serious event directly related to the catheter. So where do we use this? Well, we can use this as I mentioned for acute limb ischemia. We can use it as a primary therapy for embolic occlusions. We can use it after iatrogenic emboli.
We use it after incomplete thrombolysis when there's residual clot, so we don't have to lyse someone up further. We can save lysis time and money overnight. And we've expanded our uses out of the arterial and now we're looking at venous, pulmonary, mesenteric,
and dialysis applications. We just published our results in the pulmonary circulation from the single center. There's a retrospective study that's been completed, and now a prospective study which we're just beginning right now.
We actually have our first sites up and ready. We've had experience with DVT, and we're also using this in the mesenteric and portal circulation. A quick image of a before and after on a pulmonary embolism. There's an extensive mass of patient who came in with profound hypotension,
post-using the XTRACT system. So the benefits, simple and easy to use, highly trackable. Limitations, blood loss if you don't know how to use this right. You just can't run this vacuum in flowing blood. Once you learn that and control the switch
blood loss can be minimized. As I mentioned, the learning curve is small. A few tips, not to use the separator much in the arterial system. Just be patient with your suction. Be careful damaging the tip when you introduce it
through the sheath, there's an introducer. In conclusion, we think this is an effective method to primarily treat arterial occlusions, venous pulmonary occlusions, and more data will be coming to you on the venous and pulmonary sides but I think in the arterial side,
we actually have several publications out, demonstrating safety and ethicacy. Thank you.
- So I don't have to give you any data. I just have to tell you how we do it. So this is the easiest talk of this session. Step-by-step technical tips. Now our definition of pharmaco-mechanical may vary between us so I'll give that as we go along. These are my conflicts.
When to use it. Well certainly as you already heard, Massive PE has contraindication to full dose lytic is one area. Submassive elevated risk may be another. We've already seen multiple people put up
these guidelines so what we're really talking about at this point in time is those patients that we just talked, that those two groups that they just talked about because those are the ones that we're trying to treat. The biggest thing is don't be frozen by indecision.
Majority of patients eligible for thrombolysis do not receive it. It's amazing to me as a referral center to get the call from an outside community hospital or the patient with hypotension, abnormal RV or biomarkers and they've barely given the patient
Heparin and they just want to transfer the patient out of there and you tell them that's a massive PE. Please give them systemic thrombolysis and they go what? And I go you now have 10 times the death rate of an acute myocardial infarction. Would you give this patient lytics for acute MI?
Yes. Then give them the freaking lytics. Save their life. It's amazing what's going on in this country. So the PERT Consortium and everything, we really need to educate the community
because it's ridiculous. If you look at the utilization of thrombolysis, it's going down. Unbelievable and if you look at the in-hospital mortality for these patients that have significant PE, the in-hospital mortality is much higher
if you don't give thrombolysis. You've already seen this indirectly in a bunch of different lectures, but I just wanted to show you very quickly how to do this on an echo or CT. You want to get the center line, get it at the valve and then measure it one centimeter
below that valvular plane. This is something you don't have to depend on radiology just to do. You can just look at the transfer CT. You can look at the echo. You don't have to fight with your echo guy to give you that.
It's also very evident and often times just looking at the images. Why treat submassive elevated risk PE? You know what? I've heard all the mortality stuff. I get it.
It doesn't change mortality that much. It does and we should measure it as a primary endpoint in our trials. Change your discharge time and in this day and age, medicine is so expensive. Time in the hospital, repeat procedures,
elevated your amount of treatment for that patient really has to be looked at as part of that, not just mortality. But there's eight times more recurrent PE and four times a mortality rate if you have a PE and unresolved RV dysfunction at discharge
and that should be looked at prior to discharge, not just say well they look like they're doing okay. Treatment of IVC, higher risk PE. Certainly the other thing we have to look at is there's other things to do. You've already heard a little bit
that there's IVC filters out there. We take out 90 some percent of our IVC filters in our section. We actually as a system now are up to 60% at seven months and it only takes effort. The patients that I see die in our hospital
in the last year that shouldn't have died are patients that should've gotten an IVC filter because they got heroic things to take out their PE and nobody put a filter in even though they had significant DVT left over because they were afraid of the TV commercials?
Oh my gosh. If you look at the 27 extra deaths that we've had from IVC filters that were removable in the United States, and you take our experience and multiply it by the number of tertiary care hospitals in the United States, use them when they're appropriate.
Take them out so the risk is low, but don't go away from them. They've already been shown to be beneficial for the right patient population. But you also have embolectomy and surgery should also be considered.
Step by step. Make the decision and clinically be consistent. PERT team or other consistent mechanisms. We have an app that we use. This is throughout our entire healthcare system so all the vascular specialists have this.
It's an algorithm that's supposed to be used both in the ER and for the different vascular specialties so everybody's being treated very similarly. We have all the different definitions. We have the PESI calculator. All this is in an app
that's readily available to our constituents. Special consideration certainly is the tolerance of thrombolysis, underlying tolerance of pulmonary hypertension. Again, we need to evaluate the patient, not just label them as a PE.
And I also think there's a special population we need to study and that's the socked in pulmonary artery with no perfusion on a CT scan. I think this is a different population long term and we need to study that a little bit more. We got to get the patient back from the edge.
I think I'm opposite of Jeff. I don't want to see them get worse and then treat 'em. I want to prevent them from getting worse as long as I'm selecting that population in a thoughtful matter. We primarily use low dose TNK.
This is nothing I'm going to give you data on. This is an institutional, what do you want to call it, anecdotal experience and we lost our contracts except for TNK so we had to go to this and so we do a lot of catheter-directed. You've already seen all these trials.
There's a ton of different devices out there. The one I want to talk to you about is using a really fancy one called a pigtail catheter and another one called an ethos catheter. This is a patient that had a significant PE. You can see that they've got bilateral main PE.
This is on table. This is what we do for the vast majority of our patients. We sit there, we use ultrasound guided access to the vein so that we cut down our venous complications for access site. The patient is given 20 and 30% of a loading dose
of TNK and then we watch them. If you look at thrombus in a test tube and you give a thrombolytic therapy, it takes about 20 minutes for fibrinolysis. So this is what we do. As you're going to see, this is over 25 minutes
and we see the patient went from a pulmonary pressure of 65 and a heart rate of 115 down to 25 minutes, the patient's pulmonary pressure is about 44 and their heart rate is in the 90's. This patient then has all the catheters removed on the table even though they got lytic
and they're heparinized. This is a venipuncture, so big IV. We send them up to the unit and we typically discharge them the next day. We have an echo B4 discharge to make sure there's been a significant recovery of RV.
If not we'll watch them an extra day and then all these patients get a CT again. I'm sorry an echo again at 30 days to make sure that we're getting good resolution from that. On table results, decrease your complications. Thrombolysis has always been associated with the
duration of thrombolytic therapy and intracranial bleed. Now you can either use a pigtail catheter which is what we use for most of these people because we can measure pressure in it. We spin it around a little bit in the pulmonary arteries and give the dosage.
Again, we give 20-30% of the dose. There is no data for that. If significant improvement does not occur, they'll get dripped overnight in the ICU at usually .5 to 1 milligram per hour. You've already seen the data for EKOS.
We use this if we think we need a little bit quicker Thrombolysis such as in a socked in pulmonary artery 'cause we have no flow. We do think that may help, but we don't have any data for that. It makes us feel good.
We spend a lot more money and so we think that may be reasonable at that point in time. This is just what it looks like when you put in bilateral EKOS catheters. Certainly the patient can be put in the ICU for this. I do think that we should do a trial looking at EKOS
with a little higher dose, do it for 30 minutes, look at those pulmonary pressures right on the table. I think, again, my own opinion is after 25 years, the closer we get to being done on table, catheters out, patients doing well, the better, safer procedure we have,
the less chance of mortality, the less chance of complication and as you decrease complications, your benefit improves. We've already seen the results and you'll see more of these from non-randomized trials such as Seattle 2 which looked at 150 patients,
but they saw very quick recovery of the RV which was very important. If you look at technical success, it was very high. The dosage of thrombolytic exceedingly lower, lower than what we're giving in a PTO catheter, that's for sure.
And if you look at the RV from Ultima Trial which was randomized. There was faster RV recovery utilizing this device. Thank you very much.
- Thank you Dr. Albaramum, it's a real pleasure to be here and I thank you for being here this early. I have no disclosures. So when everything else fails, we need to convert to open surgery, most of the times this leads to partial endograft removal,
complete removal clearly for infection, and then proximal control and distal control, which is typical in vascular surgery. Here's a 73 year old patient who two years after EVAR had an aneurism growth with what was thought
to be a type II endoleak, had coiling of the infermius mesenteric artery, but the aneurism continued to grow. So he was converted and what we find here is a type III endoleak from sutures in the endograft.
