- Thank you Lowell. - Good morning, and thanks Lowell and Jose, for the invitation to come back this year. I don't have any disclosures. Well, what we're going to talk is imaging the female pelvic veneous system. And the female pelvic venous system is a complex arrangement
of four interconnected venous systems, and really you have to understand the anatomy to understand the keys to imaging it and treating it, and that's the connections between the renal vein, both the left and the right ovarian veins, the tributaries of the internal iliac veins,
and the superficial veins of the lower extremity through the saphenofemeral junction. And central to all of this are the tributaries of the internal iliac vein. Which functions as a gateway between the pelvis and the leg, and really are exactly analogous to perforating veins,
connecting the deep veins of the pelvis to the superficial veins of the leg, and you have to have an intimate knowledge of this anatomy both to image it adequately, as well as to treat it. So classically, the internal iliac vein is thought as the confluence of three tributaries.
That is, the obturator vein anteriorly, tributaries of the internal pudendal vein, sort of in the middle of the pelvis, and the superior and inferior gluteal veins, and these communicate with the legs through four escape points
that the anatomists describe anteriorly as the obturator point or the "O" point, where the round ligament vein comes through the abdominal wall, the "I point. And medially in the thigh, pudendal or the "P" point, and posteriorly the gluteal point,
which communicates both with the posterior thigh as well as with the sciatic nerve and gives rise to sciatic varices. (coughs) From our standpoint today, I'm more interested in atypical, varices, that is, pelvic source lower extremity varices,
arising from the pelvis, anteriorly for the obturator vein, and from the round ligament vein, which communicate with the vulva, branches of the internal pudendal vein, which communicate with the perineum, and the medial thigh, and posteriorly, with branches of the superior and inferior gluteal vein.
So as far as imaging goes, we're interested primarily in two clinical scenarios which the imaging requirements are somewhat different. That is, atypical pelvic source varices without any pelvic symptoms, and atypical varices with pelvic pain, and the way that we study these with venography
are quite different. Although some people do pursue blind sclerotherapy from below, I do think imaging with venography adds substantially to both the control of the sclerosant, as well as how thoroughly you're able to embolize the pelvic tributaries.
And I personally like to do sclerotherapy of the varices with venography, and use direct puncture venography using either a 23 or a 25 gage butterfly needle, that's placed under ultrasound guidance. Contrast is then injected to calibrate both
the variceal bed as well as to track the tributaries, as I'll show a minute, up into the pelvis, and usually you can embolize about to the level of the broad ligament. Simultaneously, foam sclerotherapy is performed, using a combination of Sotradecol,
and Ethiodol as a contrast media, and then is followed both by Flouroscopy, using a reverse road mapping technique to subtract the bone and other things out, and follow the contrast through as well as with ultrasound as shown here.
And just as an example, here's some vulvar varicosities, that communicate both with the obturator vein up here, with the round ligament vein through the "I" point, as well as with the saphenofemoral junction here. And although you could do this blindly, I do think you get a much better understanding
of the anatomy and the volume of sclerosant required, doing it with venography. These are posterior thigh varicosities, that communicate through the "G" point here, and you can actually see the contrast refluxing into the inferior gluteal vein shown here,
and all of this can be treated with sclerosant. The second clinical scenario, is that of atypical varices with pelvic pain, in which case you do want to make sure you treat the pelvic variceal bed completely. And for this, the venography techniques are
balloon occlusion venography performed from above. My preference is right internal jugular vein approach, because it's easier to place the occlusion balloon into the right and left internal iliac veins, which a sequentially selected, and then I use a Berenstein occlusion balloon
and then place it just below the confluence of the internal iliac vein and the external iliac veins, inflate the balloon, inject contrast, which both blocks antegrade flow, and allows reflux into the varices. Most of the time you can't see these varices if you don't have an occlusion balloon,
and then as you see the varices, sequentially select more distal tributaries with a glide wire, put the balloon down, inflate it, and perform sclerotherapy and occasionally, depending on the size of the vein, use coils if you need to. Here is an example of the balloon
in the internal iliac vein, you see the "O" point. We've already sclerosed the contralateral obturator vein, and you see this classical obturator hook here, which is classical for the obturator vein. Here the occulsion balloon is in tributaries of the internal pudendal vein,
you see it communicating through the "P" point with varices in the medial thigh, and then with the great saphenous vein here, with a type two junction. Here the balloon is in the inferior gluteal vein. You see communication with the "G" point here,
as well as communication with sciatic varices, this classic horsetail look shown here. So in conclusion, understanding anatomy is critical to the treatment of pelvic venous disorders, you do clearly have to understand the anatomy of the internal iliac vein, as well as the escape points,
and vary your venographic technique, based on the patient's symptoms. Thank you very much.
- Thank you very much, thank you Cees, that was really interesting, it's um, it's a topic close to my heart and I think that there's a great deal of work about pneumatic compression that we can learn from. These are my disclosures. Your stent choice, well,
we talk an awful lot about stents, but it is really only one part of the entire spectrum of factors that get it right. And when you get it right, you have an open vein and we believe that the open vein works, although the open vein hypothesis
seems somewhat compromised, considering where it came from in terms of open arteries. But your stent choice is just one of the factors that goes into it, and your inflow, and your outflow generally we can improve upon. Your muscle pump we'd like to improve
by using pneumatic compression boots, and then obviously getting your anti-coagulation right, as Dr. Weinberg explained, is really really key afterward. So, stent choice is one of the aspects, but it's certainly not the only aspect. You're familiar, and probably sick of these diagrams
showing the differences between radial force, crush resistance, and the trade-offs between stent flex, strengths, rather, and when I use strength it's a fairly generic term, and flexibility. And obviously in Europe, we have access to a wide variety of stents.
The Cook Zilver Vena first came out in 2010. Bard Venovo was, I think, 2016. The ABRE was just last December, but it's commercially available. The Optimed Sinus-Venous has been around for quite some time, I'm going to say 2011 if I'm correct.
And the Sinus Obliquus, then it was a little bit later, maybe 2014, 2015, and for those of you who haven't seen this before, this has got a, a closed-cell design at the top which is quite rigid, if I may, and then a very flexible sinus,
or rather open-cell design at the inferior portion, the top portion is angled to address the IVC confluence. And then the Veniti Vici, which is, (coughs) excuse me, was extensively studied in the VIRTUS trial, and this is a more closed-cell, but there's still a considerable flexibility.
So, like everything else in life, you know, you can go for the old broad who's got loads of money, or you can go for the young hot chick, and you know, she's broke. And you know, life is like that, and stents are like that too.
You know, what you get in one you lose in the other. And like a lot of the other things, you have to get everything right to make the stent work. That analogy certainly does not apply to women. But the closed-cells generally have higher force but they're slightly more rigid.
The open-cells are, perhaps, slightly weaker, but there's infinite varieties of imaginations and changes that can be made to those two very generic statements. For instance, in the newer stents, if you cut off a larger, laser cut a Nitinol tube,
you will intrinsically get thicker struts, and therefore slightly larger sheath size, but ultimately slightly more strength at the expense of slightly less flexibility. I think for me, the thing that I've learned the most about the newest venous stents,
or using the newer venous dedicated stents, is that you must do very aggressive balloon dilatation pre and post, that's absolutely essential. Regardless of what stent you use. And I'm horrified to see some of the Twitter handles of people using pre-dilatation
with an eight millimeter balloon, then putting in a 20 millimeter Wallstent and then ballooning it again to 14. Absolutely no logic to any of that. So I think you should balloon to the nominal diameter of the stent.
And it is interesting that you get a much higher force when you get that stent to the nominal diameter. The actual physical properties of the stent change when it hits that diameter. So not getting to the diameter of the stent is a huge mistake.
Now, do fractures really matter? We've been looking extensively at this in a variety of the different trials, and it's hard to know. Certainly, luminal reduction does. Fractures, not so sure about. Fractures sound like they're easy to diagnose.
They're actually very difficult. And compression at the inguinal ligament, is it real? It seems to be real. It seems to be more real than I certainly believed, in a certain proportion of patients. Typically skinnier ones, in my experience,
again, skinny females. Flexibility is obviously a big, big issue, and when you think of where your knee goes in relation to your shoulder if you're doing your yoga class, or anything else for that matter, tying your shoelaces,
there's a lot of bend required. And if you think of where we are now in aortic stent grafting compared to where we were when I last had hair, everything has changed. All of the devices have changed.
We went from Ancure, which had 64 steps, through AneuRx, and now, you know, things have moved on way past 2010 as well. So, in terms of my choices, in the USA you've got two choices, you got Wallstent and Z stent.
And if you got a rupture, use a Gore or something like that. In Europe, it's a much more, nuanced and challenging to try and figure out which ones you do. And these are just my choices. Is there any evidence to back them up?
None whatsoever. Have I had problems with most of the stents? Yes. Most of those problems were probably self-induced. I've certainly learned that pre-dilatation and post-dilatation are the essentials.
And flexibility is a lot more important than I would've thought if you had asked me five years ago. Thank you very much.
- Thank you so much. Seattle, like many other cities in the U.S. is facing a terrible, heroin epidemic crisis. We are the safety net for these patients. I was honored, when I was asked to came and share with you how we manage these patients at Harrow View Medical Center. Over the last few years, we have educated our ED doctors,
in order to avoid over-head page to vascular surgery. That they don't do any I&Ds at the bedside. If a patient with a history of IV drug use present with induration or pain on the groin. On those patients, they get triaged for sepsis, they get an IV access, can take some time.
They take labs, including blood cultures. If we can, we do ABIs, this is during the day, and we start the patient on broad-spectrum antibiotics. After that, the patient goes for a CAT Scan. The CAT Scan is really useful for us, it help us not only see the anatomy,
see if the cell is coming close to the external iliac or close to the bifurcation. But maybe even more important, it help us, and you can see the upper emissions, find a lot of needles that have broke and left over by the patients that --
It's a huge hassle for your team in the operating room. So once we have the CAT Scan. We go to the operating room, we get the patient under general anesthesia, we puncture the contralateral side, and this is our preferred method to
take care of this patient. We go up and over, we put the sheath at the end of the external iliac artery, we give some heparin, we do an angiogram that shows exactly where is the injury and we put an occlusion balloon,
usually like a 7 by 60 does the job. Once we have the ballon, we can then ride directly in the pseudoaneurysm. When you open, you take out all the clot and puss and all that tissue. And once you irrigate and debride,
you will see at the bottom, your wound. Usually you see the balloon inside the artery, with a rupture wall, and the proximal ends of the artery. So what we do with with arterial ligation, we resect to help the artery until we gain control, we paralyze vessel loops, remove the balloon
and we do the ligation both the stems and usually we try to preserve the bifurcation. It is a long puncture, it's not possible, we try to preserve our zincuflex, so the patient will have a collateral pathway to their leg. After that, we try to approximate the tissue on top,
or we do an sartorius flap. Now our patient that use black tar heroine, sometimes there's too much inflammation, too much puss, we just put the dressing and we come back in a couple of days for a wash out, to take care of the wound.
After that, the patient goes to intensive care unit, and you will notice that I didn't mention, we ever raise the foot. We don't put any pulse oximeters or do any studies. The foot is going to be okay. The patients usually have some kind of chronic compression
previously and they will tolerate ischemia pretty well. Patient goes to the ICU and the first thing that we do, we avoid hypotension, but we call ID and Pain Service. This patient's outcomes are going to be better if the pain is going to be well controlled, because they will be compliant with the treatment.
ID recommends that antibiotics treatment and helps with management other comorbidities. I know we're starting to have a lot of patients that have PE's during admission, so we try to rule out DVT study and we'll start the patients in treatment.
When we look at our cases, we have more than 50% patient that present with bacteremia, and of those, almost 40% was due to MRSA, so it's a very severe condition that the patient require several weeks of IV antibiotics. Post OP ABI, immediately,
we have a median of 0.41, so the leg is viable. And our amputation rate for these patients is very low. We have only lost 4 legs and of those 4 legs that we have to amputate, 2 patients we revascularized the immediate post-op period and both were infected.
So we actually avoid actively doing revascularizations in the accurate period. In conclusion, the vascular emergencies due to IV drug use are increasing and we as vascular surgeons should be prepared to deal with this and educate our colleagues
on how to treat them. Femoral artery ligation is well tolerated and we recommend not performing an immediate revascularization. The amputate rate is low and ID and Pain Service collaboration is essential for these procedures. Thank you so much.
- [Presenter] Okay, so you've heard two aspects of the valve, so going to give you actually two, what's called the sail valve and also the VenoValve, two other options that are out there. These are my disclosures. So if you look, these are our options in 2017,
but we really talking about these three, Amrit's already spoken about the Neovalve. All these are the indications for secondary venous problems, and usually monocusp, can be bicuspid, usually monocusp, but can be bicuspid also, and this is monocusp as well.
So want you to get the idea, a lot of monocusp is coming around even though we think theoretically, bicuspid works better, but maybe not, in terms of prosthetic valves. So this is what's known as a sail valve.
Its percutaneous is a monocusp valve. It's almost not a valve. It functions in a slightly different way. It does have a physiologic leak and it's a thin piece of PTFE and what happens is if the blood is going from here up,
when it goes up these slits become larger and when the blood wants to reflux back these become smaller slits and it's like a billowing sail so it's a self-cleaning type of valve. You don't get much on the PTFE itself and it's obviously percutaneous.
So they have done 10 pigs placed in their iliac veins. Access is six French, deployment was 100% and it expands to a 10 millimeter diameter which most of us working in this space think you need about an eight to 10 millimeter size of a stent if you're going to use a stent.
