- Relevant disclosures are shown in this slide. So when we treat patients with Multi-Segment Disease, the more segments that are involved, the more complex the outcomes that we should expect, with regards to the patient comorbidities and the complexity of the operation. And this is made even more complex
when we add aortic dissection to the patient population. We know that a large proportion of patients who undergo Thoracic Endovascular Aortic Repair, require planned coverage of the left subclavian artery. And this also been demonstrated that it's an increase risk for stroke, spinal cord ischemia and other complications.
What are the options when we have to cover the left subclavian artery? Well we can just cover the artery, we no that. That's commonly performed in emergency situations. The current standard is to bypass or transpose the artery. Or provide a totally endovascular revascularization option
with some off-label use , such as In Situ or In Vitro Fenestration, Parallel Grafting or hopefully soon we will see and will have available branched graft devices. These devices are currently investigational and the focus today's talk will be this one,
the Valiant Mona Lisa Stent Graft System. Currently the main body device is available in diameters between thirty and forty-six millimeters and they are all fifteen centimeters long. The device is designed with flexible cuff, which mimics what we call the "volcano" on the main body.
It's a pivotal connection. And it's a two wire pre-loaded system with a main system wire and a wire through the left subclavian artery branch. And this has predominately been delivered with a through and through wire of
that left subclavian branch. The system is based on the valiant device with tip capture. The left subclavian artery branch is also unique to this system. It's a nitinol helical stent, with polyester fabric. It has a proximal flare,
which allows fixation in that volcano cone. Comes in three diameters and they're all the same length, forty millimeters, with a fifteen french profile. The delivery system, which is delivered from the groin, same access point as the main body device. We did complete the early feasibility study
with nine subjects at three sites. The goals were to validate the procedure, assess safety, and collect imaging data. We did publish that a couple of years ago. Here's a case demonstration. This was a sixty-nine year old female
with a descending thoracic aneurysm at five and a half centimeters. The patient's anatomy met the criteria. We selected a thirty-four millimeter diameter device, with a twelve millimeter branch. And we chose to extend this repair down to the celiac artery
in this patient. The pre-operative CT scan looks like this. The aneurysm looks bigger with thrombus in it of course, but that was the device we got around the corner of that arch to get our seal. Access is obtained both from the groin
and from the arm as is common with many TEVAR procedures. Here we have the device up in the aorta. There's our access from the arm. We had a separate puncture for a "pigtail". Once the device is in position, we "snare" the wire, we confirm that we don't have
any "wire wrap". You can see we went into a areal position to doubly confirm that. And then the device is expanded, and as it's on sheath, it does creep forward a bit. And we have capture with that through and through wire
and tension on that through and through wire, while we expand the rest of the device. And you can see that the volcano is aligned right underneath the left subclavian artery. There's markers there where there's two rings, the outer and the inner ring of that volcano.
Once the device is deployed with that through and through wire access, we deliver the branch into the left subclavian artery. This is a slow deployment, so that we align the flair within the volcano and that volcano is flexible. In some patients, it sort of sits right at the level of
the aorta, like you see in this patient. Sometimes it protrudes. It doesn't really matter, as long as the two things are mated together. There is some flexibility built in the system. In this particular patient,
we had a little leak, so we were able to balloon this as we would any others. For a TEVAR, we just balloon both devices at the same time. Completion Angiogram shown here and we had an excellent result with this patient at six months and at a year the aneurysm continued
to re-sorb. In that series, we had successful delivery and deployment of all the devices. The duration of the procedure has improved with time. Several of these patients required an extension. We are in the feasibility phase.
We've added additional centers and we continue to enroll patients. And one of the things that we've learned is that details about the association between branches and the disease are critical. And patient selection is critical.
And we will continue to complete enrollment for the feasibility and hopefully we will see the pivotal studies start soon. Thank you very much
- So this was born out of the idea that there were some patients who come to us with a positive physical exam or problems on dialysis, bleeding after dialysis, high pressures, low flows, that still have normal fistulograms. And as our nephrology colleagues teach us, each time you give a patient some contrast,
you lose some renal function that they maintain, even those patients who are on dialysis have some renal function. And constantly giving them contrasts is generally not a good thing. So we all know that intimal hyperplasia
is the Achilles Heel of dialysis access. We try to do surveillance. Debbie talked about the one minute check and how effective dialysis is. Has good sensitivity on good specificity, but poor sensitivity in determining
dialysis access problems. There are other measured parameters that we can use which have good specificity and a little better sensitivity. But what about ultrasound? What about using ultrasound as a surveillance tool and how do you use it?
Well the DOQI guidelines, the first ones, not the ones that are coming out, I guess, talked about different ways to assess dialysis access. And one of the ways, obviously, was using duplex ultrasound. Access flows that are less than 600
or if they're high flows with greater than 20% decrease, those are things that should stimulate a further look for clinical stenosis. Even the IACAVAL recommendations do, indeed, talk about volume flow and looking at volume flow. So is it volume flow?
Or is it velocity that we want to look at? And in our hands, it's been a very, very challenging subject and those of you who are involved with Vasculef probably have the same thing. Medicare has determined that dialysis shouldn't, dialysis access should not be surveilled with ultrasound.
It's not medically necessary unless you have a specific reason for looking at the dialysis access, you can't simply surveil as much as you do a bypass graft despite the work that's been done with bypass graft showing how intervening on a failing graft
is better than a failed graft. There was a good meta-analysis done a few years ago looking at all these different studies that have come out, looking at velocity versus volume. And in that study, their conclusion, unfortunately, is that it's really difficult to tell you
what you should use as volume versus velocity. The problem with it is this. And it becomes, and I'll show you towards the end, is a simple math problem that calculating volume flows is simply a product of area and velocity. In terms of area, you have to measure the luminal diameter,
and then you take the luminal diameter, and you calculate the area. Well area, we all remember, is pi r squared. So you now divide the diameter in half and then you square it. So I don't know about you,
but whenever I measure something on the ultrasound machine, you know, I could be off by half a millimeter, or even a millimeter. Well when you're talking about a four, five millimeter vessel, that's 10, 20% difference.