So, this patient had explantations, so it is my preference to have the nordic control with an endovascular technique through the graft where the graft gets punctured and then we put a 16 French Sheath, then we can put a aortic balloon.
And this avoids having to dissect the suprarenal aorta, particularly in devices that have super renal fixation. You can use a fogarty balloon or you can use the pruitt ballon, the advantage of the pruitt balloon is that it's over the wire.
So here's where we removed the device and in spite of the fact that we tried to collapse the super renal stent, you end up with an aortic endarterectomy and a renal endarterectomy which is not a desirable situation.
So, in this instance, it's not what we intend to do is we cut the super renal stent with wire cutters and then removed the struts individually. Here's the completion and preservation of iliac limbs, it's pretty much the norm in all of these cases,
unless they have, they're not well incorporated, it's a lot easier. It's not easy to control these iliac arteries from the inflammatory process that follows the placement of the endograft.
So here's another case where we think we're dealing with a type II endoleak, we do whatever it does for a type II endoleak and you can see here this is a pretty significant endoleak with enlargement of the aneurism.
So this patient gets converted and what's interesting is again, you see a suture hole, and in this case what we did is we just closed the suture hole, 'cause in my mind,
it would be simple to try and realign that graft if the endoleak persisted or recurred, as opposed to trying to remove the entire device. Here's the follow up on that patient, and this patient has remained without an endoleak, and the aneurism we resected
part of the sack, and the aneurism has remained collapsed. So here's another patient who's four years status post EVAR, two years after IMA coiling and what's interesting is when you do delayed,
because the aneurism sacks started to increase, we did delayed use and you see this blush here, and in this cases we know before converting the patient we would reline the graft thinking, that if it's a type III endoleak we can resolve it that way
otherwise then the patient would need conversion. So, how do we avoid the proximal aortic endarterectomy? We'll leave part of the proximal portion of the graft, you can transect the graft. A lot of these grafts can be clamped together with the aorta
and then you do a single anastomosis incorporating the graft and the aorta for the proximal anastomosis. Now here's a patient, 87 years old, had an EVAR,
the aneurism grew from 6 cm to 8.8 cm, he had coil embolization, translumbar injection of glue, we re-lined the endograft and the aneurism kept enlarging. So basically what we find here is a very large type II endoleak,
we actually just clip the vessel and then resected the sack and closed it, did not remove the device. So sometimes you can just preserve the entire device and just take care of the endoleak. Now when we have infection,
then we have to remove the entire device, and one alternative is to use extra-anatomic revascularization. Our preference however is to use cryo-preserved homograft with wide debridement of the infected area. These grafts are relatively easy to remove,
'cause they're not incorporated. On the proximal side you can see that there's a aortic clamp ready to go here, and then we're going to slide it out while we clamp the graft immediately, clamp the aorta immediately after removal.
And here's the reconstruction. Excuse me. For an endograft-duodenal fistula here's a patient that has typical findings, then on endoscopy you can see a little bit of the endograft, and then on an opergy I series
you actually see extravasation from the duodenal. In this case we have the aorta ready to be clamped, you can see the umbilical tape here, and then take down the fistula, and then once the fistula's down
you got to repair the duodenal with an omental patch, and then a cryopreserved reconstruction. Here's a TEVAR conversion, a patient with a contained ruptured mycotic aneurysm, we put an endovascular graft initially, Now in this patient we do the soraconomy
and the other thing we do is, we do circulatory support. I prefer to use ECMO, in this instances we put a very long canula into the right atrium, which you're anesthesiologist can confirm
with transassof forgeoligico. And then we use ECMO for circulatory support. The other thing we're doing now is we're putting antibiotic beads, with specific antibiotic's for the organism that has been cultured.
Here's another case where a very long endograft was removed and in this case, we put the device offline, away from the infected field and then we filled the field with antibiotic beads. So we've done 47 conversions,
12 of them were acute, 35 were chronic, and what's important is the mortality for acute conversion is significant. And at this point the, we avoid acute conversions,
most of those were in the early experience. Thank you.
- You'll be pleased to know we've got a bit better at using ceiling mounted lead shields and goggles, but there's still room for improvement. These are my disclosures. I thought I'd start just by putting into context the exposures that we receive as operators. So medical diagnostics scans
can be anything up to 25 millisieverts. If you're a classified radiation worker you can only get 20 millisieverts per year. Background radiation, depending on where you live, is something between one and 10 millisieverts per year. And it varies from department to department.
But for a complex endovascular branch and fenestrated case you get typically 50 microsieverts of radiation outside the lead. What is irrefutable is that once you get to 100 millisieverts you have got a raised risk of solid cancers and leukemia.
What we do not know, we simply don't know, is what is the dose response below that 100 millisievert threshold, and is there any individual differences in sensitivity to radiation? Why don't we know?
Because we're no good at following up operators and patients after they receive an exposure. What we need is stringent study design, we need well defined populations, they need to be large studies, 10s of thousands, we need to control for
all the confounding factors for cancer, we need really high quality followup, and we need to know what dose we're receiving. This is my interventional radiology colleague. He's been there since the inception of the complex endovascular program at St. Thomas',
and I asked him to tell me what he did over the past 10 years. And you can see that this is his logbook. It excludes quite a number of perhaps lower exposure cases including GI cases, dilatations, nephrostomies. So he's done 1071 cases in 10 years.
He doesn't know his dose. But if you think per case exposure is 20, 40, or 60 microsieverts you can see that the exposures quickly build up. And in a 20-year career he's going to breach probably that 100 microsievert threshold.
So these numbers are just worth thinking about. So what evidence do we have that exposure causes DNA damage? It has been looked at in mice. If you expose mice they have an increased instance of lung tumors, for example. The radiation at low dose causes DNA damage.
It shortens the life span, and importantly, the risk is synergistic with other risks like smoking. In the course of this DNA damage and repair process, the repair process is not perfect. And eventually you get genomic instability,
and that's what causes cancer. When the cell is irradiated with low doses you also get generation of bad factors such as ROS and inflammatory factor. And we have shown in in operators that you get DNA damage before and after
you carry out fluoroscopically guided case. You can see here foci of this gamma H2AX which signal DNA damage in operators. And what happens over long term? There are markers you can look for long term that show that you're exhibiting genomic instability,
and this includes diccentrics. You can see these chromosomes are abnormal, and that happens as result of chronic radiation exposure. And micronuclei, so you can see that these cells express micronuclei. That is abnormal.
That is genomic instability and that means that your risk of cancer is increased. We haven't measured for these yet in operators, but they may well be present. So I think you need a combination of physical and biological dosimetry.
How do you do that? Well you need high throughput methods for doing it, which we don't have as yet. The current methods are laborious. You need to cont lots of cells and it takes a long time to do it.
But perhaps with the next generation high throughout sequencing this is what we'll be doing. Regular samples from operators and deciding whether there exhibiting genomic instability or not, should they be doing something other than carrying out endovascular operations.
In the meantime, radiation is really dangerous. I think that's what we've got to assume. No matter how much of a dose you're getting it's dangerous. The ALARA principles, you should hopefully all be familiar with, maximal shielding, and as mentioned,
the zero gravity suit. We've started using this. And obviously we wear leg shields. Just as something different, I mentioned that when your cell gets irradiated it produces lots of nasty factors
such as radioactive oxygen species and pro-inflammatory factors, and that can again cause DNA damage. Kieran Murphy spoke earlier on in the previous session about effective low-dose exposure. What they've done is given a cocktail of antioxidants
to patients who have cancer staging. And that actually reduces DNA damage. This is another study that came out recently, another cocktail of antioxidants, exposed to cells in vitro that were irradiated, and this is probably a less relevant study
because it's all in vitro. But again, in a very controlled situation these antioxidants do reduce the production of inflammatory factors in DNA damage. So perhaps we should all be taking a cocktail of pills before we operate.
So in summary, we live in a world of increasing radiation exposures. The health effects are unknown. We need better radiation in epidemiology, a combination of biological and physical dosimetry probably, and in the meantime we have to insist
on maximal protection and assume that all radiation is dangerous. Thank you very much.
- There's a new DCB now on the market just C-marked, and I would like to share you interim data of this brand new Kanshas DCB into the preliminary data so far available. So, as we just heard, DCB is a wide-spread accepted technology, which delivers a durable anti-restenotic efficacy
after single-balloon inflation. I think this is clear, but definitely, as we have just seen from Dr. Vermani, efficacy is not a class effect. It is critical determined by the presence and choice of the excipient of each balloon.
And we know that from different studies like here, from Jopa, we can see that outcome efficacy is different in terms of the different effects of the DCBs. So this new and novel Kanshas Drug-Coated Balloon is covered with a paclitaxel 3.2 micrograms per square millimiter.