Some of the results at four weeks did ascending venography on these pigs, not patients and they were all patent and then they did some descending of venography and eight of them, five were competent, 1 was partially competent, and two were incompetent. That was due to what they said malpositioning
or maybe it's tilting itself. More importantly at least on Histology, in pigs, not humans, there was really no microscopic thrombis on the valves so that was kind of encouraging. That is the sail valve. Then the second one that to complete the whole cycle during this segment is the VenoValve
which is a porcine derived valve. It's monocusp but it is an open insertion and it's based upon heart valve technology. One of the nice things is and that's another nice thing about the Blueleaf, you don't have a size mismatch. The Blueleaf you're doing it in the native vessel
and here you can tailor the inflow and outflow and papers show that that's really clearly important. You can't put a small valve if you have a big inflow and small outflow et cetera. You need a nice tapering so this will allow you to, when you do it open to tailor the size.
This is what it looks like. Here it's a monocusp valve that's mounted on a metal alloy frame. This is placed in the jugular veins of sheep and it's an open insertion. Clearly you suture it closed with some 7-0 sutures and then you affix it to the vein wall so it doesn't migrate also with some 7-0 sutures
and you can test it. This is a decent ascending venogram so head is up here, neck is down here in the jugular vein of the sheep. Then we can do a descending venography as well. So descending injecting from here, and there's not much leak going down.
So the FDA is submittal and hopefully do some sheep. They want to be sacrificed in 30 or 90 days and hopefully start a inhuman trial within the future. So this really goes back to the axillary valve transplant which is where I kind of started, believe it or not, 35 years ago as a, 37 years ago,
as a surgical resident doing axillary valve transplants. This is monocusp. It's an open insertion. It helps you do better inflow and outflow. But the challenges of all these are going to be, as Amrit already said it's a specialized area. And Mike (unintelligible) also.
Who needs this? Is this the first line or the final line of care in these patients and where do we place the valves or where to create the valves? Is it in the popliteal, the femoral region, or the common femoral?
Maybe some of it depends upon the profunda vein status. We've been doing this for 35 years when I was a surgical resident and I'm glad that we're finally getting to the point where we have a lot of nice options and see which ones pan out
because it'd be great for these patients. Thank you.
- Thanks very much. That's my disclosure. Let me start with this patient. 79 year old man with among other things, end-stage PAD, as you can see on the images. Previous fem-fem bypass and the like. Heavily calcified arteries everywhere,
the aorta included, severe COPD, he had been deemed medically inoperable for major aortic surgery. I had followed him for a number of years, told him that there is no way he could be fixed. He was okay with that for a while, soon his wife was.
As the aneurism grew and grew reaching almost 7 centimeters, he became increasingly concerned about this time bomb in his belly and the risk of rupture, and kept asking more aggressively and frequently about other options, so I sent him somewhere else.
And sure enough he found somebody who wanted to fix him. It was a three vessel chEVAR, extremely complex, he ended up with all sorts of complications, a horrible one week of life with three different operations terminating in death. But, he wanted that, the patient.
My experience over the many years of practice has been that, for the most part, once a patient like this, aneurism patients in particular, end up in the hands of a specialist, it is almost always all about how, and seldom, if ever, whether to repair.
There are of course exceptions to that. So I think we could take a couple of minutes to think through this which might be helpful and important at least to some of our patients. This is particularly true for complex anatomy aneurisms. So what is complex?
How would you define that? My definition of complex is something that cannot be treated with standard EVAR, or standard open repair meaning a infrarenal clamp. Look at this patient for instance, this is another part of this picture as well.
A center where everything is endo, they really didn't think about surgery, except in the face of serious complications after endo. Off label use of a device that can produce, I must say, good results even in this anatomy, but not here.
This patient wound up with a major Type 1 endoleak, so thirty days later a complex re-do intervention was performed with chEVAR. They did a good job, this was six months later. But who knows what the long term result might be. One wonders, this patient who was actually
a good medically fit patient for open repair, wouldn't he have been better served with a well-executed open operation. It's something else. The aneurysm must be large enough to represent an immediate and real threat to life.
Unlike this case, for instance, of a morbidly obese individual, I got this after the fact as failure analysis type of process whereby a 4.9 centimeter was repaired electively also causing his death 48 hours later
because of a number of serious technical issues, etc. This pushing the envelope is something that we seem to be doing increasingly all the time. To the point that now EVAR, at least in this part of the world, is estimated to represent more than 80%
of all procedures. And we continue to use diameter of course, which is an important parameter, but I hope that moving forward, we use a more nuanced approach like this one that was published a number of years ago in fact,
classifying AAA patients into Low, Average, and High risk individuals, taking into account a number of important factors beyond diameter alone. It is clear now that in men, aneurysms less than six centimeters in diameter are
at relatively low risk for rupture. Females are different though. They have a risk that is at least four times higher. We also have pretty good data for thoracic aneurysms, that those that are truly inoperable live a very short time regardless
of what we do or don't do. So I'll leave you with a few simple thoughts. I think we should always strive to weigh the risk of the procedure versus the natural history of the untreated aneurysm. Elective repair of complex anatomy AAA
requiring complex procedures should be reserved for aneurysms that are truly life-threatening. Open repair still has much to offer, and perhaps we should question the wisdom of recommending elective repair on aneurysms for patients who are truly inoperable,
almost regardless of the size of the aneurysm. Thank you.
- Folks always ask if you can do saphenous vein ablation in the presence of Deep Venous Obstruction. So, we'll talk about that a little bit. So, deep vein thrombosis, as we know, acutely, the danger, or the pulmonary embolus
is what we worry about anti-coagulation is the standard for that, but the longer fate of a DVT may be the post-thrombotic syndrome of which this is from scarring and valve damage, as we know. Mark Meissner showed us in this study back in '97
that more proximal DVT, femoral DVT fares worse than calf vein DVT as far as symptoms, and that goes out to about four years in this study. And we know that the worse actor of all is probably ileo femoral DVT,
so the more progressable the deep vein thrombosis, the greater the obstruction, the greater the symptoms. So, I always show, I like this study by Lois Killewich that she did back in 1989 basically showing the recanalization of deep vein thrombosis on a timeline.
And the message here is, that around three months, 86% of the recanalization has occurred. So, that's kind of my trigger as far as the earliest that I would even consider doing intervention on a post-thrombotic, would be at least three months to allow recanalization to occur.
We know that folks with, post thrombotic folks, do worse as far as receipt scores at five years if you compare primary deep veinous disease with post thrombotics, the post thrombotics fare poorly. And that's really the rationale between these
clot removal strategies in the ileo femoral segment to try and mitigate post-thrombotic syndrome. So, when you have a patient in front of you, the way I kind of line these things up, there going to be either obstruction dominant or reflux dominant.
You're not going to get a limb assymetry. A big, you know, one leg just clearly, larger than the other from saphenous vein reflux. It's just not going to happen. So, if you got true limb assymetry, and a saphenous vein that's 10mm and incompetent,
you're not going to improve their limb assymetry from saphenous vein ablation. So, you got to look at your indications. This patient should be looking for something ileo femoral that you can stent, but I don't think the saphenous is going to be much of a contribution.
The other thing, these folks don't have a lot of vericose veins they have more advanced skin damage. Whereas with reflux dominant, saphenous vein incompetent patient will usually present with vericose veins,
they won't have the limb assymetry, and that's why the C-3 gets a little hazy. It's swelling from superficial vein disease. It's usually just some fullness in the malleolus, maybe around the ankle, but you're not going to get full-blown edema
from saphenous vein incompetence. So, know why you're doing saphenous vein ablation. Not all refluxing saphenous veins need to be treated. Can you do saphenectomy in the presence of deep vein obstruction? We've shown this before.
This old Raju study that he did saphenectomy stripping in two groups, those with and without previous thrombosis, and they both did fairly well, did not seem to be impaired by the presence of obstruction.
This study by Puggioni on RFA ablation. She looked at some patients with DVT in a larger group that were all treated with RF ablation, and the bottom-line of her study was that RF ablation in patients with previous DVT is safe. Again, I wouldn't do it until after three months.
Does prophylactic anti-coagulation have any effect on post-thrombosis rates after saphenous vein ablation? Well, not in the study by Knipp. They used low molecular-weight heparin in folks going saphenous vein ablation, and it just increased the risk of bleeding,
and it had no effect on thrombosis. Can you do combined iliac vein stenting and saphenous vein ablation in the same setting? This is another iconic study by Neglen showed that, yes, you can. Patients with advanced disease
that underwent iliac vein stenting and saphenous vein ablation in the same operation had good symptom relief and very few complications. So, in conclusion, saphenous vein ablation may benefit
patients with previous DVT. Clearly, you're not going to do this in the acute phase of the DVT. When is it safe? I'd say the earliest you would do it, or even consider it is three months
because that's when recanalization starts to peak out. Limbs with concomitant superficial vein reflux and deep vein obstruction can be safely treated by combined treatment, at least in the Neglen series, and the DVT prophylaxis should be
administered at the surgeon's discretion. Thanks.
- Thank you Jose and Marcia. No disclosures. So the primary valve incompetence treatment techniques was started by Bob Kistner and the techinique involved a longitudinal internal valvuloplasty by longitudinal incision and tacking of the redundant valve edges.
And the next treatment available was a transverse valvuloplasty which was again under vision and the valves were tacked at the at the commissures but the incision was transverse. And a combination of the two techniques resulted in the technique of Sottiurai, the T internal valvuloplasty
which was later modified by Michel Perrin to be able to evaluate all aspects of the valve. Further to that, we developed the trapdoor internal valvuloplasty in which a trapdoor was created. All these techniques, the mainstay was reefing of the valve commissures.
On the left hand side, you can see a redundant valve, prolapsing cusps, and on the right hand side, a repaired valve after the reefing. But you can see that the commissure is quite heavily placated. So the possible disadvantage of reefing technique
is the resultant heaped up commissural junctions. This creates valvular rugal folds and obviously when healing occurs it will have increased cicatrization, it will occupy the space, and reduction of functional valve area. When we evaluated the various thrombosis results of
supra-valvular technique, modified T technique, and the trapdoor technique, we found that on an average, there was about a 4.5 to 9% incidence of valve thrombosis. And we also found that in another 6.1% patients there, the valve stations resolved. Cumulatively, these two complicates accounted
for almost 13% of all valvuloplasties. We published a new technique of reduction internal valvuloplasty on the lessons that we leared from Dr. Lugli's experience. And we wanted to quantify the repairs that we do by measuring intra valvular distances and
trans-commissural diameters preoperative as well as intra-operative by ultrasound. We used various techniques, we devised measuring forceps and this is how it's done, whereby we are able to excise the redundant valve and stitch it back onto the valve
and have no rugal folds at the end. And this can induce, this can reduce incision in high shear areas as well. And therefore, give you a good result. This is intra-operative result of competence where you can see the patient is doing valsalva
and you can see the two valve leaflets and this is the stripping technique. And a post-operative descending angiogram or venogram shows a competent valve. So when we looked at the relationship of reflux, valve repair, and ulcer healing,
we found that when we did single level repairs, we only found 50% ulcer healing. But when we did multiple level repairs, the healing was 100% in a short period of time. And the valve competency always did not correlate with ulcer healing.
In our case the valve competency levels were 87.5% and ulcer healing was 88.9% but mainly due to the single level repairs, that did not really work. So the Rival Technique in conclusion ladies and gentlemen is a complete departure from the reefing technique which has been the mainstay of valvuloplasties.
At two years, we've had 100% patency and about 87% competency of repaired valves, with a freedom from C6 ulcers at two years about 89%. Rival Technique has now replaced our technique, earlier techniques, and is the preferred technique in our center.
Thank you for your attention.
- Thanks Gustava, Fred. Thanks Frank for the opportunity. These are my disclosures. So, why are talking about aortic septotomy, and when is it necessary? It's really for treating complicated TADs with malperfusion, planning an EVAR or TEVAR when you don't have
adequate landing zones. So, certainly trying to bail out from a complication or EVAR, TEVAR. This was my first case in 2006. It was an elective case, a clot client who came with an aortic dissection.
And what I ended up doing at the time, was going from true to the false lumen at the aortic bifurcation, marching up the aorta, snaring a stent, snaring a wire from true to false lumen, and then essentially created a place where from the femoral approach, we could just apply
gentle downward traction to tear the septum. I'll show you exactly what this. The two wires come out on the femoral, from the femoral side. You essentially pull down gently and this is simply glide wire,
you could use a variety of wires. So this is something we've implemented in 2006. And of course this experience has grown. We've used it in a lot of different circumstances. Here's a completion angiogram for this case. So, what else can we do?
We can certainly do septotomies. We can put in stentgrafts or just bare metal stents to connect the true to the false lumen. The trouble with this is when aneurysms expand. These stents are really difficult to deal with.
And I'm not a big fan of putting stents in, bare metal stents across a paravisceral aorta. So, for that reason aortic septotemy is very helpful. Certainly can be used when you have infrarenal aortic aneurysms, following up with the thoricoabdominic dissections and you need
to create better landing zones. Once again, true to false lumen snare, gentle downward traction, creating single barrel lumens where you have adequate proximal and distal landing zones to obtain seals. I'll show you through a complication of a TEVAR.
Here's a patient who came in. Sudden onset chest, back pain and left foot rest pain. At the time we went in, and thought just simply getting in through the true lumen, and deploying the stentgraft all the way from the descending thoracic aorta.