Now you square that and you've got a big difference. So it's important to use the longitudinal view when you're measuring diameter. Always measure it if you can. It peaks distally, and obviously try to measure it in an non-aneurysmal area.
Well, you know, I'm sure your patients are the same as mine. This is what some of our patients look like. Not many, but this is kind of an exaggerated point to make the point. There's tortuosity, there's aneurysms,
and the vein diameter varies along the length of the access that presents challenges. Well what about velocity? Well, I think most of us realize that a velocity between 100 to 300 is probably normal. A velocity that's over 500, in this case is about 600,
is probably abnormal, and probably represents a stenosis, right? Well, wait a minute, not necessarily. You have to look at the fluid dynamic model of this, and look at what we're actually looking at. This flow is very different.
This is not like any, not like a bypass graft. You've got flow taking a 180 degree turn at the anastomosis. Isn't that going to give you increased turbulence? Isn't that going to change your velocity? Some of the flow dynamic principles that are important
to understand when looking at this is that the difference between plug and laminar flow. Plug flow is where every bit is moving at the same velocity, the same point from top to bottom. But we know that's not true. We know that within vessels, for the most part,
we have laminar flow. So flow along the walls tends to be a little bit less than flow in the middle. That presents a problem for us. And then when you get into the aneurysmal section, and you've got turbulent flow,
then all bets are off there. So it's important, when you take your sample volume, you take it across the whole vessel. And then you get into something called the Time-Averaged mean velocity which is a term that's used in the ultrasound literature.
But it basically talks about making sure that your sample volume is as wide as it can be. You have to make sure that your angle is as normal in 60 degrees because once you get above 60 degrees, you start to throw it off.
So again, you've now got angulation of the anastomosis and then the compliance of a vein and a graft differs from the artery. So we use the two, we multiply it, and we come up with the volume flow. Well, people have said you should use a straight segment
of the graft to measure that. Five centimeters away from the anastomosis, or any major branches. Some people have actually suggested just using a brachial artery to assess that. Well the problems in dialysis access
is there are branches and bifurcations, pseudoaneurysms, occlusions, et cetera. I don't know about you, but if I have a AV graft, I can measure the volume flow at different points in the graft to get different numbers. How is that possible?
Absolutely not possible. You've got a tube with no branches that should be the same at the beginning and the end of the graft. But again, it becomes a simple math problem. The area that you're calculating is half the diameter squared.
So there's definitely measurement area with the electronic calipers. The velocity, you've got sampling error, you've got the anatomy, which distorts velocity, and then you've got the angle with which it is taken. So when you start multiplying all this,
you've got a big reason for variations in flow. We looked at 82 patients in our study. We double blinded it. We used a fistulagram as the gold standard. The duplex flow was calculated at three different spots. Duplex velocity at five different spots.
And then the diameters and aneurysmal areas were noted. This is the data. And basically, what it showed, was something totally non-significant. We really couldn't say anything about it. It was a trend toward lower flows,
how the gradients (mumbles) anastomosis, but nothing we could say. So as you all know, you can't really prove the null hypothesis. I'm not here to tell you to use one or use the other, I don't think that volume flow is something that
we can use as a predictor of success or failure, really. So in conclusion, what we found, is that Debbie Brow is right. Clinical examinations probably still the best technique. Look for abnormalities on dialysis. What's the use of duplex ultrasound in dialysis or patients?
And I think we're going to hear that in the next speaker. But probably good for vein mapping. Definitely good for vein mapping, arterial inflow, and maybe predicting maturation. Thank you very much.
- Thank you very much. So, this audience certainly knows that the higher the triglyceride, the greater the cardiovascular morbidity mortality, similarly if you have a low HDL that same relation holds, and certainly for the non-HDL-C or LDL-C calculated the higher the worse outcome and there's
multiple drugs related to this. Similarly with stroke, triglyceride the same relationship. Ischemic stroke increased with low HDL and again LDL-C correlates. So the historical precedent has been that you should get a fasting lipid level
when you first encounter the patient, but to make this simple that's really probably not true. So there's various things that are measured and that are calculated, but LDL is generally calculated, HDL is measured and then the triglycerides are calculated as remnant cholesterol.
So if you compare just the measured LDL compared to calculated LDL in a non-fasting state, it's a little bit of a wider linear relationship here as compared with the fasting, it's a little bit tighter. But when you look at this in more depth, and this reference here really nicely puts it all together
but the total cholesterol really doesn't vary if you've fasted one hour or 16 hours, similarly between men and women. The only thing that varies a little bit is triglycerides and we'll go on to that in just a little bit of depth.
But again that's variable, triglycerides go up if you eat really not much difference with the other lipid levels. And if you look just in terms of triglycerides, they overlap between non-fasting and fasting, really at almost all levels
so there's not really discrepancy. Similarly with LDL, same amount of overlap here whether or not you have diabetes it doesn't seem to make a difference. So for lipid panels, profile testing, in most patients you can get a non-fasting
initial lipid profile in any patient for cardiovascular risk assessment, I'd say that's where it's most commonly done in most of our practices. Similarly with acute coronary syndrome, if preferred by the patients et cetera.