There's a unicoat technology, which is a uniform coating with micro-crystal aspects where the Paclitaxel is embedded with micro-crystal, which provides a large surface area, which facilitates a drug transfer to the lesion. It's available up to 200 millimeter.
It is a monorail balloon. You can see that in (mumbles) and some preclinical animal models, the Paclitaxel tissue concentration was definitely different in comparison to other already-established DCB, and of course, this new concept has now
to prove an efficacy and safety in the first human study. So, I can provide you now the six-months primary outcome of that KANSHAS 1 study on behalf of all the investigators. 50 patients were enrolled at six sites in Germany and Belgium. Patients will be followed up up to year, two years.
The primary endpoint is freedom from composite safety at six months. You see all the centers which enrolled patients between April 2017 and January 2018. Main inclusion criteria, Rutherford Clinical Category two to four,
lesion length up to 15 centimeter. Just want to highlight that also popliteal artery segments, could, when moved into study, I will show you also the outcome for the to P3 segment where we planted the balloon. The other baseline and lesion characteristic of the patient.
Typical risk profile, most of the patient had a Rutherford category three. On right side, you see the lesion locations, where the balloon was implanted. I see that 19 patients had a treatment with an popliteal artery.
Cumulative lesion length, 88.6 millimeter. As usual (mumbles) DSB trials classification was more on the lower side. Here the procedural characteristics. DCB per lesion 1.2. Total inflated length 72.1.
(mumbles) 14% of 14 patient, 28%, a little bit more on the higher side for that lesion length. This was due to flow limiting that section and residual stenosis. Here are the six-months outcomes in terms of hemodynamic outcomes
and Rutherford class change from a baseline. As you can see, most of the patients improved during this first six months of followup. Here's the freedom from composite safety and efficacy endpoint within couple of micro curve analyzed. This is a target of 100%,
which means freedom from device and procedure-related deaths through 30 days and freedom from target limb amputation and clinical driven TLR through six months. There were no device and procedure-related Severe (mumbles) during that six months of followup.
So let me conclude the DCB angioplasty for de novo femoropopliteal artery lesions with that new KANSHAS balloon was so far safe and efficient through six months of the procedure. It has a remarkable clinical hemodynamic improvement
at six months, but we have to wait, of course, the further followup 12 and 24 month. Thank you very much.
- Jim, thanks so much, and thanks to Doctor Veith for the opportunity to get involved. Here's my disclosure. So, certainly you don't want to be an expert on limb thromboses, however, it happens. And so, when you see these patients, no longer are we looking at fem-fem,
or even lytics, catheter-directed lytics. So how do we get from screen left to screen right in a single session therapy? Well, as we know, when these patients present, there's several different management options. You can do open thrombectomy with or without
a fem-fem, pharmacomechanical thrombectomy. There's catheter delytic and ultrasound accelerated thrombolytics, and then now, today, we have vacuum-assisted thrombectomy, as we've heard throughout this session, or continuous aspiration thrombectomy,
however you want to mention it. Regardless, when you end up with lytics, this is exactly what you're dealin' with. You're playing with fire, and if we do it long enough, you're going to see this complication. So we've really adopted a clot extraction
instead of a clot dissolution policy at our institution. I think Jim just showed you this technique that is afforded to us by the Indigo thrombectomy system, as you can see here in a Vivo model, this catheter actually does work extremely well.
It'll remove this soft thrombus, as you can see here. My first experience with this was actually for an occluded popliteal stent, as you can see here. We had a occlusion of the standard nitinol stent. This aspiration power was incredibly surprising to me. As you can see, it collapsed the standard nitinol stent.
So at that point, several years ago, we realized how good this device was, and how we want to minimize lytics for our folks. So we started in 2014 and recently this year at the Midwest Vascular forum in Saint Louis, we presented our data.
At that time, we had 73 patients over the years with acute limb ischemia. And here you can see the breakdown. For this presentation I'm going to focus on this cohort here, which is seven. But as you can see, like my panelists here,
we use it for occlusions, for not only occlusions but emboli as well, and also we had one case of an upper extremity embolism that we were able to successfully treat with this device. At that time, again, looking at all 73 patients,
you can see here that it's a very efficacious device. There were a couple folks who needed transfusion and perhaps the blood loss was a little higher than 300. However, as you can see here, the folks who had a blood loss, all five had open adjunctive interventions as well, and the ones who needed transfusion
all had catheter directed lytics as adjunctive therapy. As far as our efficacy endpoints, what we looked at was antegrade flow. As you can see here, oftentimes with your vacuum system thrombectomy, you're able to get antegrade flow. However, intermittently there's also other
adjunctive therapies that we had to use frequently as well. Going back to what, you know, my topic for today, how do you go from screen left to screen right, where here you can see one of our patients who came in. We did a retrograde ipsilateral stick,
crossed the lesion with the wire, then we delivered our eight french Indigo catheter and were able to get, in a single session, as you can see here, antegrade flow. So here's another, all this in one single session therapy. Here's another patient of ours.
As you can see to the left, one of our Gore Excluder limbs had occluded, and again, with single session therapy we were able to provide patency to that occluded right limb. Another case here, you can see one of our other Medtronic grafts.
And what you'll see here as you're looking to the right, here we are with our eight french Indigo catheter, is the separator, which is like a pipe cleaner. And we were able to clear out this clot and provide patency to this
all in a single session therapy. And again, here you can see from left to right how we were able to thrombectomize that limb. So over the years, the last three years, we do about 80 to 90 EVARs a year. During that time period, we have seven patients
come in with limb occlusions. And as you can see here, four of them were chronic, three claudicants and one res-pain, and three of them were acute limb Rutherford one, two A or two B. As you can see here, 42% of the time for these
occluded limbs, we were able to do it with no lytics, not even a pulse spray, nothing, not one drop of lytics. As you can see here, some of them we did have to do it in a single session. What we do is use a McNamara catheter.
We would squirt out, you know, anywhere from, as you can see, 14 to 18 milligrams of lytics, go get a cup of coffee, go make rounds, come back 20 minutes later, then utilize your device. And again, you can see, in a single session therapy we were able to afford patency.
And then finally, you can see here the blood loss was minimal. So this is a safe device. So in conclusion, I think that single session therapy is safe. It can facilitate achieving antegrade flow
in the management of stent graft limb occlusions. And single session therapy is the future of not only stent graft limb occlusions but all acute limb ischemia. Thanks so much.
- Thank you, Larry and Tony, for the invitation. Larry told me I should be provocative so here we go. (chuckles) Those are my disclosures, mostly in the aortic space, although I was a PI for the Humanity Phase II trial. So this is a quote that interventional nephrologists in Arizona told me one day when we were trying
to have a educational, meaningful discussion, so we provide care that is better, faster, and cheaper than what you can provide in the hospital. And we'll address this a little later. What's the roles of the access surgeon, when it comes to advocating or educating
your dialysis patients? Well, when you google advocating for anything, you're going to find mostly political references. And I think there are a number of excellent patient related groups to advocate for policies and principles. But as the surgeon, I think we have
a couple of important roles. One, we need to create the most durable, successful access possible, and as Ted just said, that needs to be individualized for the patient. We need to try and protect and maintain the access and we also have a role in protecting the patient.
We can't underestimate or underemphasize the importance of vessel mapping, both arterial and venous. We frequently get patients referred who have already had their mapping somewhere else but as the surgeon is going to be doing the procedure, we tend to repeat that in the office,
so that we can see it ourselves, because mapping can be variable, can depend on environmental conditions, how cold the patient's room is, their hydration status, so we really try and nail that down. And frequently we find a high bifurcation
of the brachial artery, that's not noted on other mapping. And, again, I think to emphasize what Ted just said, we really need to champion communication between the patient, the nephrologist, and the surgeon, just because you don't receive communication, doesn't mean you can't be the person who provokes
and stimulates communication back to the nephrologist to try and really develop a clear plan. The timing of the hemodialysis is imperative and I think we should consider early cannulation grafts in appropriate patients. What about protecting and maintaining the access,
well these slides were provided to me by Dori Schatell, who's given this talk, you need to arm your patients with information to advocate for themselves and that's really, kind of the theme of what I want to talk about later. Give them pictures of their access,
write them very clear postop instructions, teach patients about cannulation patterns, teach them how to use topical anesthetics for cannulation. Make sure they know what to do in the case of an infiltration or prolonged bleeding, or loss of the thrill.
Make sure they have your contact information, and encourage patients to learn how to self-cannulate. What about protecting the patient? Well, I think it's our, it's the team's obligation but seems to fall on us a lot to educate the patient and their family about their right to choose.
Educate the patient and their family about available providers and facilities in their area. And educate the patient and their family about what services are available at different facilities, and nephrologists , radiologists, surgeons and anesthesiologists.