From the left subclavian to the descending thoracic aorta would have been sufficient and it seemed like it was. And I think most would treat it this way. The trouble was as soon as the stentgraft was deployed, the paravisceral aorta collapsed. It was an acute dissection and now we have a very
difficult situation where the entire paravisceral aorta has really collapsed from the septum. So in this particular case, we were able to protect the celiac and the SMA with the wires that you see, where the red arrows are. And once again, put a catheter from the true to the false
lumen, snare in the descending thoracic aorta, apply gentle downward traction, to unfold and drag the septum down to the aortic bifurcation, knowing very well, as much as we were going to be able to profuse the visceral arteries, which we were able to,
we now have to deal with an occluded infrarenal aorta. And you have to be ready to do these things, especially if you are using septotomy techniques. And this particular case, we just did kissing stentgrafts, to manage this. Other scenarios could be delayed complications.
This is a patient who initially came in with a thorical dinaric dissection, which expanded into an aneurysm and underwent endovascular repair. Fairly straightforward, the coil embolisation of the false lumen. Everything went uneventful, except the patient
shows up a few days later with saddle paresthesias, bilateral lower extremity weakness, urinary incontinence, only when he ambulated. At rest, he was completely normal. This is, I think, the first case of transient ischemia and cauda conus syndrome following TEVAR.
Of course it was a daunting situation, and what we found is that the obvious dissections extended all the way to the iliac bifurcation. And this particular case, once again, going in from the right and left, true and false lumen from both sides,
I was able to snare wires and catheters into the mid aorta and you'll see this play out in the segment, and once again, gentle downward traction, create a septotomy extending to the left iliac bifurcation and to the right iliac bifurcation, and once again you see that right external iliac artery
has a prolapse septum which we treated with a stentgraft. So, there's a lot of different ways of managing these problems, and this patient's symptoms actually resolved and he recovered immediately. And I think what we need to do is be ready to deal with all sorts of potential complications that occur.
Many others have started to report on these findings as well. And obviously, there's a lot of benefit and right now, Ramon Berguer, Juan Parodi has a septotomy catheter that is currently under trial. So I think, my personal suggestions are,
this is not necessarily simple, but you have to be able to be ready to deal with all potential complications if you do aortic septotomy. And it is a very useful technique in managing complex aortic dissections.
Frank, Jackie, and the team, thank you very much. We love being in New York City at this time.
- Thanks again to the organizing committee for inviting me. There has been an extensive session this morning on ascending endografting. I think almost everything was said and will be repetition, but we'll still do so. What we learned in ascending endografts is that post surgery legions
are probably the best indications when we have pseudoaneurysm or bleeding in the ascending. Type A dissection is a rare indication, and ascending aneurysm actually doesn't work very well due to the fusion form type of these anatomies. Our experience is lended to 24 cases until 2017,
and you will notice that most of those cases were emergent, they were usually referred by a cardiothoracic surgery to our unit in order to treat those patients in a rather emergency situation. And in these cases we have mainly taken transfemoral approaches,
but you see that from transapical and trans subclavian also have been applied. There's some significant mortality tied to this treatment option, and this is due to the emergent character of the treatment. There were a lot of, a few type A dissections,
ruptures, bleedings, et cetera. Our device of choice has been the cook ascent device, which has been first published here, to be used in acute type A dissection, and is not current, not commercially available. We've also used a lot of customized grafts,
which is especially helpful when you need to tapered graft with a different proximal and distal diameters, and there you can use tapered grafts and just cut them to length that is, that fits well. There have been reports with these kind of customized
or off the shelf grafts that are commercially available, and trimmed to the length that is needed and experiences have been mainly very good. Main issue remains in over sizing and that is especially an issue because the type of CT for which they,
which is used for measuring the aorta is quite different. You need to know whether it's native or its graft, its gated or non-gated, systolic, diastolic, gated CT, the age and blood loss play a role in the pulsatility of the vessel, but generally I would like to say
that 20% over sizing's probably the right number, and this is mainly due to that already the pulsatility of this area of the aorta is, within 15%, relatively high. This is a case with the type A aortic dissection, you see that at the greater curvature, how the contrast goes into the dissection.
There's a cook ascent device that is delivered from transfemoral route, and you see here on the completion angiogram it looks quite nicely sealed, but what you also see is a problem that we frequently see is that the bare struts go into the valve
and cause a valvular insufficiency in this patient, so the patient required a TAAD that was done transapically, but the target valve did not stay where it was suppose to so it needed to be snared into a better position, and then again treated with an ascending TEVA. This time from the transapical
because we already had that access. And when this was done the patient could receive his, um, let me go back. Could receive this uh, Edwards, uh valve. Just to show you
that you can put a lot of these materials into one patient and maybe he would have been better off with open surgery, but I'm sure there was a reason why he was preferred for endo treatment. One of the big issues is inner curve apposition,
because the device is proximity, quite often not perpendicular, what is necessary in order to give them the radiant force to seal. And you see this from the, come picture this, images I got from other colleagues,
are about the Gore ARISE Studies. And what Gore is, um, is uh, is using here is a mechanism to meet this problem of the inner curvature, which I think is very helpful. We've been doing similar,
and been presented here ten years ago at the Veith-Symposium. We called it in situ bending, a bowden-cable principle to shorten the curve, the inner curvature. Medtronic has been working, Ali Khoynezhad is in the room.
He's been doing the physician sponsored IDE trial on this with really good results, and we hope to hear more from him. But if I look at the images, there's also the same issue of perpendicularity of the device, the approximate part,
and you see the same in other publications. Here from us, and again you see that the devices don't really deploy well at the inner curvature. I think I jumped over this case, which is about a transapical bridging stent,
because I have run out of time, I apologize for that. This is also imported for Martin Czerny, who has been on the podium showing today, the combination of Bolton NBS ascending graft, because its really what we need
in order to treat those patients, in order to get a safe landing zone. And to summarize, in my belief, the endovascular treatment of the ascending aorta is already beneficial in selected high risk patients, and those surgery lesions are the best aneurysms
will not work without having a valve attached to the ascending graft. Transfemoral delivery may not be the right route, in my belief the transapical was much more promising, and we see a significant process in the device development. Thank you very much.
- Good morning. Happy to discuss with you some of the issues of the currently available stents. Nutcracker Syndrome patients most frequently present with left flank pain, pelvic pain, hematuria, usually due to a significant narrowing in front of the aorta between the aorta and the superior mesenteric artery.
Open surgical treatment has been kind of a gold standard. Left renal vein transposition done most frequently followed by gonadal vein procedures or even renal auto-transplantation. Renal vein stenting, in this country, has been done using Wallstents or SMART stents.
In our experience, where we reported 37 surgical patients. We used stents only for secondary procedures. Three of the six stents had problems of either migration or in-stent restenosis. There is a systematic review in the JVS-VL, recently published, 180 patients, 7 series.
Interestingly, 175 were treated in China with good clinical results in 6-126 months. Stent migration was observed from 0 to 6.7%, depending on the series. We have seen stent migration, sometimes it's immediately during t
and that's obviously the easiest to take care of. Or immediately after, before any healing, that is also a more favorable situation. The problem is when it travels to the heart. It is not frequent, but it happens.
This is the largest series, 75 patients, stented, 5 of them had migration. Two of them to the right atrium, one of them required a medium sternotomy to remove it. Stents not only migrate, although again it's rare,
but even one patient is too frequent in this series that usually involves young, female patients. Stents in this position unfortunately can also fracture. If they don't fracture, they can thrombos. If they don't thrombos, they can be compressed.
If they don't compress, that's a stiff stent, it practically always will perforate their renal vein because of the arching configuration of the renal vein and because the unavailability of less than four centimeter long stance. So it is a problem.
It can actually cause significant, severe migration, completely occluding the inferior vena cava together with perforation of the renal vein. Obviously these cases require open surgical repair,
and have a chance to remove a few of these stents. Percutaneous retrieval, fortunately, is possible in about 90% of the cases, and sometimes, if it doesn't cause significant cardiac injury even from the heart or the pulmonary artery and
we had several case reports, of stents, especially after the TIPS procedure, early on, that migrated into the central circulation that would be removed with different types of techniques, of snaring and pulling the lost stent into a large sheath,
whether you snare it at the end or you snare it in the middle. There are good case reports. This patient that we had, we could use a balloon, pull it down to the vena cava, and then from above and below, we could remove it
with a large sheath. Current stents, if you really don't want it to migrate, the only option we see is transposition patch and using hybrid procedure to fix the stents in the renal vein.
So, in general, open surgery remains the first line of intervention. Stents have a reported high mid-term success rate but migration, fracture, perforation, thrombosis, restenosis are problems and if you go to the FDA website, you see that there are much more cases than
those that are reported. So what do we need? We need dedicated renal vein stents that are short, flexible, resist fracture and migration, and we need them urgently. Thank you.
- I try to dissect this convoluted title into two questions, basically, when is endovascular treatment of post coarctation aneurysm best, and when is an open surgical intervention required. A couple of years back in time, we looked at predictors
of aneurysmal formation in patients after surgical correction of coarctation, and we found essentially two predictors, which is previous surgical patch repair, and the age at the surgical repair, as predictors for the evolution of
a post coarctation aneurysm. In other words, these two predictors could actually become important for the selection of patient for open surgery. I come to this in a moment.
A year later, we could publish the feasibility of percutaneous endovascular repair of those post coarctation aneurysm, post surgical aneurysm, easily by a customized
or off the shelf stent graft. So that is basically accepted in the community, and reflected in guidelines, that basically come to the conclusion to the question, when is endovascular treatment
of post coarctation aneurysm best. In the case of a risk-benefit ratio high for open surgery, which is in case it's a redo surgery, of course, in presence of extensive collaterals, with a significantly increased bleeding risk,
adult patients above the age of 13.5 years, according to the statistical analysis, and when end to end anastomosis is not feasible, and of course, patients need to be suitable for an endovascular approach.
Patient preference may play a role, most recently, and of course, is conclusion of endo first should be executed in dedicated centers that have options to treat the patient even openly.
The second part of my title, or the second question is basically to the preferred use of open stents or covered stents, and in order to show our recent analysis on this, I had the privilege to compare
a group of patients from my previous institution that used self-expanding open stents, and with my current position in another place, that uses CP stents, or covered balloon expandable stent grafts
in the setting of coarctation as the first and only option. So we have no data from two different hospitals that show similar patient sets, a total of 52 in each group, that do not show any demographic differences
over a time of 10 years, collected over 10 years. Clinical presentation of comorbidities are essentially the same, so we're dealing with a comparable set of patients
and two different concepts of treating primary coarctation. The post interventional vascular events are also similar, no significant differences between the two concepts from two different sites,
with a trend towards more re-stenosis in the setting of ballon expandable stents being used as the first approach, but not significantly more. Even in hospital complications, comparing these two groups of 52 patients,
age didn't show any significant difference, with a trend for longer hospitalization in patients treated with the CP stent or covered stent. Maybe this is only a coincidental finding and a more cultural event
rather than medically driven. If you look at the outcome curves between both groups, with no mortality in either group, there is a similar shape of the Kaplan-Meier curves
over up to 90 months, with an interesting difference in the first post interventional phase, with three asymptomatic localized dissection in the balloon expandable stent graph group, however, no significant difference over time.
This next slide summarizes the ballon expandable procedure with the CP stent. After obtaining lumen and connection between this ectatic aorta, it was possible to stent the segment
with a covered CP stent very nicely. You see the result on the lower right corner. The other concept is a bare self expanding Nitinol stent placed first after recanalization of the coarctation and then potential post ballooning
to obtain an appropriate dimension and the lumen. In summary, comparing those two approaches and answering the question, when is an open operation still required, I think it's fair to say that in adult coarctation,
and endo approach should be chosen first, and bare, self-expanding Nitinol are relatively safe as a concept, and durable solution, without the risk of side branch obstruction, whereas covered ballon expandable CP stents
are also safe, and offer a durable solution, but have to respect the LSA anatomy. An open surgery I think should be reserved for infants and children younger than 13.5 years, only in view of an end-to-end anastomosis.
Thank you very much.
- Good afternoon, Mr. Chairman. Thank you for allowing me present on the topic of importance and prevention of treatment of complications of TAVR. And TAVR and TAVI are the same, transcatheter aortic valve replacement versus implantation.
So VARC stands for Valve Academic Research Consortium and they defined specifically specific details of various complications of TAVR and major vascular complications are actually one of them. This is one of the earlier publications looking at all of the outcomes, but you see
the number of, or the significant percentage of vascular complications, meaning many of them led to issues with mortality. I remember initially when we started to do TAVRs, about almost 10 years ago, it was, we had a lot of iliac ruptures.
I remember at least two or three abdominally aortic fractures that required EVAR. Those were very common. Part of it was because the devices was much larger, the profile was much bigger. We had to deal with some narrow vessels.
There was some excessive calcification, tortuosity, and we learned early on with the TEVAR as well and that you can overcome one or two of those, but it's hard to tackle when you have all the three conditions existing in a patient. Obviously, wire management was also something
that the cardiologist had to learn because many of them were not used to large devices while vascular surgeons, some of the intervention cardiologists in Europe who do a lot of EVARs and TEVARs were familiar with wire management and type of wire is very important.
Myself, as someone who was not placing many wires inside the ventricle region, we learned as well what kind of wires we need and how the wire has to be shaped and placed inside a ventricle to avoid any complications within the ventricle as well.