But really it's where the non-fasting triglycerides are highly elevated that you want to get a fasting lipid panel. So what causes secondary hyperlipidemia related particularly to hypertriglyceridemia? Certainly certain diet factors, certain drugs,
cyclosporins for example, biliary obstruction and hypothyroidism. And so, one algorithm is that in terms of screening with non-fasting, and if it's less than 200 you're good to go, you really don't need to do anything further,
and if it's greater than 200 then probably a fasting lipid profile, lipoprotein panel is indicated. So reasons that non-fasting lipid measurement is fine most of the time is that again most trials have used non-fasting levels for determination of effectiveness of various medications.
This Friedewald formula actually uses total cholesterol, HDL, and triglycerides to calculate LDL-C, and LDL really is not directly measured, it's not standardized by the CDC such as these other cholesterol moieties are. And again most CV risk factor calculators don't use LDL-C.
So again, non-fasting is acceptable for the initial risk estimation in untreated and primary prevention screening. For patients with genetic hyperlipidemia probably fasting is required. Diagnosis of metabolic syndrome, non-fasting is fine.
And again some other more highly specialized scenarios you may want a fasting profile. Thank you.
- I'm going to be speaking about indirect access sites for access intervention. I'm going to be focusing on the transjugular approach. So access interventions, typically we perform them through a direct puncture of the fistula. Sometimes you place two introducers. There are some disadvantages to the direct approach.
The crossing catheters technique that we generally use for declots is awkward and cumbersome. The introducers can obstruct flow, there's dead space behind the introducers that can trap clot, and there's radiation exposure or the direct exposure
or scatter radiation from hands near the field. Admit it, we've all had access-site complications, suture-site necrosis and infection, as well as pseudoaneurysms. There's also prolonged procedure time related to needing to obtain hemostasis
in the high-pressure segment. There are also problems particularly to immature fistulas, such as hematoma formation, spasm at the introducer site causing pseudo-stenosis, decreased flow, and fistula thrombosis. Now, the good news is that we do have options
for alternative access sites. I'm sure many of you here use arterial access for immature fistulas in particular. Brachial access can be used to, this can be used for diagnostic or therapeutic purposes. We can also utilize radial or ulnar access.
Rarely, femoral access is used, as we saw in the last presentation. But there's also pendula venous access sites. You can sometimes, as a fortuitous tributary, what I call a target of opportunity, and also, the internal jugular vein.
Now, the transjugular approach was first reported in 1998. It does have some definite advantages over direct puncture technique. You can avoid the cumbersome access, you can keep your hands away from the beam, and there's no dead space as compared
to crossing sheaths for your declot. And if the intervention is unsuccessful, you can convert your IJ access to a catheter if you already have a wire in it. There are some technical challenges associated with this technique.
You do have to overcome the valves. It can be difficult to access the cephalic vein, but you can get around this by using a snare. And there's possibly a risk of IJ thrombosis if you're using large introducers. When to use this technique?
Well, when direct puncture's going to be difficult or cumbersome, when there's a short cannulation segment, when it's an extensively stented access, and when there's inflow pathology requiring a retrograde approach or arterial empathalogy, and it's a good option for clotted access.
The technique, micropuncture access of the jugular vein, ipsilateral or contralateral, place a sheath, and an important thing to use is a reverse-curve catheter, followed by glidewire. So here, we've cannulated the jugular vein going down,
glidewire out into the arm. If you're unable to cross into the cephalic vein, you can use that snare technique. And you can get a long, stable access in this way. It's been reported about, there's about 10 publications on transjugular approach, seven retrospective studies.
There's a large study that's reported thrombectomy. Also a large study looking at immature fistulas. Smaller studies looking at dysfunctional access and pseudoaneurysms. Two case reports, one review article, but there's of course no randomized studies.
There's a recent study from this year from Ferral and Alonzo. This was a retrospective study. Over two years they performed 30 transjugular AV access interventions. This accounted for 5% of their access experience
and this series was all fistulance. Indications for the procedure, 43% were declots, 43% were arterial and fistual pathology, there were two immature fistulas and two bleeding pseudoaneurysms. The access approach was 29 for ipsilateral,
only one contralateral. The results, 97% technical success, a snare was required in 4 cases, a catheter was inserted in two of the cases. There were no episodes of jugular vein thrombosis. In the remaining time, I'd like to show
a couple of case studies. Again, from Ferral and Alonzo. This is a case of an immature fistula. This was a partially occluded, immature left upper arm fistula. The initial fistulagram shows outflow stenosis
with a multiple stenosis in thrombus, and there's an arterial in stenosis that's distal to the access point, so you're not going to be able to treat that. They performed four millimeter angioplasty. Follow-up fistulagram shows a small, but patent vein
and the arterial end could not be treated. They brought the patient back in two weeks for a staged transjugular approach. And you can see the jugular catheter coming down. The vein diameter's improved, but there's still the untreated arterial end stenosis,
which is easily treated through the jugular approach. This is a study from, a case from Dr. Rabellino, ruptured pseudoaneurysm. This is a basilic transposition with a ruptured pseudoaneurysm at an infiltration site. Pretty ugly arm, swollen, skin necrosis.
I don't think we want to be sticking that arm. They initially went with a femoral approach for the fistulagram, demonstrated the pseudoaneurysm. As you can see here, tandem outflow stenoses. Coming up from below with the femoral artery diagnostic catheter.
Down and into the arm through the jugular approach. And here, you can see the venous outflow after angioplasty, covered stent deployed through the jugular access. So in summary, the transjugular approach is a useful but underutilized technique. The advantages include single-puncture intervention,
does not involve the outflow vein directly, simplified hemostasis, it's a low pressure system. It does have the advantage that you can use large introducers, there's less radiation for the operator, and you can convert to a catheter easily if needed. It is a useful technique for fistula maturation,
thrombectomy, and access maintenance. I say go for the jugular.