- Okay, I went to my nephrologist. He told me I needed to get this fistula put in, and then I was directed to the access center, because the way he said it, that's where I had to go to get it done, after I'd already talked to another doctor about doing it,
I was told I had to go to the access center. Okay-- - Oop, let's see. - Um, what she didn't say is that, she didn't like the center in the first place, because originally the doctor that saw her there for the fistula, didn't give us any help.
So he said, I can't do it for you, I don't know what's going to happen, and every time we would ask him, well, is there any solution for her to get a fistula, he wouldn't answer our question and he's like, well, I can't, I can't help you, I'm not going to take it.
So, when they told her told to go to that center, she had told him, can I go somewhere else, somewhere where they're a little bit more professional? And they said, no, you have to go there, they're the specialists. - So, going back to the original comment.
We provide care that is better, faster, and cheaper than what you can provide in the hospital. Well, when you're talking about better, that's really measured only by safety and durability of the interventions, not opinions. And faster, unfortunately, in our area,
some of our access centers are closed on Wednesdays, some of them are closed on Fridays and the weekend. And it's interesting, we often, the surgeons in town often get pummeled on Friday because the access center is closed. And I can tell you that my weekend on call,
I spent about half my day Saturday doing access interventions. And cheaper, cheaper's really only a function of how payers have decided to reimburse. You pay the same amount for staff, electricity, and supplies, whether you're at a hospital,
a surgery center, or an OBL. Unfortunately, some access centers frequently choose therapies that are less effective but cheaper to protect their margins. And perfect examples of these are stent grafts, and drug-coated balloons.
I think hemodialysis patients really want care that is safe, effective and durable. And really, where that's going to be best achieved will depend on what's available in a particular community or region. And most importantly, and I think,
as Ted highlighted, they're really the commitment to providing excellence in access care. And I'll finish with one more little vignette from one of my patients, and these patients, actually this was unsolicited, they just happened to be going off in the office one day
and I had gotten this assignment, I said, you mind if I video this and use it in my presentation? - Basically, in my opinion, what it is, it needs to be patient education. The ones that do talk to me, 'cause I do take control
of my treatments completely. That's why my fistula's in such good shape, 'cause I'll only run 16 gauge needles, which slows down my treatment, which keeps my heart in better shape. That's why I'm still up, walking, doing what I do.
- Thank you very much.
- Thank you, Dr. Ouriel, Dr. Lurie. Ladies and gentlemen. Brian, that was a very fair overview of the ATTRACT trial as it was published in the New England Journal, so thank you. And these are my disclosures. So Dr. DeRubertis did a very nice review of this paper
that was published in the New England Journal December 7th of last year. He went over very nicely that it was NIH sponsored, phase III, randomized, controlled, multicenter, 692 patients randomized, anticoagulation alone versus anticoagulation plus catheter-based techniques.
Now one thing I want to call your attention to is the fact that patients with deep venous thrombosis, acute deep venous thrombosis, who were eligible for randomization, were stratified before they were randomized into two different groups, iliofemoral DVT or fem-pop DVT.
So in my opinion, these are not subgroups because the randomization of one group had no effect on the randomization of another, so I would argue that these are independent groups. That makes a big difference when you do statistical analyses.
The other important issue that I want to point out is that the outcomes were pre-determined to what we were going to analyze. We had to choose one as a primary endpoint and the others as secondary, but these were pre-determined end points that were up for analysis, not post hoc analyses.
And post-thrombotic syndrome was determined at the time, 12 years ago when we wrote the protocol, to be the primary end point. I would submit that we would not choose that as a primary end point if we wrote the protocol today. Moderate to severe post-thrombotic syndrome
certainly would be more appropriate. Leg pain, swelling, health-related quality of life, certainly important. This is the outcome, and unfortunately, it did not reach significance. There was no difference between the two groups
and there was an increased risk of bleeding, but this is the outcome that drove opinion about ATTRACT, but we don't really do catheter-directed thrombolysis for fem-pop DVT. Therefore, the results of the iliofemoral patients will be the most meaningful and that paper was written
and that paper has been accepted by circulation. It should be out shortly, but there were 391 iliofemoral DVT patients and the primary outcome was no different than the primary outcome in the overall trial. But are they?
If we had chosen the Venous Clinical Severity Score in place of the Villalta score for analysis of that primary end point, it would've been a positive study. So if we chose a different tool to analyze, our primary end point would've been positive for the iliofemoral DVT patients.
If we look at moderate to severe post-thrombotic syndrome, a significant difference. Control patients had a 56% increased risk of moderate to severe PTS versus the control patients. If we look at severe post-thrombotic syndrome, control patients had a 72% increased risk
of severe PTS versus control. If we look at the overall severity of the Villalta score in PTS, we can see that there is a significant difference favoring percutaneous catheter-directed thrombolysis. When we look at pain, the patient's pain was significantly reduced in the PCDT patients compared to control.
We look at edema, significant reduction in edema at day 10 and day 30 in patients who received catheter-directed thrombolysis compared to control. Disease-specific quality of life significantly favored patients who had PCDT compared to control. So we look at moderate to severe, severe, pain,
quality of life. There was a price to pay. Major bleeding was increased, but the P-value was no different. I will not argue that patients are not at increased risk. They are at increased risk for bleeding,
but this is an historically low bleeding rate for catheter-directed thrombolysis and there were no intracranial bleeds. No difference in recurrent deep venous thrombosis. No difference in mortality at 24 months between the two groups.
So in conclusion, the primary end point, reduction of any PTS defined by a Villalta score of 5 or more, no difference, but an item that has not reached the level of discussion that we will need to consider is that 14% of our patients had a normal Villalta score coming into the study.
It's impossible to improve upon that, but there is a significant reduction in any PTS if you use the Venous Clinical Severity Score, reduction of moderate and severe post-thrombotic syndrome, reduction of pain and swelling, and improved disease-specific quality of life compared to controls.
And I think these are the meaningful end points that patients appreciate and these are the points of discussion that will be covered in the article in circulation that will be published very soon. Thank you for your attention.
- So my charge is to talk about using band for steal. I have no relevant disclosures. We're all familiar with steal. The upper extremity particularly is able to accommodate for the short circuit that a access is with up to a 20 fold increase in flow. The problem is that the distal bed
is not necessarily as able to accommodate for that and that's where steal comes in. 10 to 20% of patients have some degree of steal if you ask them carefully. About 4% have it bad enough to require an intervention. Dialysis associated steal syndrome
is more prevalent in diabetics, connective tissue disease patients, patients with PVD, small vessels particularly, and females seem to be predisposed to this. The distal brachial artery as the inflow source seems to be the highest risk location. You see steal more commonly early with graft placement
and later with fistulas, and finally if you get it on one side you're very likely to get it on the other side. The symptoms that we are looking for are coldness, numbness, pain, at the hand, the digital level particularly, weakness in hand claudication, digital ulceration, and then finally gangrene in advanced cases.
So when you have this kind of a picture it's not too subtle. You know what's going on. However, it is difficult sometimes to differentiate steal from neuropathy and there is some interaction between the two.
We look for a relationship to blood pressure. If people get symptomatic when their blood pressure's low or when they're on the access circuit, that is more with steal. If it's following a dermatomal pattern that may be a median neuropathy
which we find to be pretty common in these patients. Diagnostic tests, digital pressures and pulse volume recordings are probably the best we have to assess this. Unfortunately the digital pressures are not, they're very sensitive but not very specific. There are a lot of patients with low digital pressures
that have no symptoms, and we think that a pressure less than 60 is probably consistent, or a digital brachial index of somewhere between .45 and .6. But again, specificity is poor. We think the digital pulse volume recordings is probably the most useful.
As you can see in this patient there's quite a difference in digital waveforms from one side to the other, and more importantly we like to see augmentation of that waveform with fistula compression not only diagnostically but also that is predictive of the benefit you'll get with treatment.
So what are our treatment options? Well, we have ligation. We have banding. We have the distal revascularization interval ligation, or DRIL, procedure. We have RUDI, revision using distal inflow,
and we have proximalization of arterial inflow as the approaches that have been used. Ligation is a, basically it restores baseline anatomy. It's a very simple procedure, but of course it abandons the access and many of these patients don't have a lot of good alternatives.
So it's not a great choice, but sometimes a necessary choice. This picture shows banding as we perform it, usually narrowing the anastomosis near the artery. It restricts flow so you preserve the fistula but with lower flows.
It's also simple and not very morbid to do. It's got a less predictable effect. This is a dynamic process, and so knowing exactly how tightly to band this and whether that's going to be enough is not always clear. This is not a good choice for low flow fistula,
'cause again, you are restricting flow. For the same reason, it's probably not a great choice for prosthetic fistulas which require more flow. So, the DRIL procedure most people are familiar with. It involves a proximalization of your inflow to five to 10 centimeters above the fistula
and then ligation of the artery just below and this has grown in popularity certainly over the last 10 or 15 years as the go to procedure. Because there is no flow restriction with this you don't sacrifice patency of the access for it. It does add additional distal flow to the extremity.