One of the things we learned to improve outcomes are really access management, which is critical. Many of these are done percutaneously, as you know, and having an ultrasound guided and access to this area is very important. And fluoroscopy, while being helpful in many patients,
especially with palsis femoral arteries, many people feel that the ultrasound adds additional accuracy to avoid high or low stick. But this usually with a micro-puncturist, I usually do an angiogram, confirm that we don't have a high or low stick
and that's particularly upgraded to 035 in a you know five or eight French sheath, depending on. Next thing particularly is following the wires for unfavorable tracking, like you see in this case, for example. That depends, it mostly has to do with the wire you choose
to track this device over, but also sometimes anatomy and vessel consistency. Now direct iliac access has been used in the past, and I think there is a useful for certain number of patients as an alternative, but today rarely used for any TAVR
just because of the profile going down. Exo-conduit is very commonly used and I think is a good and helpful situation for patients requiring large device. And most of its ations is actually, I used to leave the ilio-femoral artery bypass,
because it hopes not only provide profusion to that leg, but also can be helpful for future re-intervention of that patient. Now endo-conduit has become also popular, which means basically we go in from inside with an Igor or similar devices,
we crack open the iliac arteries and this may be an opportunity as well. Having said that if you have a graft past iliac inguinal canal, that may or may not be good because it tends to bend in that area. Dissections we have seen frequently with TAVR,
and that's typically treated with stents as well. With percutaneous options with TEVARs and EVARs, we see a lot of femoral artery stenosis that needs to be followed up with these patients. So the position of these devices are very important when you do a perclose and tuberclose devices.
Dissections, fistula, we talk about pseudo-aneurysm and other issues can happen with TAVR and those need to be monitored and watched for, obviously, as well. Same thing with embolization of some closure devices. But open surgical repair has its own issues as well.
We can have lymphocelle. We can have venous obstruction, arterial stenosis, neuropathy, infection. So none of this exposure, either percutaneous or open is without complication, and we've got to keep an eye on those particularly.
Retrograde dissection, I've put on. It's mostly a complication of TEVAR, but as we described already with TAVR, with the TAVR as well, you have, predictably, especially with devices who have bare wires in the STJ area can cause localized,
penetrative, aortic lesions, but also dissections that needs to be watched for and cared for. And sometimes the echo, the trans-thoracic echo, will fail to show that because you pass the lesion site,
where the echo will show. So if you pass a certain area, you may not be able to see with the trans-thoracic echo, but he hopefully should show it. But if not, an angiogram or intravascular ultrasound should be an alternative.
And there's a couple of ways to deal with this, obviously, besides, using ascending stent graft is also. Hemiarch replacement, or what we did in the past extra-anatomic bypass in a zone zero. Make it a zone zerotitus. With that said, I want to say the TAVR has
significant complications that has thankfully reduced, but they are a major source of complications and mortality within this patient population. Thank you.
So I'm a consultant for both of those. Okay, so repair of coarctations. So surgical repair is effective, has a low procedural mortality and morbidity, and so does stent implantation. But the mortality is very, very low with stents, and the morbidity is also lower in general.
Whatever method you choose, though, both methods are going to be complicated by hypertension, re-intervention for stenosis and aneurysm formation, which is normally just a question of time if you follow up the patient for long enough because the post-stenotic dilatation,
cystic medial necrosis, calcification, it's a sick wall. So the potential advantages of using a covered versus a bare stent versus angioplasty is that the angioplasty just tears, and we don't do angioplasty on native coarctations. But you put a stent in and you get this creation
of a longitudinal framework, and if you have a covered stent you're going to control the integrity of the vessel at the coarctation and below it, which is normally a very dangerous area, the poststenotic dilatation area. And they're particularly useful using covered stents
when there's an aneurysm which is present. However, there's no good studies to say that's really the right thing to do. So recently Tretter and McElhinney, they looked at all the reports that had been done for endovascular therapy for aortic coarctation,
and they noted that aortic rupture was particularly rare, less than 1%. Acute aneurysm formation, when intervening for endovascular therapy, was about up to 13% for angioplasty, up to 5% for bare metal,
and less than 1% after covered stents. But it depends on the reporting bias and there's a lot of inconsistent definitions. And overall, the acute wall injury seems to be going down for coarctation due to better delivery systems, more use of covered stents.
And there are really only three covered stents, which are balloon expandable, and the CP covered stent, which comes bare and covered, and it's stuck on quite loosely, the Atrium V12LD which is not available for the last two years,
which goes up to 22 millimeters, and the aortic BeGraft which comes in a whole range of sizes and covered. This is the Atrium V12LD with stainless steel covering the inside and the outside, and the BeGraft is chromium cobalt
and it's covered on just the outside. So, when you're doing the covered stents, you need to consider the vascular access damage that can be done because you need a relatively large delivery system, and I'm a pediatric cardiologist,
so using these in small kids you have to be very careful, and the CP stent can take even 11 to 12-French system. The stent integrity, because the CP Platinum-Iridium stents tend to fracture, the Atrium has a problem of infolding, and the Bentley is quite a strong stent and I've had no problems with it,
but it's early days yet. And the other thing is the covering integrity. The CP is incomplete while the Atrium and the Bentley seem to have a better cover. So looking at the COAST I study, which was a look at the CP stent,
which was a bare stent, they did 105 patients underwent attempted implantation, and just looking at sort of the aneurysm, the aortic wall injury, they did balloon dilatations just for some compliance testing, which I never do, and they generated some small
aortic aneurysms showing that that area is a problem. And in intermediate followup when they put in bare stents, they had a total of six aortic aneurysms, five were successfully treated with a covered stent placement and one resolved without intervention,
and they had some stent fractures. Then what they did, they did a COAST II study, which was looking at the CP covered stent, which was used, and they used it in a total of 158 patients. 83 had had previous intervention and had some aortic wall injury.
And when they were using that stent, complete coverage of the pre-existing aortic wall injury was achieved only in 92% of the patients, and seven patients had minor endoleaks. The other thing is, so that shows that the covering wasn't that good.
The other thing was is it takes a large delivery system four patients experienced important vascular site injury. In the Advanta trial the covered stents were very good, in general, for getting the blood pressure down, getting the gradient down, and increasing the diameter. And also, comparing sort of the long-term followup,
we followed the blood pressure for three years, the blood pressure stayed down and we had a very good result. The major problem was they had very small problems with femoral artery occlusion only in one patient compared to the four in the CP stents.
So there was one small aortic hematoma treated with a second stent, but the major problem was the stent wasn't robust enough in the aorta and had infolding. Two of which required urgent reintervention. The Bentley, which is a relative,
and we've had it since January 2017, so this is, let's say, a complex native coarctation. So we treated that with a BeGraft. And here you can see this is another patient, a little Bedouin girl, that had an endovasculitis and a coarctation,
and she was treated with a CP stent, which was covered, but you can see the aneurysm stayed. We put the, another Bentley stent in there. So you can see that the covering, even when using covered stent, is not necessarily always the right thing.
We've done now 22 patients with a Bentley BeGraft. You can see the median age and all different types of coarctations which have been previously treated or native. Overall, it gets down the gradient and the coarctation diameter stays up.
We had no acute wall injury and no other immediate complications. Patients that had pre-existing aneurysms, ones which you saw, was successfully treated, and at median followup things look good. So in conclusion, surgery, in my institution,
is the primary choice of intervention in patients who endovascular stenting is not possible. So infants and small children we won't do a balloon angioplasty because it tears the intima and they have aneurysms afterwards. If we can put in a covered stent,
that's our first choice. Safe and effective acute treatment of coarctation and associated with less aortic wall injury than bare metal and balloon angioplasty, but you need a lot of reintervention. The choice of the covered stent,
you need to consider delivery system, the maximum diameter of the stent, the stent integrity, whether it's going to fracture or infold, and the covering integrity. And when all is said and done we still need to have long-term followup imaging.
Thank you very much.
- Just going to do a little bit of a deeper dive into the types of nutcracker syndrome. I think most everyone knows this one. The anterior nutcracker syndrome in which the left renal vein is compressed as it passes between the aorta and the SMA, and this is definitely the most common
and certainly the most written about, but there's also posterior nutcracker syndrome in which there's a left renal vein which is retroaortic, and in this case it's compressed between the aorta and the spine, and then even more rare is the atypical nutcracker
in which there is a truncular vascular malformation trapping the left-sided IVC and renal vein between the SMA and aorta. Why do I mention these? I mention these because they inform the decision for open surgical repair when necessary.
All treatment options for nutcracker are directed to reduce venous hypertension, and we have the generally armamentarium of vascular procedures as I've listed here. Today my task is to discuss the open surgical options and really the two most important ones
are the versions of left renal vein transposition that I've listed here and have been discussed by Dr. Gloviczki and then gonadal vein transposition which, in our institution, is preferred if the anatomy is suitable. So since I'm following Dr. Gloviczki
I had to list all the papers from his institution, but this is the one that's most (mumbles) to my talk. This is their experience with left renal vein transposition versus conservative management in 23 patients, about 50/50, and what they found, if you look at their results and the characteristics of the patients that they treated,
were that if they selected their patients well, and by that I mean patients with appropriate anatomy and appropriate symptoms, they had excellent results when using left renal vein transposition to treat nutcracker syndrome. This is the other manuscript that Dr. Gloviczki mentioned,
so this is a version of open repair that includes stenting plus left renal vein transposition with suturing the stent in place that I think they hope will deal with the issues of migration in renal vein stenosis. So far their early results are excellent.
And then this is a meta-analysis, also mentioned by Dr. Gloviczki, and one of the elements of this meta-analysis was a surgical arm, if you will, although it wasn't really an arm since it's not a study, but they describe those patients
that were treated surgically. So what did that look like? Well in this meta-analysis they found that open surgical approach was associated with resolution of symptoms in the majority of patients, there were very few complications,
no renal failure or mortality, few postoperative complications in this manuscript as well as in our experience. By far (mumbles) the most common postoperative complications are ileus and hematoma, and freedom from re-intervention was fairly good.
75% at a year and 70% at 12 months. So with regard to surgery, I think the selection of the surgical approach needs to based on the patient anatomy and the patient clinical characteristics. Ideally, master all techniques
so you can offer all of them to the patient. I'd like to highlight my favorite operation for this condition which is gonadal vein transposition. I'll go over how to do it in just a moment, but the idea is that you transect the gonadal vein. You mobilize it completely from
the pelvis to the left renal vein, and you transpose it onto the inferior vena cava, and this both achieves a decrease in pelvic hypertension and it decompresses the left renal vein beautifully but doesn't put the left renal vein itself at risk for thrombosis.
It also, which is important in young people, does not require a great saphenous vein harvest which sometimes may be necessary in certain versions of the left renal vein transposition. So here's the technique. You make a mini-laparotomy,
do standard retroperitoneal exposure, mobilize the gonadal vein, and implant it onto the IVC. Here is a case of posterior nutcracker syndrome. You can see that renal vein transposition would be really hard here. There's the gonadal vein.
This patient was successfully treated, and then another patient with atypical anatomy who was successfully treated with a right gonadal vein transposition, and we actually wrote this up in case reports. So lastly, I just wanted to quickly review our experience.
We've done 15 gonadal vein transpositions. We've had excellent success, 100% technical and 93% clinical. The caveat with that is we have a really short follow-up, so it's hard to say yet whether we'll have the problems with clinical recurrence and restenosis.
So in summary, I think we are waiting a good renal stent, but gonadal vein transposition currently, I think if it's a large gonadal vein, is the treatment of choice if you're going to go this surgical route. Thank you.
- This, yeah, I'm not quite sure why I seem to always get this talk. Maybe its because I do have more screw-ups or just show them in a more ridiculous fashion. There's no significant disclosures relative to this, apart from the fact that I'm seriously embarrassed. I'm actually not going to talk about stent migration,
because in the last year or two there's an absolute epidemic of stents being reported in the right atrium, pulmonary artery, floating in the IVC. In one state alone, there's been a 10,000, sorry 1,000% increase in the amount of venous stents placed in the past year,
or past two years. So that is somewhat worrying to me. I'm frankly amazed when iliac stents migrate and I'm always amazed when renal stents don't migrate. And there's a nice image of an echo of, I think that's a wall stent in the right atrium.
That heart doesn't look so good. And here's one being fished out very cleverly out of a pulmonary artery. How they ever got there is kind of amazing. I think patients either with no stenosis or totally mis-sized stents were being used.
No, I'm going to talk about something even worse, and that is, not worse in terms of patient outcome, but it is more embarrassing. So typical patient that we see who was managed conservatively with an iliofemoral deep vein thrombosis and presented about nine months later
with weight gain, venous claudication for which we have no objective measure. But no ulcers and no visible post-thrombotic syndrome. And for reasons that known only to myself and I don't know why I did it, I decided to go up and over from the right groin to try and cross
this left iliofemoral venous obstruction. And I'm not sure how well it projects, but essentially we're getting a TriForce Cook device and a roadrunner wire down here, and in due course we crossed the lesion, and we did a videogram And that looks pretty good.
And so we go on, pardon me, I'll try and go on. And this is a venogram from an oblique view. And again, nothing difficult about this. This is all fairly straightforward. We do a balloon dilatation and there is our final completion stent.
And I'm feeling fairly good. She was feeling quite uncomfortable because the urethral catheter we had difficulty getting in and it's possibly a little bit not concentrating hard enough on that. And so I saw the next day as per standard practice
and was doing my ultrasound. But her leg clinically hadn't improved much at all. And I was, I just wasn't happy with the ultrasound. There wasn't, I couldn't figure out exactly what was wrong. There was certainly flow in the stents and there was flow below.
But it just didn't look right. So I did a CT and admittedly there is a radiation cost here, but just we'll have a little look at this and, yeah, okay. So we'll look at that again, because it isn't quite humiliating enough the first time around. Let's just concentrate just in here, um, yeah.