- Thanks Fieres. Thank you very much for attending this session and Frank for the invitation. These are my disclosures. We have recently presented the outcomes of the first 250 patients included in this prospective IDE at the AATS meeting in this hotel a few months ago.
In this study, there was no in-hospital mortality, there was one 30-day death. This was a death from a patient that had intracranial hemorrhage from the spinal drain placement that eventually was dismissed to palliative care
and died on postoperative day 22. You also note that there are three patients with paraplegia in this study, one of which actually had a epidural hematoma that was led to various significant and flacid paralysis. That prompted us to review the literature
and alter our outcomes with spinal drainage. This review, which includes over 4700 patients shows that the average rate of complications is 10%, some of those are relatively moderate or minor, but you can see a rate of intracranial hemorrhage of 1.5% and spinal hematoma of 1% in this large review,
which is essentially a retrospective review. We have then audited our IDE patients, 293 consecutive patients treated since 2013. We looked at all their spinal drains, so there were 240 placement of drains in 187 patients. You can see that some of these were first stage procedures
and then the majority of them were the index fenestrated branch procedure and some, a minority were Temporary Aneurysm Sac Perfusions. Our rate of complication was identical to the review, 10% and I want to point out some of the more important complications.
You can see here that intracranial hypotension occurred in 6% of the patients, that included three patients, or 2%, with intracranial hemorrhage and nine patients, or 5%, with severe headache that prolonged hospital stay and required blood patch for management.
There were also six patients with spinal hematomas for a overall rate of 3%, including the patient that I'll further discuss later. And one death, which was attributed to the spinal drain. When we looked at the intracranial hypotension in these 12 patients, you can see
the median duration of headache was four days, it required narcotics in seven patients, blood patch in five patients. All these patients had prolonged hospital stay, in one case, the prolongation of hospital stay was of 10 days.
Intracranial hemorrhage in three patients, including the patient that I already discussed. This patient had a severe intracranial hemorrhage which led to a deep coma. The patient was basically elected by the family to be managed with palliative care.
This patient end up expiring on postoperative day 21. There were other two patients with intracranial hemorrhage, one remote, I don't think that that was necessarily related to the spinal drain, nonetheless we had it on this review. These are some of the CT heads of the patients that had intracranial hemorrhage,
including the patient that passed away, which is outlined in the far left of your slide. Six patients had spinal hematoma, one of these patients was a patient, a young patient treated for chronic dissection. Patient evolved exceptionally well, moving the legs,
drain was removed on postoperative day two. As the patient is standed out of the bed, felt weakness in the legs, we then imaged the spine. You can see here, very severe spinal hematoma. Neurosurgery was consulted, decided to evacuate, the patient woke up with flacid paralysis
which has not recovered. There were two other patients with, another patient with paraplegia which was treated conservatively and improved to paraparesis and continues to improve and two other patients with paraparesis.
That prompted changes in our protocol. We eliminated spinal drains for Extent IVs, we eliminated for chronic dissection, in first stages, on any first stage, and most of the Extent IIIs, we also changed our protocol of drainage
from the routine drainage of a 10 centimeters of water for 15 minutes of the hours to a maximum of 20 mL to a drainage that's now guided by Near Infrared Spectroscopy, changes or symptoms. This is our protocol and I'll illustrate how we used this in one patient.
This is a patient that actually had this actual, exact anatomy. You can see the arch was very difficult, the celiac axis was patent and provided collateral flow an occluded SMA. The right renal artery was chronically occluded.
As we were doing this case the patient experienced severe changes in MEP despite the fact we had flow to the legs, we immediately stopped the procedure with still flow to the aneurysm sac. The patient develops pancreatitis, requires dialysis
and recovers after a few days in the ICU with no neurological change. Then I completed the repair doing a subcostal incision elongating the celiac axis and retrograde axis to this graft to complete the branch was very difficult to from the arm
and the patient recovered with no injury. So, in conclusion, spinal drainage is potentially dangerous even lethal and should be carefully weighted against the potential benefits. I think that our protocol now uses routine drainage for Extent I and IIs,
although I still think there is room for a prospective randomized trial even on this group and selective drainage for Extent IIIs and no drainage for Extent IVs. We use NIRS liberally to guide drainage and we use temporary sac perfusion
in those that have changes in neuromonitoring. Thank you very much.
- Good morning, I would like to thank Dr. Veith, and the co-chairs for inviting me to talk. I have nothing to disclose. Some background on this information, patients with Inflammatory Bowel Disease are at least three times more likely to suffer a thrombo-embolic event, when compared to the general population.
The incidence is 0.1 - 0.5% per year. Overall mortality associated with these events can be as high as 25%, and postmortem exams reveal an incidence of 39-41% indicating that systemic thrombo-embolism is probably underdiagnosed. Thrombosis mainly occurs during disease exacerbation,
however proctocolectomy has not been shown to be preventative. Etiology behind this is not well known, but it's thought to be multifactorial. Including decrease in fibrinolytic activity, increase in platelet activation,
defects in the protein C pathway. Dyslipidemia and long term inflammation also puts patients at risk for an increase in atherosclerosis. In addition, these patients lack vitamins, are often dehydrated, anemic, and at times immobilized. Traditionally, the venous thrombosis is thought
to be more common, however recent retrospective review of the Health Care Utilization Project nationwide inpatient sample database, reported not only an increase in the incidence but that arterial complications may happen more frequently than venous.