It's definitely a more morbid procedure. It involves generally harvesting the saphenous vein from patients that may not be the best risk surgical patients, but again, it's a good choice for low flow fistula. RUDI, revision using distal inflow, is basically
a flow restrictive procedure just like banding. You're simply, it's a little bit more complicated 'cause you're usually doing a vein graft from the radial artery to the fistula. But it's less complicated than DRIL. Similar limitations to banding.
Very limited clinical data. There's really just a few series of fewer than a dozen patients each to go by. Finally, a proximalization of arterial inflow, in this case rather than ligating the brachial artery you're ligating the fistula and going to a more proximal
vessel that often will accommodate higher flow. In our hands, we were often talking about going to the infraclavicular axillary artery. So, it's definitely more morbid than a banding would be. This is a better choice though for prosthetic grafts that, where you want to preserve flow.
Again, data on this is very limited as well. The (mumbles) a couple years ago they asked the audience what they like and clearly DRIL has become the most popular choice at 60%, but about 20% of people were still going to banding, and so my charge was to say when is banding
the right way to go. Again, it's effect is less predictable than DRIL. You definitely are going to slow the flows down, but remember with DRIL you are making the limb dependent on the patency of that graft which is always something of concern in somebody
who you have caused an ischemic hand in the first place, and again, the morbidity with the DRIL certainly more so than with the band. We looked at our results a few years back and we identified 31 patients who had steal. Most of these, they all had a physiologic test
confirming the diagnosis. All had some degree of pain or numbness. Only three of these patients had gangrene or ulcers. So, a relatively small cohort of limb, of advanced steal. Most of our patients were autogenous access,
so ciminos and brachycephalic fistula, but there was a little bit of everything mixed in there. The mean age was 66. 80% were diabetic. Patients had their access in for about four and a half months on average at the time of treatment,
although about almost 40% were treated within three weeks of access placement. This is how we do the banding. We basically expose the arterial anastomosis and apply wet clips trying to get a diameter that is less than the brachial artery.
It's got to be smaller than the brachial artery to do anything, and we monitor either pulse volume recordings of the digits or doppler flow at the palm or arch and basically apply these clips along the length and restricting more and more until we get
a satisfactory signal or waveform. Once we've accomplished that, we then are satisfied with the degree of narrowing, we then put some mattress sutures in because these clips will fall off, and fix it in place.
And basically this is the result you get. You go from a fistula that has no flow restriction to one that has restriction as seen there. What were our results? Well, at follow up that was about almost 16 months we found 29 of the 31 patients had improvement,
immediate improvement. The two failures, one was ligated about 12 days later and another one underwent a DRIL a few months later. We had four occlusions in these patients over one to 18 months. Two of these were salvaged with other procedures.
We only had two late recurrences of steal in these patients and one of these was, recurred when he was sent to a radiologist and underwent a balloon angioplasty of the banding. And we had no other morbidity. So this is really a very simple procedure.
So, this is how it compares with DRIL. Most of the pooled data shows that DRIL is effective in 90 plus percent of the patients. Patency also in the 80 to 90% range. The DRIL is better for late, or more often used in late patients,
and banding used more in earlier patients. There's a bigger blood pressure change with DRIL than with banding. So you definitely get more bang for the buck with that. Just quickly going through the literature again. Ellen Dillava's group has published on this.
DRIL definitely is more accepted. These patients have very high mortality. At two years 50% are going to be dead. So you have to keep in mind that when you're deciding what to do. So, I choose banding when there's no gangrene,
when there's moderate not severe pain, and in patients with high morbidity. As promised here's an algorithm that's a little complicated looking, but that's what we go by. Again, thanks very much.
- I will be talking about new KDOQI guidelines. I know many of you have heard about KDOQI guidelines being revised for the past maybe over a year or maybe two. Yes, it is being done, and it is going slow only because it's being done in a very different way. It's more than an update.
It's going to be more of an overhaul for the entire KDOQI guidelines. We in KDOQI have looked at access as a solitary problem like we talked about grafts, catheters, fistulas for access, but actually it sort of turns out
that access is part of a bigger problem. Fits into a big ESKD lifeline of a patient. Instated distal patients come in many varieties. It can affect any age, and they have a lot of other problems so once you have chronic renal failure, renal replacement mortality fits in
only when it becomes Stage IV or Stage V. And renal replacement mortality is not just access, it is PD access, it's hemo access, it is transplant. So these things, we need to see how they fit in in a given person. So the new KDOQI guidelines concentrates more
on individualizing care. For example, here the young Darien was an 11 year old with a prune belly syndrome. Now he has failed PD. Then there's another person here who is Lydia who is about 36 or 40 year old lady
with a insulin dependent diabetes. Already has bad vascular pedicle. Lost both legs. Needs access. Now both these patient though they need access, it's not the same.
It's different. For example, if you think of Darien, he was in PD but he has failed PD. We would love to get him transplanted. Unfortunately he's got terrible social situation so we can't get him transplanted.
So he needs hemo. Now if he needs hemo, we need to find an access that lasts for a long time because he's got many years ahead of him. On the other hand we have Lydia, who has got significant vascular disease.
With her obesity and existing infectious status, probably PD won't be a good option for her. So she needs hemo, and she's obviously not a transplant candidate. So how are we going to plan for hemo? So these are things which we are to more concentrate
and individualize when we look at patients, and the new guidelines concentrate more on these sort of aspects. Doing right access for right patient, right time, and for right reasons. And we go about planning this keeping the patient first
then a life plan ESKD lifeline for the patient, and what access we are looking at, and what are the needs of the patient? Now this is also different because it has been done more scientifically. We actually have a evidence review team.
We just poured over pretty much 1500 individual articles. Recent articles. And we have looked through about 4000 abstracts and other articles. And this data is correlated through a workgroup. There a lot of new chapters.
Chapter specific surgery like peri-operative, intra-operative, post-operative, cat issues, managing complication issues. And we started off with the coming up with the Scope of Work. The evidence review team took the Scope of Work
and tried to get all the articles and sift through the articles and came up and rated the evidence using a certain rating system which is very scientific. The workgroup then kind of evaluated the whole system, and then came up with what is clinically relevant.
It's one thing for statisticians to say how strong evidence this is, but it's another thing how it is looked upon by the clinicians. So then we kind of put this into a document. Document went through internal and external review process.
This is the process we have tried to do it. Dr. Lok has been the Chair of the group. Myself and Dr. Yevzlin are the Vice-Chairs. We have incredible workgroup which has done most of the work. And here are the workgroup members.
We comprised of nephrologist, transplant surgeons, vascular surgeons, Allied Health personnel, pediatric nephrologist so it's a multi interventional radiologist and interventional nephrologist. This is a multi disciplinary group which has gone through this process.
Timothy Wilt from Minnesota was the head of the Evidence Review Team, who has worked on the evidence building. And now for the editorial sections we have Dr. Huber, Lee, and Dr. Lok taking care of it. So where are we today?
We have pretty much gone through the first part of it. We are at the place where we are ready for the Internal Review and External Review. So many of you probably will get a chance to look through it when it comes for the External Review and would love
to have your comments on this document. Essentially, we are looking at access in the context of end stage renal disease, and that is new. And obviously we have gone through and done a very scientific review, a very scientific methodology to try
to evaluate the evidence and try to come up with guidelines. Thank you.
- First of all I'd like to thank the organizers for inviting me to give this presentation. These are my disclosures. I'm going to divide this presentation into three main parts. I will initially make the case that at the present time we are providing relatively poor value in ESRD and Vascular Access Care.
I'll then submit to you that one way to address this issue is through Patient Centered Device Innovation and then I'll tell you a little bit about some regulatory initiatives in this area. If you define value as being outcomes over cost
then I would argue that in vascular access we actually provide very poor value in that we have pretty bad outcomes and in order to achieve these bad outcomes we actually spend a huge amount of money at about 1.5 billion dollars per year and these is no talk at all
in the construct before you about quality of life. How can we break this cycle of a lack of innovation resulting in poor quality and outcomes and a high cost burden? I would submit to you that one way that we may be able to break the cycle
is through patient centered innovations. Patient centered innovation, whether it's discovery or process of care innovation, is basically innovation that targets the issues that are important to patients, not necessarily the issues that are important to physicians,
or payors, or regulators, or to industry. The reason that this is important is that the things that are relevant and critical to patients are often very different from the things that are important to the other stakeholder groups that I mention. If you look at hemodialysis for example
the things that are important to a patient on hemodialysis are ability to travel, and dialysis free time, and not feeling washed out post dialysis. On the other hand, if you're an nephrologist as I am, the things that are important to me are survival, and hospitalization, and being a nephrologist
I completely obsess about blood pressure which is really not something that patients are that worried or bother about. The next question is, of course, how do we develop therapies that address the issues that are important to patients? I got this slide from Frank Hurst at the FDA.