This is one of these unusual Irish patients where the femoral vein in fact passes posterior to the inferior pubic ramus, otherwise known as the obturator vein. Somewhat embarrassing, and on a sagittal reformatted, it looks just even that bit better. So, you can see it coming in beautifully,
right out the back here. So she was actually incredibly cool about it, I just said, you know, I've screwed up and we've made a mess here. And that's a single shot of it there. You can see that I've placed it into the obturator vein.
And, so then at that stage I go from above and its partially thrombosed. I puncture from below and get access to the stent. And then you can see here we've gone in the correct access here, through the interstices, and now we have actually a straight shot
and then I'm snaring my wires so you're back to first principles and just do things properly after that. And then ballooning here and now this is the only same time you'll see a bifurcated stent of this fashion. And you can see here that we have eventually good flow
in a correct orientation. I've taken out my little sheath here, so there's a small leak here. This is what cone-beam CT looks like. You've got a double stent system here, which then splits right there into the occluded obturator
and the patient common femoral. And she's actually done very, very well since that time. And this her own follow-up and you can see the stent is widely patent. So, although the stent didn't get away, it certainly was misplaced.
Lessons for me, trust your gut. If you think there's something wrong, there is usually is. And I remember Mike Dick years and years ago saying, "Just sit down, take off all your leads, and go into your room, and just think for a few minutes,
before you do the next step." And I wish I had done that at the time. Thank you very much.
- Thanks very much Ali, and good morning. Kommerell was a German radiologist who made the first clinical diagnosis of this lesion in 1936, however, anatomically the existence of this anomalous right subclavian artery was first described
in the middle of the 1700s. One can see in some cases where these lesions attain a very large size why as they course behind the esophagus swallowing difficulties can be a prominent clinical symptom. The abnormal course of this vessel
is behind the esophagus in the vast majority, about 80%. Between the trachea and the esophagus, in 15%, and in front of the trachea occasionally, 5%. The diverticulum is a remnant of the embryonic dorsal aorta and it is always, by definition, associated with an aberrant subclavian artery.
One cannot exist with the other. To take home this is the easiest, best way to remember on these things. There are essentially two types of comorals. K type one is the one associated with a normal anatomy, aortic arch but an anomalous,
a bearing right subclavian artery. In the endovascular era it is relatively straightforward to treat this. As you can see they are excluding from within the aorta with an endograft and closing off the subclavian artery
beyond the diverticular, either surgically or endovascularly. A new iteration that is quite interesting to me, and we've had an opportunity to use it once, is Mario Lachat's periscope technique that actually can be used very well anatomically
from a transfemoral approach as you can see for this configuration. Comoral type two is a different animal altogether. Associated with a totally abnormal anomalous aortic arch anatomy, so-called right-sided, or right side aortic arch.
More rare certainly than the type one. And this is complex of course, but it is a type two, right-sided arch that we see with certain regularity than the one that we are talking about and usually associated with the comorals diverticulum
associated with a bearing left subclavian artery in such a case. It is amazing that almost every time we have seen a case like this the anatomy is essentially identical. This is the configuration that we see
on a regular basis. We had an opportunity to treat about seven such cases between the two in the last decade. And this is a good case in point, a patient presenting with a very large comoral type two. A cardiothoracic surgeon had attempted to approach this
from a right thoracotomy approach six months previously. Not clear what his thinking had been but thank goodness he bailed out before doing too much damage or killing the patient. He recovered from that.
We treated him. Here's the anatomy by the way which again is extremely consistent in everyone of these cases. Almost always almost identical to what you see there. K type two.
We treated this in a staged fashion. One of the main difficulties in dealing with this endovascularly is that invariably the aortic arch is sharply angulated so navigating and deploying things across that anatomy can be difficult,
- Continuing along this theme of kind of show and tell, we're going to to talk about some options for flap management in infrarenal aneurysms following dissection. So this is a patient who presented to us with modest-sized abdominal aortic aneurysm but large iliac aneurysms, no prior repair, with a Type B dissection of unknown duration.
He's only in his mid-50s. Had a large but not aneurysmal descending thoracic aorta. Common and internal iliac artery aneurysms bilaterally, almost five centimeters. And so the question is, since the dissection went all through the aneurysm zone
what was the best way to manage this? So, we describe this technique of percutaneous endovascular septotomy. Where we get to access to true and false lumens from below, as well as arm access. Confirm we're in the true lumen,
use a Chiba needle to cross the dissection flap, with an 014 wire, snare it on the false lumen, so we now have an 014 wire going across the fenestration true to false lumen. We can now create a single lumen in the infrarenal abdominal aorta
by essentially tearing the dissection flap down to the bifurcation, call this Endoluminal septotomy. We can then deploy a unibody bifurcation device, in this case Endologix. Put in a large Gore cTAG cuff proximally,
to get proximal seal, put parallel grafts in the hypogastric arteries bilaterally, to maintain bilateral internal iliac artery aneurysm flow. There's your completion aortogram, six months CT scan, and at two years we continue to have stable proximal thoracic aorta, stable diameter at the supraceliac segment.
And a single lumen infrarenal abdominal aorta, with good proximal seal. And patency in the internal iliac arteries bilaterally. So this is just one patient, we described a similar patient previously in a case report in Annals of Vascular Surgery.
More recently, now we've reported a small series of these patients. We've had good results with these procedures, other people have reported complications. One of the issues that can occur is when the septum comes down like that,
it can occlude one of the common iliac arteries and cause a mass effect in the distal aorta. It can also damage the aorta. I'm not saying this is the best way to manage all these patients, but, as I said, we now have the series of approximately
half a dozen or so of these patients which have done reasonably well using this technique. What are our alternatives if the flap has been present for a longer period of time and is less likely to be amenable to this septotomy technique?
So in this case this patient had a proximal aneurysm repaired 15 years ago, after a Type B dissection, and now has progressive aneurysmal dilatation of the infrarenal aorta, with the now 15-year-old septum in that area, which we thought would not be amenable
to endoluminal septotomy. So we tried a different approach for this particular patient. In this case we get access to the true lumen, we deploy the device in the true lumen. You can see the device is almost
completely non-deployed distally because of the very little space there. So if you come up and over you can then, after a few attempts, catheterize the contralateral limb. You can then expand that distal aorta
with kissing balloon techniques. You now have room to deploy your distal limbs. That actually worked out okay distally, where we now have access to both common iliacs, below the level of the section with good profusion, but obviously a massive Type 1 endoleak here
where we're still limited by the dissection flap. So we tried ballooning that several times with a Coda balloon, which only made it slightly smaller but wasn't able to completely resolve the problem. And so the solution to this is start using endoanchors
in the area where you have good fixation around the graft to the true lumen. And as you get around the false lumen side, is you gradually deploy these endoanchors as you go around the circumference, you can eliminate that false lumen.
So we can get a 30-day CT scan which now shows no residual Type 1A endoleak, good apposition there, and good distal fixation there. So obviously for some of these patients open repair is going to be the best solution, but for both acute and chronic dissections
there are endovascular options which allow for appropriate management. The variables to be considered are duration, location, the presence of prior interventions, bi-directional access from arm and femoral areas obviously important.
To summarize you can either tear or compress the flap to create a single proximal lumen in the infrarenal aorta. And as I mentioned we've had good results in a small number of selected patients. Thank you very much for your attention.
- I like this title because I do think this is probably the final study we're going to see on a large scale for pharmacomechanical thrombectomy and catheter-directed thrombolysis for acute DVT treatment. These are my disclosures. So, the CaVenT trial came on the heels
of a number of smaller single center series and sort of case studies on catheter-directed thrombolysis. And of course this was a randomized study in 24 different Norway hospitals that showed a patency advantage and a reduction in PTS on both early and late term, even out to five years
in patients treated with catheter-directed thrombolysis rather than anticoagulation alone. The ATTRACT trial of course is the follow up to this study in a sense, it was a large US trial, an NIH-funded multicenter trial that used a strategy of thrombus removal with
adjunctive catheter-directed thrombolysis for acute DVT and essentially this accrued over 50 or so hospitals throughout the US. Using either pharmacomechanical thrombectomy and/or catheter-directed thrombolysis versus standard treatment of anticoagulation.
Enrollment completed in 2014 was presented at SIR and has been published in a New England Journal article I show there. Inclusion criteria essentially involved acute DVT's defined as symptomatic DVT of less than 14, or less than or equal to 14 days duration
including the femoropopliteal and iliofemoral segment and I think that's kind of important, these two locations, so you could have isolated femoropopliteal disease. Randomization was a one to one between anticoagulation versus pharmacomechanical thrombectomy plus anticoagulation
and the analysis was stratified by plus or minus common femoral involvement. So you could have a group stratified to no iliac and no common femoral involvement. The PMT treatment was basically infusion first for IVC or popliteal vein thrombosis,
but everything else was treated with an attempt at single session pharmacomechanical thrombectomy followed by lytic therapy if needed to clear residual thrombus for up to 24 hours with adjunctive measures afterward including stunting, et cetera.
No IVIS imaging or any of that was prescribed. These are the primary efficacy and secondary efficacy endpoints, and these are important, I think, because it effects the outcome of our perception of the results of this trial. The primary efficacy endpoint was a binary presence of PTS
at any time point between six and 24 months. Defined as Villalta score of greater than five or a venous ulcer. Whereas secondary endpoints were not binary so much, but continuous, so severity of PTS, proportion of patients with moderate to severe, et cetera.
And then of course there are some quality of life measures, as well as symptoms: leg pain and leg size. These are the primary safety endpoints, primarily episodes of, issues of bleeding, recurrent thromboembolism, and death. So looking at the sort of meat of the study,
or the primary efficacy endpoint, this was considered a negative trial in the sense that this primary endpoint of reduction of the incidents of PTS did not occur in those patients undergoing pharmacomechanical thrombectomy or thrombolysis, and so there's no difference
between these two groups in this regard. On an other hand, there was an unfortunate increase in bleeding risk, both early on as well as any bleeding. So early major bleeding, and any bleeding within the first ten days.
So this was a finding that lead to, or, these two findings lead to the conclusion in the paper, that among patients with acute proximal deep-vein thrombosis, the additional pharmacomechanical catheter-directed thrombolysis to anticoagulation did not result in a lower risk of post-thrombotic syndrome.
And did in fact lead to higher bleeding rates. So this is real and true, but looking deeper into the study, I would say that there are some other important secondary efficacy endpoints, and if you look at this, you see that along the continuous variables, and if you look at severity of PTS,
this was favored in the more aggressively treated arm across all time points. And so, if we're looking at degree of PTS, I think there's quite a difference. It's also true that there was a difference in leg pain severity, so subjective reporting of
pain as well as the actual index limb circumference. If you look at some other secondary endpoints, even though there was no difference in the binary metric of any PTS, across all-comers, if you looked at moderate to severe PTS, there was a significant difference, and this seemed to be more true in the patient
with the proximal iliofemoral DVT, rather than those patients with simply femoropopliteal DVT. So I think there are a lot of criticisms of the ATTRACT trial that we've probably heard and discussed. Large selection bias, large number of patients screened for those who were randomized, devices changed
over the course of time, no IVIS in the protocol, no patency assessment in majority of subjects, and probably the biggest issue is inclusion of femoropopliteal DVT, which is done largely to drive enrollment. And I would argue these issues are common to all
randomized trials, randomized trials do strike a balance between broad applicability to different patient populations while trying to still answer specific questions that are manageable. And so I think these are reasons why we have to look deeper into the trial results with some of the secondary endpoints,
rather than just focusing on that major headline. So I would say that in terms of lessons learned, the ATTRACT trial does confirm that this aggressive strategy of thrombus removal may not be appropriate for all patients with iliofemoral and femoropopliteal DVT
in part because of this increased risk of bleeding. I think this something that we know, and ATTRACT has confirmed that. Finally, this bleeding risk is extraordinarily low overall, so that makes me believe there are some patients who very much warrant it due to their symptoms
and their active status. And I do think it did show that the results in less severe PTS in those patients treated with aggressive strategies of thrombus removal. So this is what we want to avoid, a patient like this, who is very symptomatic,
very young, and very active, who has never had any discussion of thrombolytic therapy offered to him, and then referred only three months later or six months later, when there's really not as much we can do about that patient. So it's in conclusion the ATTRACT trial was well-designed
and rigorous with broad clinical scope. It confirms that decision to offer aggressive strategies of thrombus removal continue to require us to make artful clinical decisions in a patient specific manner. And I think it does illustrate that a certain subset of patients,
especially those younger active patients, probably do warrant thrombolytic therapy, thanks.
- My disclosures are not relevant. Joe showed this slide, this is the original SVS guidelines, which really, as he mentioned, is a lesion-based evaluation of what the trauma looks like. And, for the purposes of this discussion, we'll be focusing on grade three injuries. Which really means there's blood outside the aortic wall.
There is loss of integrity of all layers and there's a pseudoaneurysm. We've all transitioned to delayed TEVAR for grade one and two. But, what do we do with these grade three injuries? Where's the boundary between medical therapy
that puts the patient at risk of interval rupture and early repair? Which may, as I'll show, put them at risk of other problems. This is a pretty widely adopted prac the idea of treating traumatic pseudoaneurysms,
at least initially, with some medical therapy. This is a review of 18 studies, almost 1,000 patients. It showed really one in five were managed non-operatively. There is a very low rate of aorta-related mortality which will be a recurring theme on all the data I show you. And, there's a really low rate
of required late interventions. As true for many of our trauma-related literature, there's a really poor long-term follow-up rate. The AAST studies have shown us that delayed repair really can improve outcomes. There's a significant selection bias in
these are non-randomized trials for, I think, exclusively. But the reality is, if a patient can wait until stabilization of their other injuries, they do better if you can wait on repairing the aorta, both mortality and the paraplegia rates are lower.