I was going to present four patients over the course of one year, that were treated at my institution. The first patient is 25 year old female with Crohn's disease, who had a transverse colectomy one year prior to presentation. Presented with right flank pain, she was found to have
right sided PE, a right sided pulmonary vein thrombosis and a left atrial thrombosis. She was admitted for IV heparin, four days later she had developed abdominal pains, underwent an abdominal CTA significant for SMA occlusion prompting an SMA thrombectomy.
This is a picture of her CAT scan showing the right PE, the right pulmonary vein thrombosis extending into the left atrium. The SMA defect. She returned to the OR for second and third looks, underwent a subtotal colectomy,
small bowel resection with end ileostomy during the third operation. She had her heparin held post-operatively due to significant post-op bleeding, and over the next three to five days she got significantly worse, developed progressive fevers increase found to have
SMA re-thrombosis, which you can see here on her CAT scan. She ended up going back to the operating room and having the majority of her small bowel removed, and went on to be transferred to an outside facility for bowel transplant. Our second patient is a 59 year old female who presented
five days a recent flare of ulcerative colitis. She presented with right lower extremity pain and numbness times one day. She was found to have acute limb ischemia, category three. An attempt was made at open revascularization with thrombectomy, however the pedal vessels were occluded.
The leg was significantly ischemic and flow could not be re-established despite multiple attempts at cut-downs at different levels. You can see her angiogram here at the end of the case. She subsequently went on to have a below knee amputation, and her hospital course was complicated by
a colonic perforation due to the colitis not responding to conservative measures. She underwent a subtotal colectomy and end ileostomy. Just in the interest of time we'll skip past the second, third, and fourth patients here. These patients represent catastrophic complications of
atypical thrombo-embolic events occurring in IBD flares. Patients with inflammatory disease are at an increased risk for both arterial and venous thrombotic complications. So the questions to be answered: are the current recommendations adequate? Currently heparin prophylaxis is recommended for
inpatients hospitalized for severe disease. And, if this is not adequate, what treatments should we recommend, the medication choice, and the duration of treatment? These arterial and venous complications occurring in the visceral and peripheral arteries
are likely underappreciated clinically as a risk for patients with IBD flares and they demonstrate a need to look at further indications for thrombo-prophylaxis. Thank you.
- Thanks Bill and I thank Dr. Veith and the organizers of the session for the invitation to speak on histology of in-stent stenosis. These are my disclosures. Question, why bother with biopsy? It's kind of a hassle. What I want to do is present at first
before I show some of our classification of this in data, is start with this case where the biopsy becomes relevant in managing the patient. This is a 41 year old woman who was referred to us after symptom recurrence two months following left iliac vein stenting for post-thrombotic syndrome.
We performed a venogram and you can see this overlapping nitinol stents extending from the..., close to the Iliocaval Confluence down into Common Femoral and perhaps Deep Femoral vein. You can see on the venogram, that it is large displacement of the contrast column
from the edge of the stent on both sides. So we would call this sort of diffuse severe in-stent stenosis. We biopsy this material, you can see it's quite cellular. And in the classification, Doctor Gordon, our pathologist, applies to all these.
Consisted of fresh thrombus, about 15% of the sample, organizing thrombus about zero percent, old thrombus, which is basically a cellular fibrin, zero percent and diffuse intimal thickening - 85%. And you can see there is some evidence of a vascularisation here, as well as some hemosiderin deposit,
which, sort of, implies a red blood cell thrombus, histology or ancestry of this tissue. So, because the biopsy was grossly and histolo..., primarily grossly, we didn't have the histology to time, we judged that thrombolysis had little to offer this patient The stents were angioplastied
and re-lined with Wallstents this time. So, this is the AP view, showing two layers of stents. You can see the original nitinol stent on the outside, and a Wallstent extending from here. Followed venogram, venogram at the end of the procedure, shows that this displacement, and this is the maximal
amount we could inflate the Wallstent, following placement through this in-stent stenosis. And this is, you know, would be nice to have a biological or drug solution for this kind of in-stent stenosis. We brought her back about four months later, usually I bring them back at six months,
but because of the in-stent stenosis and suspecting something going on, we brought her back four months later, and here you can see that the gap between the nitinol stent and the outside the wall stent here. Now, in the contrast column, you can see that again, the contrast column is displaced
from the edge of the Wallstent, so we have recurrent in-stent stenosis here. The gross appearance of this clot was red, red-black, which suggests recent thrombus despite anticoagulation and the platelet. And, sure enough, the biopsy of fresh thrombus was 20%,
organizing thrombus-75%. Again, the old thrombus, zero percent, and, this time, diffuse intimal thickening of five percent. This closeup of some of that showing the cells, sort of invading this thrombus and starting organization. So, medical compliance and outflow in this patient into IVC
seemed acceptable, so we proceeded to doing ascending venogram to see what the outflow is like and to see, if she was an atomic candidate for recanalization. You can see these post-thrombotic changes in the popliteal vein, occlusion of the femoral vein.
You can see great stuffiness approaching these overlapping stents, but then you can see that the superficial system has been sequestered from the deep system, and now the superficial system is draining across midline. So, we planned to bring her back for recanalization.
So biopsy one with diffuse intimal thickening was used to forego thrombolysis and proceed with PTA and lining. Biopsy two was used to justify the ascending venogram. We find biopsy as a useful tool, making practical decisions. And Doctor Gordon at our place has been classifying these
biopsies in therms of: Fresh Thrombus, Organizing Thrombus, Old Thrombus and Diffuse Intimal thickening. These are panels on the side showing the samples of each of these classifications and timelines. Here is a timeline of ...
Organizing Thrombus here. To see it's pretty uniform series of followup period For Diffuse Intimal thickening, beginning shortly after the procedure, You won't see very much at all, increases with time. So, Fresh Thrombus appears to be
most prevalent in early days. Organizing Thrombus can be seen at early time points sample, as well as throughout the in-stent stenosis. Old Thrombus, which is a sort of a mystery to me why one pathway would be Old Thrombus and the other Diffuse Intimal thickening.