It basically makes the point that we need to have patient input at every point in the product development process, from initial ideation, to clinical trial design, to patient preferences, to patient centered outcomes. The FDA actually has a number of programs
in this area, one example is their Patient Focused Drug Development Initiative which allows the FDA to speak with patients and patient groups in different therapeutic areas. Closer to home, the Medical Device Innovation Consortium is extremely interested in Patient Preferences
and in a Risk-Benefit analysis. Within the kidney health initiative, which is a public-private partnership between the American Society of Nephrology and the FDA, we are also very interested in patient preferences for renal devices, and the background for this is
that an individual patient's tolerance for risk actually varies tremendously. Patients on home hemodialysis, for example, may be happy to sacrifice some degree of safety with regard to, say, vascular access, in order for an improved
or a more independent quality of life. But if you're a regulator there needs to be a way that you can get insight in to how patients perceive the risk/benefit ratio so that it can be incorporated into the regulatory pathway, and at least at the present time
the tools for this do not exist. The Kidney Health Initiative hosted an extremely successful patient preference workshop in the Baltimore area a couple of years ago. We asked three main questions: how can patients assist in the development
of a new medical device? How can they ensure the success of future clinical trials? And how can they help with the decision to make a new device available? The proceedings of this workshop have been published, and I'm really not going to go into details there.
I'm going to share with you a video that was made to try and attract patients to this webinar, and I think it really epitomizes the importance of patient centered innovation. - Hello, I'm CeCe, a fellow kidney disease patient. For 33 years I've done dialysis, both hemo and PD.
I had a transplant for 10 years and as you can imagine too many pills, shots, and accesses to mention. As kidney patients you and I both know that a few things in life are not optional. Strength, courage,
persistence, and determination. No matter what life throws at us, we try to stay balanced, maintain our routine, and remain positive. But let's face it, we are often in a holding pattern. Kidney disease treatments have not
changed much over the years. The options for patients like us have largely remained the same for many years. You want to help change that? We need you. Each day we're asked to share our lives with our treatment. But now, let's share our voice, ideas, opinions.
From patients like us, they matter. Key people are realizing our voices matter too. Here's what I found out. The Food and Drug Administration, often known as the FDA, is looking for patients living with kidney disease like you and me, to provide input
on how potential treatments of the future could look. Picture a big table. Around it are dialysis caregivers, researchers, doctors, nurses, and companies providing new products and treatments. They want us and our families to sit beside them
and have a seat at this table. We'll work together to bring potential new treatment options, safe and effective ones, and ones that patients like you and me want and need. Imagine the future of your treatment. What does it look like?
How does it improve your day-to-day life? This future doesn't have to remain just a dream. Join me and other patients to contribute our thoughts and make our ideas a possible reality. - The driving force and also the voice behind that video was the lady on the right, Celeste Lee.
She was a dialysis patient for over 30 years, she was a member of the KHI board of directors, and Celeste died a year and a half ago, she basically withdrew from dialysis because of bone disease from the 30 years of dialysis. I really think that her death
should be a charge for all of us really to try and develop therapies that target the things that are important to patients. Thank you very much for your attention.
- Thank you. Here are my disclosures. Our preferred method for zone one TAVR has evolved to a carotid/carotid transposition and left subclavian retro-sandwich. The technique begins with a low transverse collar incision. The incision is deepened through the platysma
and subplatysmal flaps are then elevated. The dissection is continued along the anterior border of the sternocleidomastoid entering the carotid sheath anteromedial to the jugular vein. The common carotid artery is exposed
and controlled with a vessel loop. (mumbling) The exposure's repeated for the left common carotid artery and extended as far proximal to the omohyoid muscle as possible. A retropharyngeal plane is created using blunt dissection
along the anterior border of the cervical vertebra. A tunneling clamp is then utilized to preserve the plane with umbilical tape. Additional vessel loops are placed in the distal and mid right common carotid artery and the patient is systemically anticoagulated.
The proximal and distal vessel loops are tightened and a transverse arteriotomy is created between the middle and distal vessel loops. A flexible shunt is inserted and initially secured with the proximal and middle vessel loops. (whistling)
It is then advanced beyond the proximal vessel loop and secured into that position. The left common carotid artery is then clamped proximally and distally, suture ligated, clipped and then transected. (mumbling)
The proximal end is then brought through the retropharyngeal tunnel. - [Surgeon] It's found to have (mumbles). - An end-to-side carotid anastomosis is then created between the proximal and middle vessel loops. If preferred the right carotid arteriotomy
can be made ovoid with scissors or a punch to provide a better shape match with the recipient vessel. The complete anastomosis is back-bled and carefully flushed out the distal right carotid arteriotomy.
Flow is then restored to the left carotid artery, I mean to the right carotid artery or to the left carotid artery by tightening the middle vessel loop and loosening the proximal vessel loop. The shunt can then be removed
and the right common carotid artery safely clamped distal to the transposition. The distal arteriotomy is then closed in standard fashion and flow is restored to the right common carotid artery. This technique avoids a prosthetic graft
and the retropharyngeal space while maintaining flow in at least one carotid system at all times. Once, and here's a view of the vessels, once hemostasis is assured the platysma is reapproximated with a running suture followed by a subcuticular stitch
for an excellent cosmetic result. Our preferred method for left subclavian preservation is the retro-sandwich technique which involves deploying an initial endograft just distal to the left subclavian followed by both proximal aortic extension
and a left subclavian covered stent in parallel fashion. We prefer this configuration because it provides a second source of cerebral blood flow independent of the innominate artery
and maintains ready access to the renovisceral vessels if further aortic intervention is required in the future. Thank you.
- Thank you very much. Well this is a series that was actually published five years ago. And it outlined 45,000 patients after carotid endarterectomy, as well as open and closed thoracic abdominal procedures and infrainguinal bypasses.
And you can see here, that the VTE rate, and this is emblematic of a lot of studies. If you take everything together in a ball, you get an average result. And as you can see, the peripheral bypasses had a low incidence.
Carotids, very low incidence. But open procedures had a higher incidence than endovascular procedures. But here is the nub. Here is what's really important and why you need to do risk assessment.
Look at what happened to these percentages if the patients had any morbidity during hospitalization, as high as 7.8%. And here's the list after they went home. Again, it's not the .5 tenths of a percent or 1%, and this is what it's all about.
It's about the extra risk factors that the patient has. So now, anybody that's starting to do work with the Caprini Score, you've got to go to the patient-friendly form. Because we don't just do it,
if the patient comes in for surgery, and somebody does a preoperative evaluation in the holding area, stop it! It's ridiculous! Have you ever been in the holding area? What are you worried about?
You're worried about having the operation. Are they going to find cancer? Will the surgeon have a bad day? How much pain am I going to be in? How long am I going to be out of work? They're not going to talk to you
about their family history or their obstetrical misadventures. So you have them fill a form out ahead of time with their family, and then when they come in, you just double-check it. And we've studied this, it's in five languages,
and it's got perfect correlation with trained observers doing the same thing. And remember, if you fail to carefully interrogate your patients regarding the history or family history of venous thromboembolism, vascular surgery or not, sooner or later you may
be faced with a fatal PE. And the idea that you're giving anticoagulants during your procedure that's going to protect them is not valid. The relative risk of thrombosis increases with the number of risk factors identified.
A combination of genetic and acquired risk factors in a person without a history of a thrombosis personally, but with a family history, has a 60-fold higher chance than those that have a negative family history. And a positive family history increased
the risk of venous thrombosis more than 2-fold, regardless of the other risk factors. Don't forget the history of thrombosis. You won't need to look this article up. It's 183,000 patients over 25 years and it shows that both in first, second,
and third-degree relatives, as well as cohabitants in the household, there's an increased risk of venous thromboembolism. Lowering down, getting lower for each degree of a relative.
But a DVT in a cousin, there may also be a thrombopathic condition in that patient. So you better pay attention to that. National Surgical Quality Improvement Program, wonderful program. The database has no information on history
or family history of VTE, use of perioperative VTE prophylaxis, intraoperative anticoagulation, or perioperative use of antiplatelet agents. How are you supposed to make any sense out of DVT-related studies?
Finally, due to the lack of routine screening for VTE, the incidence of VTE may be underestimated in this NSQIP database, which only makes the need for further study more pressing. This is an important consideration because
more recent data indicates that two-thirds of the patients are found to have DVT during screening and after vascular operations, have no signs or symptoms of the problem. And I'd like to remind you, so this is based on the Boston data, which is the best data.