But, it's not just completely a selection bias. There are maybe some other benefit here. And, one of the things that plays into play is: What are their other injuries like? What is their traumatic brain injury look like? And, we use this as a defining point at Grady
about figuring out whether someone really should be figured for early repair or not. If you look at this series of 300 patients with traumatic aortic injury, 248 had a concomitant brain injury, and those are obviously of a variety of different grades,
from a little blip on the CT scan to a potentially devastating neurologic insult. But, it's not uncommon to have to manage both injuries at the same time. That is the rule rather than the exception. They can be pretty significant
and, again, there's significant selection bias in this series out of Maryland. But, there's about a one third, one third, one third early repair, delayed repair or non-operative strategy. If you look at the non-op patients and the delayed patients, you can see
that we get to that very, very low mortality rate. The early repair patients, as you can imagine, are often associated with a fatal outcome. Now, that fatal outcome is not always a it is usually related to something else
and highlights the selection bias of series like this one, that show us that if you're sick when you come in with an aortic tear, you're going to continue to be sick regardless of whether we fix your tear or not. But, there is some other benefit, potentially. The traumatic brain injury is one piece that I've mentioned,
but it's not uncommon, I think we've all experienced situations like this where the trauma physician and the orthopedic physician and everyone who is taking care of these patients is really focused on a grade three aortic injury. And, it oftentimes allows for neglect
or missing of other injuries that may be more life-threatening. How do we avoid delay? There's a few areas where we can think about intervening. The first thing is getting a good radiographic grade, as Joe alluded to, and there's a variety
of different scoring systems. This ultimately amounts to a simplification of the Harborview scoring system which is the one that I personally have gravitated to over the last two years. Which demonstrates that for the old grade one and two
there is probably no benefit of repeat imaging, there is probably no benefit of intervention, and pseudoaneurysms should be fixed when they are stable and severe ongoing-rupture patients should be fixed right away. That assessment of stability is an important part of this.
Part of Dr. Crawford's interest, in particular, was evaluating the size of the pseudoaneurysm and the size of the hematoma. And so, all of these are things that we've seen before but they all probably behave a little bit differently. So, how do we look and see:
Are there specific types of injury that are more prone to rupture with non-operative therapy? And one of the things that's been assessed is the diameter ratio. I think Joe showed this data a second ago. Another is the size of the periaortic hematoma.
In this large series, if you had two of these three factors: a lactate greater than four, a mediastinal hematoma greater than 10 millimeters or a lesion to normal aortic ratio of greater than 1.4. That was 90% accurate in terms of theoretically predicting early rupture.
Which, if you just look at clinical judgment alone, goes down to 65%. Keeping in mind that clinical rupture, true rupture is very often a fatal event. There is a lot of value in moving that number from 65 to 90. If we can get good modeling that tells us
who is at particularly high risk of rupture in this selected group, there is a lot of potential benefit. Just as importantly, as I've mentioned earlier, if you have a higher aortic grade of injury, you are more likely to die but it does not predict aorta-related mortality.
Much of that is the selection bias that people with higher grades of aortic injury are fixed sooner and therefore are not candidates to die from aorta-related mortality. Let's skip through this. And then again, (audience member coughing)
the idea that we need additional information and we need better imaging, better physiologic data that predicts the need for early repair is the take-home message. The answer, as you can imagine, is more information. Part of what the Aortic Trauma Foundation is doing
is going to be evaluating: Are patients really going to do better with non-operative therapy if they have very specific criteria that allows them to be selected out? Are there high-risk criteria that we can figure out besides just eyeballing the CT scan and saying:
This is someone who's not going to do well if we sit on them. Thank you very much.
- Good afternoon. So as we've already heard, traumatic injuries are the leading cause of death and disability in children over the age of one. Fortunately, these types of injuries are relatively infrequent, most commonly involving the lower extremities, for example femur fractures,
causing disruption of the SFA or popliteal artery, or the upper extremities, supracondylar humeral fractures will cause damage to the axial or to the brachial artery. Retrospective review of a children's registry from 1993-2005 with 103 patients all of whom were under the age of 18, most were males.
The majority are penetrating wounds. And most frequently, the extremities were involved. Open surgical repair was favored, primary repair when possible, vein patches for use for those under the age of six, and an interposition graft or bypass was used
for those over the age of 12. Non-operative management was selectively chosen in about 10%, and the outcome in this cohort, 10% mortality, 11 amputations, and limb length discrepancy did become a problem over time, necessitating revascularization in 23%.
A nationwide Swedish registry from 1987-2013 looked at 222 patients, children under 15. In this scenario, 2/3 were male, 2/3 had blunt trauma. Once again, upper extremity injuries were more commonly seen in those under 10. Lower extremity injuries more frequently seen
in those between the ages of 11-15. With that cohort that we talked about, 96% were treated with open surgical repair, similar to what we saw before. Interposition grafts, vein patches for the young, and primary repair whenever possible. However, endo therapy was introduced in this scenario,
with eight patients undergoing intervention for axillary, subclavian artery, iliac, and aortic trauma. A summary of four large series was pooled here, and essentially shows you once again the majority of the injuries are in the extremities. The gold standard to date remains open surgical repair,
either with patch, endo anastomosis, or interposition graft, depending on the age and the location. Lajoie presented this abstract, which is a single center retrospective review, nine years, 60 patients, all under the age of 18. And once again with vascular trauma pediatric group,
majority of treatment is with open, however 16% underwent endovascular intervention with embolization, stents, and stent grafts utilized. None of the stents were implanted in anyone under the age of 13. Follow-up six weeks showed no difference
in the amputation rates or the mortality rates, however reinterventions were certainly higher in those who underwent endovascular therapy. National Trauma Databank from 2007-14 of pediatric trauma under the age of 16. 35,000, so it's a very large cohort.
And you're going to see here, it's not just a trend. This was statistically significant. There is an increase endovascular therapy utilization across the board in that time frame, and specifically for blunt trauma, increasing from 5.8% up to 15.7%.
And what you can take away from this is that the increased endovascular therapy was utilized in children over 12, larger hospitals, level one trauma centers, and those who resided in northeast. In addition to that, those who had a higher
injury severity score also underwent endovascular therapy. The most common procedures, embolization of the internal iliac, and TEVAR for blunt aortic trauma. Unfortunately, despite this, the in-hospital survival failed to improve.
So now there's a plethora of data out there, and multiple single-site institutional reviews of their own experience. Here's what I can say. I think there are some select indications for which endovascular therapy appears to be advantageous.
Without question, as you've heard already, the blunt thoracic aortic trauma. Here's a 17-year-old, fell from a seven-story building and successfully underwent endovascular intervention. Another case, a 16-year-old gunshot wound to the thigh, injury to the profunda femoris was a large
false aneurysm in the anteromedial thigh, who underwent coil embolization successful exclusion of this area where the pseudoaneurysm happened to be, but maintained perfusion through the SFA and the remaining branches of the profunda. Is there a role here for blunt femoral trauma in the child?
Well, I'm not a big fan of it, doing it in adults, but there is a paper on it. 13-year-old popliteal artery trauma, high ISS score, this occlusion was recanalized and a self-expanding stent placed. And I will note that a bridging technique was utilized.
Once the other injuries were addressed, the patient underwent bypass. 12-year-old with polytrauma, iatrogenic orthopedic screw injury to the SFA, successfully treated with a Jomed stent, and then planned bridging procedure,
who underwent open repair a few days later with an interposition vein graft from the contralateral leg. One more case, 14-year-old polytrauma, self-expanding covered stent placed for an axillary artery injury, and this was a planned procedure as a bridging technique. He, unfortunately expired prior to that opportunity
to perform the bridging technique on him with a bypass. So, in summary, I do think pediatric vascular injuries are uncommon. Open repair, once again, remains the gold standard. Endovascular therapy appears to be increasing, especially TEVAR and embolization.
Endovascular therapy in the extremities is an option as a bridge in older people over 12 who have higher ISS scores. And a nationwide pediatric database for arterial trauma would be beneficial. Thank you.
- Thanks, so we've talked about open techniques, and as Marsham mentioned, wouldn't it be nice if we could develop some type of endovascular valve replacement or any reflux procedure. There are a subset of patients that require this, as we get out in these more severe disease severity, is when start seeing more
of a higher prevalence of deep venous incompetence. This tends to be a mix of primary deep venous incompetence and post-thrombotic, which also gives you a mix of the pathology of reflux and obstruction along the axial vein tree. And really, it's to find the most critical
site of disease for repair. As you've heard, the open surgical techniques have been the mainstay now, conservative would be compression, and we're now going to talk about implantable valves. Kistner, as we know, has been the father of this,
and really, his concept has been that in the deep axial system, that we have the, really, the external iliac, 25% percent of the time, has one valve. But, in general, the iliac system is valveless. But, we're choosing the common femoral vein,
the femoral vein profunda, or popliteal, that we need one competent valve somewhere along those axial segments to get the control of venous hypertension. That's really the goal. We've heard about external repair, or reefing,
that's available if the valve is intact. However, if the valve is not intact, and destroyed, then you need to bring in a new valve, either transplanted from the axillary, or transposing from good valve, to an axial segment. And really, this has been the data with open repair.
Yes, you can get ulcer healing, but there's a pretty rapid fall off at about three to five years with all these open techniques, with valve fatigue, or scarring, or enamel hyperplasia, or thrombosis. This is really, so Dusan Pavcnik at Dotter Institute
in Oregon, has been working on this for a while, the bioprosthetic valve. The first-generation, he was using sub intestinal submucosa, which basically gave you a collagen skeleton, with growth factors sewn onto a metal frame.
And then that gets implanted, and the idea was that hopefully, it'll repopulate with endothelial cells and mimic a human valve. The problem with this one was mostly tilting of the frame in vivo.
And this is kind of what it looks like, developed, delivered through its delivery system. The second-generation valve, they worked more on the frame, and still, you know, with a prosthetic in here, you do see good incorporation of the bioprosthetic valve in a vein wall with population of endothelial cells.
They've also looked at transplanting native valve to native valve on a frame, so using jugular of one side, taking it out, sewing it onto a frame, and placing it on the other side in sheep.
And that was mixed with a variety of problems, as always enamel hypoplasia and thrombosis are the main two actors that cause these to fail. Then the last thing that I've seen, that I haven't seen any results on, was this idea of the autologous endothelial monolayer
on a valve, which, when you then put it in the circulation, then you've got flow conditions, and then you worry about the sheer and the flow disrupting the populated cells from the valve. So, I asked Tim Liem, who's,
whom you've met earlier, he's out there in Oregon, and knows the Dotter institute, and I wanted to see the fate of these valves that we just talked about, with autologous, and they've implanted some in Korea and Europe. They lasted for about three months
and they all go on to fibrose or thrombose. So, it's been a challenge with the autologous valves. We've heard about neovalves already, which again is open monocusp, and now there's an endovascular system under development, where they use
intra-vasc or ultrasound mounted on a catheter, a blade, and a balloon, to create an endovascular monocusp valve. So, that's been under development for a while. But, in conclusion, a percutaneous valve is an unmet need in a small subset of patients
who come to us with wide open deep venous incompetence, ulceration, and a miserable quality of life, and currently there's not a great option, except for open surgery, which doesn't last more than five years or so. Thank you.
- I've got the privilege of trying to discuss some of our more interesting complications that we see. These are my disclosures. Obviously, renal salvage has changed in the way we look at it. Originally, when a renal graft occluded, we thought we had one to two hours of warm ischemia time
before it was irreversibly ischemic. We've now seen some reports of salvage going out for hours to even months, and with endovascular techniques such as thrombectomy, angioplasty, stenting, and if necessary, bypass, we've found that we have been able to go on and
actually create salvage in longstanding renal occlusions. This is a retrospective review over the last six years. We had eight patients that were referred to us or were presented to us with renal artery thrombosis or occlusion. Four were after complex endovascular repair
with parallel grafts or chimneys or fenestrations, and two were standard EVARs, mainly with cuffs or with anchoring devices. One thing we found is that, as part of this review, we always tried to identify that there was in fact the preservation of renal function,
even though many of these patients were on dialysis, so we had either a renal duplex showing arterial flow, the renal CT scan showing uptake of contrast, or a split-function renal perfusion scan, showing uptake in the affected renal artery or renal parenchyma. Renal duplex was our mainstay.
We did identify not only the presence of flow within the renal parenchyma, but also get an idea of renal size, and then is there an active arterial flow within the renal artery itself. So here are the eight patients,
four males, four females, mean age was around 82. Follow-up was over almost three years now with these patients. Mean duration of ischemia was right around two months going up to three months, prior to actually undergoing intervention.
Four of these eight patients were actually on hemodialysis already. Of that, three of the four patients, we actually got off hemodialysis. Pre-operative, pre-intervention creatinine was 3.6, went down to 1.2 in post-intervention.
So, four had thrombolysis and new stent placement, three had angioplasty and stenting, these were mainly those that were covered, and one patient did undergo iliorenal bypass. Here's how those eight patients broke out, with a stent occlusion generally kinking and then crush,
or coverage with aortic cuffs, and I'll try and walk through two of these case presentations for you. The first patient presented was actually my patient, and I put one of my first pivot-graft fenestrated aortic stent-grafts in.