We have to work that out, I hope. Calcification is generally a very late feature in this process. Thank you very much.
- These are my disclosures. So central venous access is frequently employed throughout the world for a variety of purposes. These catheters range anywhere between seven and 11 French sheaths. And it's recognized, even in the best case scenario, that there are iatrogenic arterial injuries
that can occur, ranging between three to 5%. And even a smaller proportion of patients will present after complications from access with either a pseudoaneurysm, fistula formation, dissection, or distal embolization. In thinking about these, as you see these as consultations
on your service, our thoughts are to think about it in four primary things. Number one is the anatomic location, and I think imaging is very helpful. This is a vas cath in the carotid artery. The second is th
how long the device has been dwelling in the carotid or the subclavian circulation. Assessment for thrombus around the catheter, and then obviously the size of the hole and the size of the catheter.
Several years ago we undertook a retrospective review and looked at this, and we looked at all carotid, subclavian, and innominate iatrogenic injuries, and we excluded all the injuries that were treated, that were manifest early and treated with just manual compression.
It's a small cohort of patients, we had 12 cases. Eight were treated with a variety of endovascular techniques and four were treated with open surgery. So, to illustrate our approach, I thought what I would do is just show you four cases on how we treated some of these types of problems.
The first one is a 75 year-old gentleman who's three days status post a coronary bypass graft with a LIMA graft to his LAD. He had a cordis catheter in his chest on the left side, which was discovered to be in the left subclavian artery as opposed to the vein.
So this nine French sheath, this is the imaging showing where the entry site is, just underneath the clavicle. You can see the vertebral and the IMA are both patent. And this is an angiogram from a catheter with which was placed in the femoral artery at the time that we were going to take care of this
with a four French catheter. For this case, we had duel access, so we had access from the groin with a sheath and a wire in place in case we needed to treat this from below. Then from above, we rewired the cordis catheter,
placed a suture-mediated closure device, sutured it down, left the wire in place, and shot this angiogram, which you can see very clearly has now taken care of the bleeding site. There's some pinching here after the wire was removed,
this abated without any difficulty. Second case is a 26 year-old woman with a diagnosis of vascular EDS. She presented to the operating room for a small bowel obstruction. Anesthesia has tried to attempt to put a central venous
catheter access in there. There unfortunately was an injury to the right subclavian vein. After she recovered from her operation, on cross sectional imaging you can see that she has this large pseudoaneurysm
coming from the subclavian artery on this axial cut and also on the sagittal view. Because she's a vascular EDS patient, we did this open brachial approach. We placed a stent graft across the area of injury to exclude the aneurism.
And you can see that there's still some filling in this region here. And it appeared to be coming from the internal mammary artery. We gave her a few days, it still was patent. Cross-sectional imaging confirmed this,
and so this was eventually treated with thoracoscopic clipping and resolved flow into the aneurism. The next case is a little bit more complicated. This is an 80 year-old woman with polycythemia vera who had a plasmapheresis catheter,
nine French sheath placed on the left subclavian artery which was diagnosed five days post procedure when she presented with a posterior circulation stroke. As you can see on the imaging, her vertebral's open, her mammary's open, she has this catheter in the significant clot
in this region. To manage this, again, we did duel access. So right femoral approach, left brachial approach. We placed the filter element in the vertebral artery. Balloon occlusion of the subclavian, and then a stent graft coverage of the area
and took the plasmapheresis catheter out and then suction embolectomy. And then the last case is a 47 year-old woman who had an attempted right subclavian vein access and it was known that she had a pulsatile mass in the supraclavicular fossa.
Was noted to have a 3cm subclavian artery pseudoaneurysm. Very broad base, short neck, and we elected to treat this with open surgical technique. So I think as you see these consults, the things to factor in to your management decision are: number one, the location.
Number two, the complication of whether it's thrombus, pseudoaneurysm, or fistula. It's very important to identify whether there is pericatheter thrombus. There's a variety of techniques available for treatment, ranging from manual compression,
endovascular techniques, and open repair. I think the primary point here is the prevention with ultrasound guidance is very important when placing these catheters. Thank you. (clapping)
- Thank you very much. I'm going to talk on Improper and Suboptimal Antiplatelet Therapy which is probably currently the standard on most carotid angioplasty stent trials and I'm going to show you how it could potentially affect all of the results we have seen so far. I have nothing to disclose.
So introduction, based on the composite end point of stroke/death in our technical trials, they're always, in all randomized trials Endarterectomy always did marginally better than Carotid angioplasty and stenting. However, a small shift, just about a one person shift
could make carotid artery stenting better could shift the results of all these carotid stent trials. Let's just look at CREST. I think it's the gold standard for randomized trial comparing endarterectomy with stenting. You can see the combined death, streak and MI rate.
For endarterectomy, it's 6.8%, for CAS, 7.2%. For stroke, again 2.3, 4.1. Again, it's a one person shift in a direction of making stents better could actually show that stents were favorable, but comparable to it, not just inferior.
Now if you look at the data on CREST, it's very interesting that the majority of the strokes, about 80% of the strokes happened after about 24 hours. In fact, most of them happened on the third day period. So it wasn't a technical issue. You know, the biggest issue with current stenting
that we find is that we have filters, we have floor reversal. They're very worried about the time we place the stent, that we balloon, pre- and post-, but it wasn't a technical issue. Something was happening after 24 hours.
Another interesting fact that no one speaks about is if you look at the CREST data a little bit in more detail, most of the mortality associated with the stenting was actually associated with an access site bleed.