Patients with a low score pneumatic compression during hospitalization. Moderate score, of 7-10 days of anticoagulation. Don't make any difference if they're inpatient or outpatient. And 28 days if their score is over nine.
They lowered their incidence on the surgical services from 2.2% to a tenth of a percent at 30 days. And finally, and I think this is really, really important. Take a look at all these risk assessment scores.
To my knowledge, there's only two scores. It's not the Padua, it's not the IMPROVE that have a history of obstetrical misadventures which can reflect antiphospholipid antibody syndrome, as well as family history
in various degrees of relatives. So with that, thank you very much.
- I have nothing to disclose. So, just as a matter of background, you've heard a lot about catheter-directed thrombolysis as a means to improve RV function in patients with acute pulmonary embolism. I think there's a lot of limitations to a catheter-directed thrombolytic strategy,
including need for ICU stay for catheters, need for thrombolytics, which even at low dose do carry a finite risk of intracerebral hemorrhage, and other cost related issues. And so, again, to reiterate the last two speakers, a single session, non-lytic based therapy
that's definitive for pulmonary embolism certainly could have a lot of use. And so, I don't really need to outline the importance of the RV to LV ratio as a marker for high risk in pulmonary embolism other than to say that it is very difficult to do a randomized prospective
clinically blinded study in pulmonary embolism for this fact that in the submassive population we're used, unfortunately, used to having surrogate markers for clinical improvement, such as improvement in RV LV ratio. Nevertheless, it is a good outcome
in that it is very reproducible. CT scanning has been shown to be the best way to really get reproducible results with RV to LV ratio. I will talk about the FlowTriever System, which in its original design consisted of an aspiration catheter which is a 20 French catheter
directed from the femoral vein typically into the pulmonary arteries and then the FlowTriever Device which is these nitinol disks that can grasp the clot and help it withdraw and then the retraction aspiration system which is a manual suction based system to withdraw the nitinol frame
as well as to aspirate the clot. So, this procedure and device were studied in the FLARE Study. We wanted to evaluate the safety and efficacy of this device. We looked at 106 patients in 18 sites.
It was prospective single arm multi-center, and we looked at outcomes at 48 hours and 30 days, primarily looking at efficacy with the primary outcome being reduction in RV to LV ratio at 48 hours as well as safety which was a composite major adverse event rate, including device related death, major bleeding
according to the VARC-2 definition, as well as treatment related adverse events such as clinical deterioration, pulmonary vascular injury, cardiac injury, all of the things, the dreaded complications that we worry about when instrumenting these patients who are acutely ill.
We measured these outcomes at 48 hours and followed the data with the typical Data Safety Monitoring Board and Clinical Events Committee that were all independent. So, the inclusion criteria were typical patients aged 18 to 75.
They had to have evidence of proximal pulmonary embolism by CTA. Most of these patients would probably fit into what we would call an intermediate high risk by modern definition. We did exclude patients who were profoundly hypotensive,
patients that had evidence of perhaps chronic pulmonary embolism. They did have to have heart rates less than 130 as well. The exclusion criteria, we didn't want to blur the results with patients who had failed thrombolysis. So that was excluded.
We didn't want to have patients with severe pulmonary hypertension greater than 70, which perhaps might be an indication of chronic pulmonary embolism. Vasopressor requirements, people who had FiO2s greater than six liters per minute to keep their sats up, patients who were profoundly anemic,
patients who had recent cardiac or pulmonary surgery, as well as actively progressive cancer. Of note, patients with a high bleeding risk other than what I had mentioned were included in the trial. We had a very successful enrollment as you can see. We had 106 patients that were enrolled, one of which was
enrolled but unfortunately did not meet eligibility. She had undiagnosed metastatic breast cancer at the time of her enrollment, and so, that was the one patient that ended up resulting in a study related death. We had two patients who received thrombolytics adjunctively
as part of the procedure. That data was analyzed separately. So really the core of the patients were 104 patients who were treated only with the FlowTriever and did not get any adjunctive thrombolytics. As far as baseline characteristics,
we treated 106 patients. The average age was 55.6. The mean BMI was 36.1. I'm based in Louisville, Kentucky and that's below average for our BMI. But unfortunately, DVT and PE is a disease
of obesity, which is only increasing in this country. You had the typical other comorbidities including hypertension, coronary artery disease. 73 patients or 69% had concurrent DVT. Several patients had a history of prior DVT or a prior pulmonary embolism.
As far as the characteristics, we had sPESI score of one in about 45% of the patients, positive troponin in 60%, D-Dimer of 75%, elevated BNP in 73%. Most of these patients had bilateral pulmonary emboli. And as far as prior treatment, most of them got unfractionated heparin.
Some of them got low molecular weight heparin. Almost all of them had femoral access from the right. The other alternative access was from the left. We did not have any patients in this trial that were treated from the internal jugular approach, although that is possible with this procedure.
As far as the devices used, there were a mean of 1.7 devices. We had three sizes, small, medium, and large with an average number of passes of four passes for the treatment, a mean procedure time of one hour and 39 minutes ranging from 39 minutes up to three hours,
and we had zero technical complications in terms of success for delivery, deployment, or retraction of the disks. Here's the example of the delivery of the catheter. You can see in real the advancement of a 20 French catheter from the femoral venous approach over a stiff guide wire into the pulmonary artery.
So, as far as delivery this proved to be quite technically successful and feasible. You can now see that the FlowTriever disks are deployed within the pulmonary artery. You can see that there are two disks deployed. One disk remains retracted into the aspiration guide
catheter and it turns out for our technical point that was the most important thing was to place the aspiration guide catheter close to the clot and then you can see examples of the type of clot removed here. As far as the main efficacy outcome we had
a decrease in the RV LV ratio from 1.5 at baseline to 1.15 with a reduction of .39, which falls in line with all of the other devices and catheter-directed thrombolytic therapies which also seemed to result in a improvement into the RV LV ratio of very similar magnitude.
As far as the clinical outcomes, most patients stayed about one day in the ICU. 44 out of the 106 had zero ICU time. There was three days to discharge on average and we had one patient of all cause mortality, which turned out to be a patient that
died in hospice due to metastatic breast cancer. As far as major adverse events, we had no intracranial hemorrhage, no access site major bleeding, no decide related death, pulmonary injury or cardiac injury. We had one patient with a bleeding event and three patients with treatment
related clinical deterioration. The adverse bleeding event occurred very early in the clinical experience. This patient had hemoptysis and hemothorax after the procedure, and ended up being treated with a lobectomy.
We had three patients with clinical deterioration including worsening PE requiring surgery, cardiogenic shock requiring treatment for cardiogenic shock, and then one patient became agitated and VF-ed prior to actually having the procedure and was treated with defibrillation.
Of note, all four of these patients despite their major adverse clinical outcomes survived to the 30 day end point. I already talked about the relative improvement in RV to LV ratio. Relative to some of the other trails you've seen it falls directly in line and the safety,
I think the big safety note is that the major bleeding rate was quite low in this procedure with no major device related bleeding. So in conclusion, catheter-directed mechanical thrombectomy using the FlowTriever without the use of thrombolysis is safe and effective in improving RV function
in patients with intermediate risk PE. It's associated with a low ICU time, a low total hospital time, and I think it establishes a non-thrombolytic basis for acute, for treatment of acute pulmonary embolism. Certainly there's more investigation needed.
Thank you very much.
Thank you, Mr Chairman. In order to avoid unnecessary repetition, I'm going to try to move forward with some of my slides. There we go. And, again, in order to avoid that, we're just going to move through the cases. I have some cases that are different
to the ones presented before. It seems that everybody's happy with this technology. This is a CTO recanalization of a patient with subacute total occulsion of the SFA that previously had a stent in place,
in the distal SFA. And here you can see how we are able to reopen the vessel and look at the clot in the entire length at the end of the catheter there. So, this technology really works.
Let me show you now an acute bowel ischemia case. A patient that comes with abdominal pain. A CTA shows that the patient has an occlusion of the proximal SMA. We put a catheter there,
we do a diagnostic angiogram confirming the occlusion, then we cross the lesion and we inject distali showing that the branches are patent. And then we put in place
an oscar directional sheath that will give us great stability to work and through that one we use a Cat Eight, from Penumbra. As you can see here, advancing the catheter in combination with the separator,
and this is the final angiogram showing complete opening of the main SMA and you can see very clearly the elements that were occluding the MSL. We are also using this technology in DVT, acute DVT, with proprietal access
and here you can see the before, and then, sometimes we use it alone, sometimes we use it in combination with angiojet and with the bull spray, followed by this technology for the areas that did not respond.
But this is usually a technology that is helping us to get rid of most of the clot. Like here, you see there is some residual clot. And after Penambra, you can direct the catheter and you can really clean the entire vein. Same here, before and after.