He was 63 years of age, did quite well, and then presented in his follow-up with a five day history of left flank pain. Unfortunately this was during Hurricane Sandy, so he was received in an outside facility, and once we were actually able to get transport available,
he was sent to our institution. He had a total ischemia time of 14 days. As shown in this angio here, he had kinking of his renal stent, as you can see right here as the stent comes out, and then we did not put enough
of a flexible stent going down, and that led to occlusion of the renal artery. Here's a nice CT representation of that renal kink at the distal aspect of the stent. This was with an iCast stent. We then went in and gave tPA, actually
Angiojet thrombectomy, angioplasty and stent extenstion. So here, you can see the thrombus that was in the... Once we actually catheterized the stent, we came in and there's the clot that we saw with the tPA. We then did Angiojet, and actually were able to get flow. Later on we were actually as stable as more cortical flow.
And then follow-up, we actually show persistent perfusion in this, and this has now gone out to about four years. Second patient was seen in an outside hospital. She'd had a left nephrectomy due to cancer, prior to her presentation underwent aortic endograft, and they inadvertently covered her right renal artery,
and since she had a left nephrectomy, she became anuric, went on hemodialysis, and presented to us about a month and a half, referred by a nephrologist who had gotten another one of his patients off dialysis, and sent her to, now with a creatinine of eight on dialysis. And here you can see, I think this is where we saw
the mistake of the interventionist. When they put the stent-graft in, they'd mistaken the hypatic artery for the lone renal artery, and so they ended up covering that renal artery. There's a small perfusion slit there. Duplex still showed that we had a 12 cm plus kidney
with patent renal flow, and so we were able to come in, we had to work with reverse-curve wire and get a wire into that renal artery, angiogram, balloon and stent it and maintained preservation. Finally, we were coming through, we had left brachial access for another patient with renal occlusion, here coming in.
And again, showing a very small renal artery here, getting behind it, short renal stump, but able to stent and reestablish flow and perfusion. And now that patient's doing well and is off dialysis with a creatinine of one. And there's the CTA showing excellent flow
to that right kidney. And in conclusion, renal preservation is possible, even when you have prolonged ischemia going into term of months, provided you document there's still perfusion of the kidney itself. And I think with endovascular techniques,
we can salvage in some of these patients, and they don't want to give up on these occluded stents or covered stent renals during endovascular repair. Thank you very much for your attention.
- I don't know whether I am supposed to be the judge here in this debate, because our paper was quoted by both discussants. (laughing) I have no disclosures. Oh sorry, that was one too fast. We have heard this morning about
arterial reinterventions after EVAR. They are of great concern, and we have focused during the last decade very much on the top stent and the neck of the aneurysm, but very little has actually been paid attention to the distal landing zone.
And about 20% of the patients having an EVAR for AAA do also have an aneurysm of their common iliac artery, if we use the definition 16mm as an areasmatic. But having said that, we know that up to 25mm diameter of common iliac arteries can be treated with flared limbs. So the question is, whether you have a patient with
a common iliac artery of 16-25mm, whether you're going to give him a flared limb or if you're going to use an IBD. So, we looked at our patients having had a standard EVAR, and we looked at the rate of type 1b endoleak, and we divided the patients into two groups,
those having iliac limbs larger than 20mm and those having iliac limbs smaller than 20mm in diameter. It is a retrospective analysis between the years 2006-12 and the endpoint was, as I've said, type 1b endoleak. Now in order to be able to study this in a proper way, we wanted to have available size information
on the iliac stent grafts, and we also needed to have a three year follow-up at least of a CT scan of the treated aneurysm. So, if you look at the top, we have 692 limbs, and then we go to the bottom right and then you will see that we could investigate 239 limbs altogether.
So that's about 1/3. Out of those 239 limbs, 178 had a stent graft limb that was smaller than 20mm, and in 61 patients or limbs it was larger than 20mm. This is just to show you that we used all different kinds of stent grafts, but mainly Cook Zenith device,
the Gore Excluder, and the Vascutek Anaconda. So, now to the results of the measurements. The preoperative diameter of the distal common iliac artery was 14.5mm and the used stent graft limb was in mean 17mm. Which means that we had a mean oversize for the iliac limb of almost 18%.
During follow-up there was no immediate post-operative type 1b endoleak at the first CT scan being performed before discharge. And then we had mean CT follow-up of about 53 months. There was over this time a 7.5% type 1b endoleak overall, and that appeared after three years, and the mean oversize
in that group who had an endoleak was 12.5%. And this is the summary of the results, where you can see that the rate of type1b endoleak in those limbs that were smaller than 20mm, was close to 4%. And it was 4 times higher in the group
with a limb larger than 20mm. And this was highly statistically significant. And this is just a graphical view of what I just said. Four of the included patients died during follow-up. There were two ruptures due to type 1 endoleak, and one patient died.
So in conclusion, Mr Chairman, ladies and gentlemen, EVAR with flared limbs has a significantly higher risk for type 1b endoleak in a long-term follow-up. And follow-up is therefore mandatory, and I wanted to consider whether if an IBD should be used in common iliac arteries that are larger
than 16 or 18mm in diameter. Thank you very much for your attention.
- I have no disclosures. So I'm going to show you some pictures. Which of the following patients has median arcuate ligament syndrome? A, B, C, D, or E? Obviously the answer is none of these people.
They have compression of their celiac axis, none of them had any symptoms. And these are found, incidentally, on a substantial fraction of CT scans. So just for terminology, you could call it celiac compression
if it's an anatomic finding. You really should reserve median arcuate ligament syndrome for patients who have a symptom complex, which ideally would be post-prandial pain with some weight loss. But that's only I think a fraction of these patients.
Because most of them have sort of non-specific symptoms. So I'm going to say five things. One, compression of the celiac artery is irrelevant in most patients. It's been found in up to 1/3 of autopsies, MRIs, diagnostic angiography, CT.
This is probably about par, somewhere in that 5% or 10% of CT scans that are in asymptomatic patients will have some compression of the celiac axis. The symptoms associated with median arcuate ligament syndrome are non-specific,
and are really not going to tell you whether patients have the disease or not. So for instance, if you look here's like 400 CT scans, 19 of these patients had celiac compression. But the symptom complex in patients
who had abdominal pain for other reasons looked exactly the same as it did for people who had celiac compression. So symptoms isn't going to pull this apart. So you wind up with this kind of weird melange of neurogenic, vascular,
and you got to add a little psychogenic component. Because if any of you have taken care of these people, know that there's a supertentorial override that's pretty dramatic, I think, in some fraction of these people. So if you're not dizzy yet, the third thing I would say,
symptom relief is not predicted by the severity of post-operative celiac stenosis. And that's a little distressing for us as vascular surgeons, because we think this must be a vascular disease, it's a stenotic vessel. But it really hasn't turned out that way, I don't think.
There's several papers, Patel has one just in JVS this month. Had about a 66% success rate, and the success did not correlate with post-op celiac stenosis. And here's a bigger one,
again in Annals of Vascular Surgery a couple years ago. And they looked at pre- and post-op inspiratory and expiratory duplex ultrasound. And basically most patients got better, they had an 85% success rate. But they had patients,
six of seven who had persistent stenosis, and five of 39 who didn't have any symptoms despite improved celiac flow. So just look at this picture. So this is a bunch of patients before operation and after operation,
it's their celiac velocity. And you can see on average, their velocity went down after you release the celiac, the median arcuate ligament. But now here's six, seven patients here who really were worse
if you looked at celiac velocity post-op, and yet all these people had clinical improvement. So this is just one of these head scratchers in my mind. And it suggests that this is not fundamentally a vascular problem in most patients. It goes without saying that stents are not effective
in the presence of an intact median arcuate ligament. Balloon expandable stents tend to crush, self-expanding stents are prone to fracture. This was actually published, and I don't know if anybody in the audience will take credit for this.
This was just published in October in Vascular Disease Management. It was an ISET online magazine. And this was published as a success after a stent was put in. And you can see the crushed stent
because the patient was asymptomatic down the road. I'm not discouraging people from doing this, I'm just saying I think it's probably not a great anatomic solution. The fifth thing I'd say is that comorbid psychiatric diagnoses are relatively common
in patients with suspected median arcuate ligament syndrome. Chris Skelly over in Chicago, they've done an amazing job of doing a very elaborate psych testing on everybody. And I'll just say that a substantial fraction of these patients have some problems.
So how do you select patients? Well if you had a really classic history, and this is what Linda Riley found 30 years ago in San Francisco. If they had classic post-prandial pain with real weight loss and a little bit older patient group,
those people were the easiest and most likely to have a circulatory problem and get better. There are some provocative tests you can do. And we did a test a few years ago where we put a catheter in the SMA and shoot a vasodilator down,
like papaverine and nitroglycerin. And I've had patients who spontaneously just said, "That's the symptoms I've been having." And a light bulb went off in our head and we thought, well maybe this is actually a way you're stealing from the gastroduodenal collaterals.
And this is inducing gastric ischemia. I think it's still not a bad test to use. An alternative is gastric exercise tonometry, which is just incredibly elaborate. You got to sit on a bicycle, put an NG tube down to measure mucosal pH,
get an A-line in your wrist to check systemic pH, and then ride on a bike for 30 minutes. There's not many people that will actually do this. But it does detect mucosal ischemia. So for the group who has true circulatory deficiency, then this is sort of a way to pick those people up.
If you think it's fundamentally neurogenic, a celiac plexus block may be a good option. Try it and see if they react, if maybe it helps. And the other is to consider a neurologic, I mean psychologic testing. There's one of Tony Sadawa's partners
over at the VA in Washington, has put together a predictive model that uses the velocity in the celiac artery and the patient's age as a kind of predictive factor. And I'll let you look it up in JVS. Oddly enough,
it sort of argues again that this is not a circulatory problem, in that the severity of stenosis is sort of inversely correlated with the likelihood of success. So basically what I do is try to take a history,
look at the CTA, do inspiratory and expiratory duplex scans looking for high velocities. Consider angiography with a vasodilator down the SMA. If you're going to do something, refer it to a laparoscopist. And not all laparoscopists are equal.
That is, when you re-op these people after laparoscopic release, you often times find a lot of residual ligament. And then check post-operative duplex scans, and if they still have persistent symptoms and a high-grade stenosis,
then I would do something endovascular. Thank you.
- [Speaker] I wanted to talk about a specific subset of what we've just been talking about, last we talked, so traumatic aortic injuries. I have no relevant disclosures. As you know, most of these occurred just distal left subclavian, which has a fixation point and then the more mobile distal thoracic aorta,
which leads to the tear with blunt trauma. The purpose what we looked at is the traumatic aortic injuries of the chest that are distal to that first five centimeters by the subclavian. So we looked at our trauma registry for a little over six years and included patients that had
blunt trauma either car crash, motorcycle, pedestrian versus auto or falls. And on their trauma center CTA had evidence of an aortic disruption in adult patients. We did divide the groups based on five centimeter length from the take off of the left subclavian artery.
Measuring the distal point to the left subclavian to the first point of the intimal injury seen on the CTA. We did this measurement on the modified sagittal view of the CTA in order to standardized the measurements. And these were all the CTA's done within the trauma center. We chose this five centimeter length based on
radiologic data from a number of studies, two of which are listed here. That generally show the entry that usually occurs somewhere around 15-16 millimeters from the left subclavian and then all stop before five centimeters or most all stop at four centimeters.
That way we had two separate groups that truly appear to be different, different subsets of the same problem. This is a typical lesion that you would see and most of these were further down from the arch so that was very little trouble separating these two groups.
So we found 74 patients and the total 60 of which were in the usual zone what we call the first five centimeters. And then the interest group what we called the Unusual Site there were 14 patients or 19% of the 74. We looked at a number of characteristics
the first thing that came evident, was that although age and race made little difference, this was a disease that predominated by women. Two thirds of the women with unusual location injuries. Two thirds of the patients with unusual location injuries were women, where the standard for the
usual location was about 75% male. We then looked at the mechanism have a role in this unusual site of injury at car crashes and all the usual mechanisms found no difference in their statistical p value. You saw the age was around 40 median age.
And so we thought maybe preconditions.. Premedical conditions might have a role but that was not found either. Then we looked at basic physiologic characteristics as they came in and they are all listed here. And you can see none of these were statistically different.
You can note that the most of them were slightly tachycardic but as a rule were not hypotensive. We also looked at solid organ entries associated with these unusual unusual location aortic tears. And we found no difference in pulmonary, cardiac, spleen or liver entries.
We did find a difference in looking bony fractures in that we found thoracic spinal fractures were present in 50% of time with these aortic injuries in unusual locations. Which was the only fractures that we found statistically different between the two groups.
Again we used SVS classification and here was a major difference in that the unusual site had 80% were grade one or grade two, and most of them were grade one. Where as the usual location we had over half were grade three so there was a significant difference there.
And that results in a difference in management for 14% of the patients with blunt injuries at the unusual locations actually ended up getting a stent graft, where 66% at the usual location did. And then we have talked about grade two being somewhat arbitrary and judgmental,
we found that none of these patients grade two lesions had unusual side needed a stent graft or it was a side that they didn't need one. Where three out of seven at the usual location did. As far as mortality is concern it was also a higher mortality with the unusual location.
Although the length of stay was less, just possibly the effect of those patients died early on. They did not die though from aortic injury. They died from other cause, particularly traumatic brain injury and then later on in the ICU. So our conclusion are that when you look at these injuries
of the thoracic aorta. We didn't include abdominal. They can be divided into two groups. Those that are within five centimeters and those distally. The unique group tend to be lower grade, they tend to not need intervention,
they do have a worse mortality not related to the injury itself, they are associated with thoracic spinal fractures, and more common in female patients. So I think we need to look at this as two different entities.