So if you could really decrease the late strokes, if you can decrease the access site bleeds, I think stents can be performed better than endarterectomies. The study design for all stent trials, there was a mandatory dual antiplatelet therapy.
Almost all patients had to be on aspirin and Plavix and on CREST, interestingly, they had to be on 75 milligrams BID for Plavix so they were all on very high dose Plavix. Now here's the interesting thing about Plavix that most people don't know.
Plavix is what is called a pro-drug. It requires to be converted to its active component by the liver for antiplatelet effect. And the particular liver enzyme that converts Plavix to its active metabolic enzyme is very variable patient to patient
and you're born that way. You're either born where you can convert its active metabolite or you can't convert it to its active metabolite and a test that's called 2C19 is actually interesting approved and covered by Medicare and here's the people
that read the black box warning for Plavix, that looked at the package insert. I just cut and paste this on the package that said for Plavix. I'm just showing you a few lines from the package insert. Now next to aspirin, it's the commonest prescribed drug
by vascular specialists, but most people probably have not looked at the package insert that says effectiveness of Plavix depends on activation by a liver enzyme called 2C19 and goes on to say that tests are available to identify to 2C19 genotype.
And then they go on to actually give you a recommendation on the package insert that says consider alternative treatment strategies in patients identified as 2C19 poor metabolizers. Now these are the people who cannot metabolize Plavix and convert them to its active metabolite.
So let's look at the actual incidents. Now we know there is resistance to, in some patients, to aspirin, but the incident is so small it doesn't make worth our time or doesn't make it worth the patient's outcome to be able to test everyone for aspirin resistance,
but look at the incidents for Plavix resistance. Again, this is just a slide explaining what does resistance mean so if you're a normal metabolizer, which we hope that most of us would be, you're going to expect advocacy from Plavix at 75 milligrams once a day.
Other hand, let's say you're a rapid or ultrarapid metabolizer. You have a much higher risk of bleeding. And then if you go to the other side where you are normal, intermediate or poor metabolizer, you're not going to convert Plavix to its active metabolite
and poor metabolizers, it's like giving a placebo. And interestingly, I'm a poor metabolizer. I got myself tested. If I ever have a cardiac interventionalist give me Plavix, they're giving me a placebo. So let's look at the actual incidents
of all these subsets in patients and see whether that's going to be an issue. So we took this from about 7,000 patients and interestingly in only about 40%, NM stands for nominal metabolizer or normal metabolizers. So only 40% get the expected efficacy of Plavix.
Let's look at just the extremes. Let's just assume people with normal metabolizers, normal intermediate and the subgroup between the ultra rapid, the normals, they're all going to respond well to Plavix. Let's just look at the extremes.
Ultra rapid and poor metabolizers. So these are the people who are going to convert Plavix to a much higher concentration of its active metabolite, but have a much higher risk of bleeding. Ultra rapid metabolizers. Poor metabolizers, Plavix doesn't work.
4%, 3%. That's not a small incidence. Now in no way am I saying that carotid stent trials itselves are totally based on Plavix resistance, but just look at the data from CREST. Let's say the patients with poor metabolizers,
that's 3%, so these people did not get Plavix. Plavix does not affect you in doses of up to 600 milligram for people with poor metabolizers. Incidents of embolic events in CREST trial for carotid stents was 4%. This happened after three days.
I believe it's possibly related to platelet debris occurring in the stent on people who did not receive a liquid anti-platelet therapy. How about the people who had the groin bleed? Remember I told you that access site bleeds were most highly predictable mortality.
If you're the ultra rapid metabolizers, that incidence was 4%. So these were the people that convert Plavix with a very high dose of active metabolite, very high risk of bleeding. Access site bleed rate,
if you look at the major/minor rates, 4.1%, very close to the ultra rapid metabolizers. So fact remains that carotid angioplasty stenting post procedure events are highly dependent on appropriate antiplatelet therapy to minimize embolic events and to decrease groin bleeds.
So in conclusion, if we just included 2C19 normal metabolizers, as was recommended by the packaging insert, so just test the people, include the people on normal metabolizers, exclude the rest, we are probably going to shift the results in favor of carotid angioplasty and stenting.
Results of all carotid angioplasty stent trials need to be questioned as a significant number of patients in the carotid angioplasty stent arm did not receive appropriate antiplatelet therapy. Thank you very much.
- Thanks Dr. Weaver. Thank you Dr. Reed for the invitation, once again, to this great meeting. These are my disclosures. So, open surgical repair of descending aortic arch disease still carries some significant morbidity and mortality.
And obviously TEVAR as we have mentioned in many of the presentations has become the treatment of choice for appropriate thoracic lesions, but still has some significant limitations of seal in the aortic arch and more techniques are being developed to address that.
Right now, we also need to cover the left subclavian artery and encroach or cover the left common carotid artery for optimal seal, if that's the area that we're trying to address. So zone 2, which is the one that's,
it is most commonly used as seal for the aortic arch requires accurate device deployment to maximize the seal and really avoid ultimately, coverage of the left common carotid artery and have to address it as an emergency. Seal, in many of these cases is not maximized
due to the concern of occlusion of the left common carotid artery and many of the devices are deployed without obtaining maximum seal in that particular area. Failure of accurate deployment often leads to a type IA endoleak or inadvertent coverage
of the left common carotid artery which can become a significant problem. The most common hybrid procedures in this group of patients include the use of TEVAR, a carotid-subclavian reconstruction and left common carotid artery stenting,
which is hopefully mostly planned, but many of the times, especially when you're starting, it may be completely unplanned. The left common carotid chimney has been increasingly used to obtain a better seal
in this particular group of patients with challenging arches, but there's still significant concerns, including patients having super-vascular complications, stroke, Type A retrograde dissections and a persistent Type IA endoleak
which can be very challenging to be able to correct. There's limited data to discuss this specific topic, but some of the recent publications included a series of 11 to 13 years of treatment with a variety of chimneys.