We are also using it for PE. I know that you guys in Miami are doing the same and we are happy with the results. And then, just to finish, I think this is a really nice case that was done by one of our partners in vascular surgery.
A patient with an occluded carotid subclavial bypass. So you see access from the brachial artery on one side. And this person, the person who did this, was smart enough to also came from the groin
and put the filter in the internal carotid artery, just in case. So then he starts to manipulate that occluded subclavial carotid bypass. As you can see here. And at a certain point,
he does a follow-up angiogram showing that the entire carotid, including the internal and external, is totally occluded. So, because he was prepared, he had a filter,
he didn't panic, he went and used the indigo device, and he was able to get all that clot out and re-establish nice anterial flowing in the carotid artery,
completely clean. The carotid subclavial bypass. And he did a final angiogram in AP and lateral view, confirming that there is no distimbolisation at the intercranial level. So, this technology really works.
I think that we all agree. And these are good examples on how we can help patients with that technology. Thank you for your attention.
- Thank you very much again, I greatly appreciate the honor to be able to be here and be able to present these data. These are my they're my conclusions, thank you very much. So, what I think is really very important for all of us
is to remember this Chinese Proverb, never kill a friend, never treat a stranger. And what that means is that you have to learn a lot about that patient before you just go ahead and operate on them.
Then they're not strangers anymore. And if God forbid the CT scanner is broken, you're going to have to do a history and physical. We know that chart review I hate to look at reviews of the Caprini scores going back with retrospective chart reviews,
because they're terribly flawed. We have one of the only risk assessments that looks at the history of obstetrical complications and if you look at chart review, nobody asks the questions. Six tenths of a percent,
13 percent face to face. Same thing with family history of thrombosis. Five point two percent, 17 percent live. Personal history of DVT even doubled in live versus chart review. These questions aren't asked
and of course in the National Surgical Quality Improvement Project and the American College of Surgeons. These things aren't even in there. And they have five million patients. And they talk about DVT studies, and they don't know about what's going on.
We have 39 factors in the Caprini score and that's judged to be too many. You can't have too good a history and physical. The better your history and physical, the better you can take care of the patient. So if devised in a patient friendly form,
it's in five languages. The patients fill it out ahead of time. And then, this was compared to professionals filling it out. There's excellent correlation except for a couple of problems.
And that is that the patient fills the form out, then when they come in, we reemphasize history of family history, B.M.I., obstetrical history, and then see if they have pitting edema or varicose veins.
And so that takes less than five minutes. The last thing in the world you want to do, and I would say anybody that has preoperative surgical nurses in the holding area that Caprini scores, that's flawed. Stop it.
That's no place to be doing that. Because people are worried about their surgery, are they going to get through it, are they going to find cancer, how long are they going to be out of work. You can't ask them about this at that time.
So, these are the scores that we use. Part of this is also reinforced by stuff that's been done. God bless that we would need a moment of silence for the University of Michigan. All the fabulous work that they've done there
in this regard. And we also, this is how we score these patients. Got a lot of operator error here today. Age, as you can see, and contraceptives or hormonal therapy and so forth. This, everybody needs to get this study and to read it.
This is 183000 individuals in the Scandinavian system followed for 25 years. And what they showed is, that there's an increased incidence. If you take a look at a person that's never had a clot, if they have a first degree relative with a clot,
they have an increased risk of thrombosis, slightly less for second degree relatives, slightly less for third degree relatives, and believe it or not, even slightly more compared to controls for people that are living together but of course with the person's lifestyles and so forth
so it's not totally understandable. The point of this is, the point of this is, pay attention to family history of thrombosis. Because that might uncover a whole thrombopathic family that you don't realize. And that'll be the difference in these low risk
procedures between life and death. I've seen a number of patients die with simple procedures because nobody asked about the family history. So, what we recommend is Caprini scores of one to four. You can use compression stockings when they're
if they're in the hospital if it's for ablation. You can use compression stockings according to your protocol, whatever you do. If the patient's at moderate risk, five to eight, low molecular weight heparin for seven to ten days and compression stockings.
And if they're high risk, over nine, then we also like to do a duplex scan before stopping the low molecular weight heparin. And so in conclusion, risk assessment using the score, utilize patient-friendly form,
avoid chart review, face to face critical. And remember that some of these simple procedures, these patient's are very high risk if they're thrombopathic. Provide prophylaxis for at least one week in those at risk for a score of over five.
And then extended prophylaxis for history of VTE, family history of VTE and thrombophilia. Now, I put 14 to 28 days because you have to take these situations individually. Somebody's had four family members in their past history that have had thrombosis.
That's a thrombopathic family. I would go for 30 days. If it's only one incident and one patient, then maybe two weeks. Thank you very much.
- I want to thank the organizers for putting together such an excellent symposium. This is quite unique in our field. So the number of dialysis patients in the US is on the order of 700 thousand as of 2015, which is the last USRDS that's available. The reality is that adrenal disease is increasing worldwide
and the need for access is increasing. Of course fistula first is an important portion of what we do for these patients. But the reality is 80 to 90% of these patients end up starting with a tunneled dialysis catheter. While placement of a tunneled dialysis catheter
is considered fairly routine, it's also clearly associated with a small chance of mechanical complications on the order of 1% at least with bleeding or hema pneumothorax. And when we've looked through the literature, we can notice that these issues
that have been looked at have been, the literature is somewhat old. It seemed to be at variance of what our clinical practice was. So we decided, let's go look back at our data. Inpatients who underwent placement
of a tunneled dialysis catheter between 1998 and 2017 reviewed all their catheters. These are all inpatients. We have a 2,220 Tesio catheter places, in 1,400 different patients. 93% of them placed on the right side
and all the catheters were placed with ultrasound guidance for the puncture. Now the puncture in general was performed with an 18 gauge needle. However, if we notice that the vein was somewhat collapsing with respiratory variation,
then we would use a routinely use a micropuncture set. All of the patients after the procedures had chest x-ray performed at the end of the procedure. Just to document that everything was okay. The patients had the classic risk factors that you'd expect. They're old, diabetes, hypertension,
coronary artery disease, et cetera. In this consecutive series, we had no case of post operative hemo or pneumothorax. We had two cut downs, however, for arterial bleeding from branches of the external carotid artery that we couldn't see very well,
and when we took out the dilator, patient started to bleed. We had three patients in the series that had to have a subsequent revision of the catheter due to mal positioning of the catheter. We suggest that using modern day techniques
with ultrasound guidance that you can minimize your incidents of mechanical complications for tunnel dialysis catheter placement. We also suggest that other centers need to confirm this data using ultrasound guidance as a routine portion of the cannulation
of the internal jugular veins. The KDOQI guidelines actually do suggest the routine use of duplex ultrasonography for placement of tunnel dialysis catheters, but this really hasn't been incorporated in much of the literature outside of KDOQI.
We would suggest that it may actually be something that may be worth putting into the surgical critical care literature also. Now having said that, not everything was all roses. We did have some cases where things didn't go
so straight forward. We want to drill down a little bit into this also. We had 35 patients when we put, after we cannulated the vein, we can see that it was patent. If it wasn't we'd go to the other side
or do something else. But in 35%, 35 patients, we can put the needle into the vein and get good flashback but the wire won't go down into the central circulation.
Those patients, we would routinely do a venogram, we would try to cross the lesion if we saw a lesion. If it was a chronically occluded vein, and we weren't able to cross it, we would just go to another site. Those venograms, however, gave us some information.
On occasion, the vein which is torturous for some reason or another, we did a venogram, it was torturous. We rolled across the vein and completed the procedure. In six of the patients, the veins were chronically occluded
and we had to go someplace else. In 20 patients, however, they had prior cannulation in the central vein at some time, remote. There was a severe stenosis of the intrathoracic veins. In 19 of those cases, we were able to cross the lesion in the central veins.
Do a balloon angioplasty with an 8 millimeter balloon and then place the catheter. One additional case, however, do the balloon angioplasty but we were still not able to place the catheter and we had to go to another site.
Seven of these lesions underwent balloon angioplasty of the innominate vein. 11 of them were in the proximal internal jugular vein, and two of them were in the superior vena cava. We had no subsequent severe swelling of the neck, arm, or face,
despite having a stenotic vein that we just put a catheter into, and no subsequent DVT on duplexes that were obtained after these procedures. Based on these data, we suggest that venous balloon angioplasty can be used in these patients
to maintain the site of an access, even with the stenotic vein that if your wire doesn't go down on the first pass, don't abandon the vein, shoot a little dye, see what the problem is,
and you may be able to use that vein still and maintain the other arm for AV access or fistular graft or whatever they need. Based upon these data, we feel that using ultrasound guidance should be a routine portion of these procedures,
and venoplasty should be performed when the wire is not passing for a central vein problem. Thank you.
- 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.
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