- Symptomatic post-thrombotic disease affect at least 30-50% of patients with deep vein thrombosis. Regular wearing of individually selected compression garments with regular follow-up alleviate symptom in many patients. However, compression therapy doesn't eliminate chronic structural post-thrombotic changes,
implies lifelong treatment, ineffective of many cases, and low overall patient compliance remain a serious challenge. Raju S. Et., alia Asia. Percutaneous balloon angioplasty and stenting of iliofemoral venous segment have recently improved
the outcomes for patients with severe PTS, related to venous outflow obstruction. Postinflammatory vein wall remodeling and destruction of the venous value is considered to be the morphological substrate for PTS. Auto transplantation of valve-containing venous segment
demonstrated good five year results of half of patients, 50%. Maletti., Perrin., 10 years ago. However, there is currently low correlation between hemodynamic effect and clinical success of deep vein surgery in published literature.
The main goal of this study is to develop a novel surgical technique on venous neo-valve formation to correct deep axial reflux and improve venous outflow in post-thrombotic disease We perform the first series of in vitro experiments
using methods of mathematical modeling to develop a novel surgical technique on venous neo-valve formation. Five macroscopically intact common femoral veins were taken out autopsies from individuals without history of venous thrombosis.
And five common femoral veins were taken off autopsies from individuals with PTS. It was very difficult. The surgical technique involves complete transection of the common femoral vein, eversion of the proximal end of the vessel
with simultaneous endo-phlebectomy and creation of neo-leaflets from the inverted vein wall by interrupted sutures. Transection of the femoral vein and eversion of the approximal end of the vessel. During mathematical modeling appropriate dimensions
of the neo-valve were determined to resemble morphology of a native valve. An optimal vein wall thickness for neo-leaflets was determined to enable appropriate elasticity and coaptation. The hydraulic probe demonstrated good competency
of the neo-valve at 1.5 atmospheric in vitro. The absence of outflow obstruction was predicted as less than 20% stenosis during the maximal valve leaflets separation. In conclusion: A novel experiment model was autologous deep
venous neo-valve was created and evaluated in vitro. In vivo experiments to evaluate hemodynamic effect, thrombosis risk, and long term hemodynamic effect. Thank you very much.
- Good afternoon. These are my disclosure. We all know that ectatic common iliac arteries especially in presence of an abdominal aortic aneurysm tend to dilate with time. For example, if you look at the yellow line, in a common iliac artery of 20 millimeters
is growing five millimeters in five years. If this is not important in open repair, it's crucial for endovascular repair, because it represents the landing zone of the procedure. We have already that if you look at the patient for 14 months you don't find any degree of dilation
in patients treated with a bell-bottom. Again, we heard about these long-term results, but actually, only eight patients reached the five year follow up in this paper. So time is crucial. And we, now and then, encounter many patients
following them up along their life, that when we land in short, ectatic iliac sealing zones, then we encounter these type one endoleak for migration of the iliac limb inside the angiograft. Recently reviewed our experience of 610 patients, with a mean follow-up of 99 months
and we found that one-fourth of the patients are still alive after 14 years. So you have to afford very long-term good results. And this is only possible if you have trustable sealing zones. If you want to avoid type one endoleaks and rupture
in case of ectatic iliac arteries, you have to follow them all, and you have to be very aggressive in treating the complication. Two months ago we published this paper, presented at the ESVS meeting.
And we divided our cohort of patients in those with an ectatic iliac artery and those with normal iliac arteries. What we found was that the patient with ectatic iliac arteries, of course, were a little bit at higher risk
in terms of heart disease, cerebrovascular disease, and kidney disease. But in the late outcomes of these patient, was found that Type Ib endoleak was much higher than those in patients with normal iliacs. Reintervention rate was also higher.
In terms of overall mortality, patient with the larger iliacs showed worse survival because of their preoperative risk factors. But in terms of EVAR failure, this patient presented lower success if compared to standard common iliac arteries.
And this is also true in terms of overall reintervention. But coming to the iliac related reintervention, patient with ectatic iliac arteries had a three-fold incidence of reinterention at Type I endoleaks in the long run after 99 months. We have also some iliac-graft failure,
defined as iliac-related reintervention, occlusion, related death, or aneurysm rupture. Patient with ectatic iliacs had 14% risk of failure after 11 years, while patient with ectatic iliacs had only 4% risk of failure in the long run. Is it not known?
No, actually, if you look at the St. George Vascular Institute's risk score, the main determinant of failure is the common iliac diameter. And we have already other experiences reporting the same values.
Is it typical from one graft? Not at all. This is a patient with Talent graft in which one limb migrated into the opposite common iliac aneurysm and we were able to treat it with an extension.
But most of the patient getting old, they don't come back for follow up. They don't come back and we can check the position of the iliac limb in the long run. Is there any other alternative? Yes it is.
We now have the iliac branch endografting that showed that after 10 years, the reintervention needed in only 8% of the patients, so we can afford the durable results in patients like this. So in conclusion we can say that iliac arteries
tend to dilate with time, especially if they are ectatic. EVAR are prone to late failure in these cases, so rigid follow-up protocol is needed for this kind of patients. And probably if you want a long-term result,
you have a consider safer landing zone, like iliac branched device. Thank you for your attention.
- So these are my disclosures. So I tried to divide this talk up into four areas that are common that occur in our practice at Mayo. One will cover guidelines. What do the chest guidelines and SIR guidelines show?
And a statement by the AHA, and then patients with PE that are presenting in different phases, and then patients that have a subset of CHF and then obviously special patients such as pulmonary embolectomy.
And so let's talk about the guidelines. And I think it's really important to understand a few factors when you're considering putting filters in. One is obviously the workup of the patient, and what are their anatomical considerations?
Number two the extent of clot burden, and then number three the hemodynamics of the patient for their age and how did they get to you? And then fifth you can look at the guidelines to help you.
So, what is the circumstances that a provoked DVT, unprovoked DVT, with and without malignancy, what is their age? I'm not going to cover that, but that's in the setting of what you should be considering as you think about that.
So these are the guidelines the chest guidelines are on the top, and then the SIR guidelines and there's pretty good uniformity between the two guidelines at least for placement of filters and I've highlighted those.
For example acute proximal DVT if you can't anticoagulate because of risk of bleeding. So that's a 1C recommendation. Part C there is in the treatment of PE acute PE if anticoagulation is not possible because of risk of bleeding.
And then SIR guidelines recommend absolute indication for proven VTE, recurrent VTE despite anticoagulation or contraindication to anticoagulation. So these are really guidelines to help us think about how we would manage these patients
and where we would place filters. And again the other thing that we have to remember is that some of these guidelines were written when we were still doing a fair bit of permanent filters and now with the FDA recommendations
for temporary filters if you put a temporary filter in, or an optional filter you're obligated to schedule the patient for a return to your office to come back for removal. And that creates another set of challenges
for our patient. How do you get em back? How do you schedule em for a return? When do you schedule em for a return? And then obviously does every patient need a filter removal?
Does a 90 year old patient with a optional IVC filter need an aggressive treatment for filter removal than a 50 year old for example. And so these are the guidelines. And these are the relative indications.
If you're not sure, these are sort of on the... Depending on where you're at for example large free-floating proximal DVT ilio clot in transit gets a filter placed as well. So I want to talk about a scientific statement
that Mike, Dr. Jaff co-chaired. And this was a statement from American Heart, and it really also provided some guidelines also for IVC filters in the setting of acute PE, and it listed different scenarios
of when you might place a filter. Adult patients with an acute PE very similar to what the SIR guidelines and AACP were. This was class one level B that could not be contraindicated or anticoagulated
due to excessive bleeding. Number two was anticoagulation should be assumed in patients with an IVC filter once contraindications to anticoagulation or active complications have been resolved. And we're going to talk a little bit about
how they got to this. And then patients who have retrieval filters should be evaluated periodically. That's very important I sort of alluded to this. If you place a filter, you need to somehow have a mechanism in place to bring em back.
In our facility every patient that gets an optional filter placed, has a nurse assigned to making sure once their care has resolved and they're ready for filter removal that they're scheduled for a return with an office visit.
And then number four recurrent acute PE despite therapeutic anticoagulation. It's reasonable to place an IVC filter very similar to the chest guidelines, and I won't repeat the rest. So how did we get here?
So this is the first paper that I'm going to review. This was a clinical trial of permanent filters in patients with proximal DVT. So permanent filter this was 200 patients randomized to permanent filters for preventing clots.
And what this paper showed was that if you had an iliofemoral DVT and a clot and you got a filter, that it put you at a higher risk for filters and really didn't prevent PE. And so this is number one paper that's
very important that we should recognize. So this is again permanent filters four different types of filters that are basically not used that often. One of them is the Bird's Nest. And this was a New England Journal paper
a PREPIC 1 trial, and this is what the age group were and the filters are very well matched. This was the gender as you can see the baseline characteristics very well matched. And this is table two this was the endpoint
within the first 12 days. And if you look at the filter group, you'll see that there was PE: two symptomatic in the filter group, five in the non-filter group P value 0.03, major bleeding was about the same
nine in the filter group versus six. So again, filter plus anticoagulation versus filter alone. And then there's death no difference in death. And so this really helped set the stage in the early or late 90s early 2000s
of how to manage permanent filters. And this is principle endpoints at two-year follow-up in the filter group versus non-filter group. And you can see symptomatic PE no difference. Recurrent DVT there was a difference,
and this sort of changed the way we managed filters and our temporary filters. We used this data set to help us with iliofemoral DVTs for example, and this is major bleeding and death. So again, no difference between
filter and no filter. And this is within 12 days. This is the principle endpoint within first 12 days after randomization. Between Heparin and Unfractionated Heparin because patients were treated with either
of the therapy again showing no difference. And this is the last table from that paper which is endpoints during the two-year follow-up of Low-Molecular Weight Heparin again showing no differences between Low-Molecular Weight Heparin
and Unfractionated Heparin. How about retrievable filters? The French group the same set of authors looked at the same problem, but looked at it with retrievable IVC filters. And what they wanted to do is evaluate
the efficacy and safety of retrievable IVC filters plus anticoagulation versus anticoagulation alone for preventing PE. In patients who were at risk for acute PE and a high risk for, or had acute PE and were at a high risk.
So this is retrievable IVC filters, and what is this study shows. So this was a study again done outside the US. It was randomized, open label, blinded endpoint, PREPIC2 with a six-month follow-up. Took seven years to enroll 400 patients.
Patients had to have an acute symptomatic PE with a lower limb DVT, and have at least one criteria for severity. They were assigned to retrievable IVC filter implantation plus anticoagulation or anticoagulation alone,
and they had to have a planned retrieval of filter at three months, six month follow-up data. The primary endpoint was symptomatic recurrent PE at three months and secondary outcomes were recurrent PE
at six months, symptomatic DVT, major bleeding, death at three and six months and filter complications. And the results showed that in the filter group the filter they had a few patients that couldn't get the filter so they
could have placed 193 filters out of 200, and they were retrieved 153 were retrieved of the 164 in which retrieval was attempted. So again you're seeing patients not getting filters retrieved. By three months recurrent PE had occurred
in six patients in the filter group versus three. So you saw a prevention of recurrent PE in patients with a filter, and the results were very similar at six months. So you see the confidence intervals there. There was no difference observed among
the two groups regarding the other outcomes. And filter thrombosis occurred again in three patients. So what about IVC filter and PE plus or minus thrombolysis? So I'm going to show you a couple of studies
that suggest that patients that are with PE and thrombolysis may do better with a filter. And these are large databases. The first one was alluded to by our previous speaker is Paul Stein
Paul Stein's group. And they looked at in hospital all-cause fatality rate according to the use of vena cava filters as determined using the nationwide in-patient sample, and patients across the US.
And this is very interesting. As I was getting ready for this talk, this was an interesting observation that they made. So this is all-cause mortality in patients with PE across the country,
and patients were either categorized according to unstable or stable and you can see that across the X axis, and whether or not they got lytic therapy or not. And on the Y axis you can see fatality, in the hospital fatality based on filter
and non filter. And as you look across the different groups if you had an unstable patient who did not get lytic therapy, patients with filters did better than patients without filters.
If you had an unstable patient who had planned lytic therapy, unstable patients did better with filters than not. And even in the stable lytic group there was a difference in the groups.
So this suggests that there is a treatment benefit for patients with PE that are stable or unstable that are getting planned lytic therapy or not getting planned therapy. There is no difference if you are stable
with no lytic therapy. So it's implying that there may be an effect from the lower extremity or clot outside of where you're treating that may be contributing to the fatality. Here's another paper from the same group.
And this is using a premier health care database over 2010 to 2014, and they classified patients into similar groups based on ICD 9 codes and whether they were unstable or stable. So these were patients with PE
and an admitting diagnosis of PE, as well as a primary diagnosis of PE. And they used a time-dependent analysis according to the date of insertion of the IVC filter to control for the immortal time bias.
I don't understand all that but this is what the authors showed. So they had 266,000 patients with PE. 4,200 were unstable, PE admitting and primary diagnosis was down to 479 and those were divided
into thrombolytics versus non thrombolytics and if you saw if you got a filter eight patients died versus in the first group in thrombolytic group versus 42. Again in the non thrombolytic group, less patients died 27 versus 80.
So again showing a protection in patients with PE who are getting, who are unstable and who are getting admitted with filters. So there are other subsets, I'm not going to speak about them.
But I want the audience to understand there's patients with heart failure that may be that filters may be protective for. So if you present with heart failure in the setting of PE, that there is a large paper
large data set showing that patients should receive filters. And another sub special group patients undergoing pulmonary embolectomy that filters may also be protective for. So I want to be cognizant of the time,
and I'm going to stop there. Thank you.
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