And these publications suggest that the left common carotid chimneys are the most commonly used chimneys in the aortic arch, being used 76% to 89% of the time in these series. We can also look at these and the technical success
is very good. Mortality's very low. The stroke rate is quite variable depending on the series and chimney patency's very good. But we still have a relatively high persistent
Type IA endoleak on these procedures. So what can we do to try to improve the results that we have? And some of these techniques are clearly applicable for elective or emergency procedures. In the elective setting,
an open left carotid access and subclavian access can be obtained via a supraclavicular approach. And then a subclavian transposition or a carotid-subclavian bypass can be performed in preparation for the endovascular repair. Following that reconstruction,
retrograde access to left common carotid artery can be very helpful with a 7 French sheath and this can be used for diagnostic and therapeutic purposes at the same time. The 7 French sheath can easily accommodate most of the available covered and uncovered
balloon expandable stents if the situation arises that it's necessary. Alignment of the TEVAR is critical with maximum seal and accurate placement of the TEVAR at this location is paramount to be able to have a good result.
At that point, the left common carotid artery chimney can be deployed under control of the left common carotid artery. To avoid any embolization, the carotid can be flushed, primary repaired, and the subclavian can be addressed
if there is concern of a persistent retrograde leak with embolization with a plug or other devices. The order can be changed for the procedure to be able to be done emergently as it is in this 46 year old policeman with hypertension and a ruptured thoracic aneurism.
The patient had the left common carotid access first, the device deployed appropriately, and the carotid-subclavian bypass performed in a more elective fashion after the rupture had been addressed. So, in conclusion, carotid chimney's and TEVAR
combination is a frequently used to obtain additional seal on the aortic arch, with pretty good results. Early retrograde left common carotid access allows safe TEVAR deployment with maximum seal,
and the procedure can be safely performed with low morbidity and mortality if we select the patients appropriately. Thank you very much.
- Good morning everybody. Here are my disclosures. So, upper extremity access is an important adjunct for some of the complex endovascular work that we do. It's necessary for chimney approaches, it's necessary for fenestrated at times. Intermittently for TEVAR, and for
what I like to call FEVARCh which is when you combine fenestrated repair with a chimney apporach for thoracoabdominals here in the U.S. Where we're more limited with the devices that we have available in our institutions for most of us. This shows you for a TEVAR with a patient
with an aortic occlusion through a right infracrevicular approach, we're able to place a conduit and then a 22-french dryseal sheath in order to place a TEVAR in a patient with a penetrating ulcer that had ruptured, and had an occluded aorta.
In addition, you can use this for complex techniques in the ascending aorta. Here you see a patient who had a prior heart transplant, developed a pseudoaneurysm in his suture line. We come in through a left axillary approach with our stiff wire.
We have a diagnostic catheter through the femoral. We're able to place a couple cuffs in an off-label fashion to treat this with a technically good result. For FEVARCh, as I mentioned, it's a good combination for a fenestrated repair.
Here you have a type IV thoraco fenestrated in place with a chimney in the left renal, we get additional seal zone up above the celiac this way. Here you see the vessels cannulated. And then with a nice type IV repaired in endovascular fashion, using a combination of techniques.
But the questions always arise. Which side? Which vessel? What's the stroke risk? How can we try to be as conscientious as possible to minimize those risks? Excuse me. So, anecdotally the right side has been less safe,
or concerned that it causes more troubles, but we feel like it's easier to work from the right side. Sorry. When you look at the image intensifier as it's coming in from the patient's left, we can all be together on the patient's right. We don't have to work underneath the image intensifier,
and felt like right was a better approach. So, can we minimize stroke risk for either side, but can we minimize stroke risk in general? So, what we typically do is tuck both arms, makes lateral imaging a lot easier to do rather than having an arm out.
Our anesthesiologist, although we try not to help them too much, but it actually makes it easier for them to have both arms available. When we look at which vessel is the best to use to try to do these techniques, we felt that the subclavian artery is a big challenge,
just the way it is above the clavicle, to be able to get multiple devices through there. We usually feel that the brachial artery's too small. Especially if you're going to place more than one sheath. So we like to call, at our institution, the Goldilocks phenomenon for those of you
who know that story, and the axillary artery is just right. And that's the one that we use. When we use only one or two sheaths we just do a direct puncture. Usually through a previously placed pledgeted stitch. It's a fairly easy exposure just through the pec major.
Split that muscle then divide the pec minor, and can get there relatively easily. This is what that looks like. You can see after a sheath's been removed, a pledgeted suture has been tied down and we get good hemostasis this way.
If we're going to use more than two sheaths, we prefer an axillary conduit, and here you see that approach. We use the self-sealing graft. Whenever I have more than two sheaths in, I always label the sheaths because
I can't remember what's in what vessel. So, you can see yes, I made there, I have another one labeled right renal, just so I can remember which sheath is in which vessel. We always navigate the arch first now. So we get all of our sheaths across the arch
before we selective catheterize the visceral vessels. We think this partly helps minimize that risk. Obviously, any arch manipulation is a concern, but if we can get everything done at once and then we can focus on the visceral segment. We feel like that's a better approach and seems
to be better for what we've done in our experience. So here's our results over the past five-ish years or so. Almost 400 aortic interventions total, with 72 of them requiring some sort of upper extremity access for different procedures. One for placement of zone zero device, which I showed you,
sac embolization, and two for imaging. We have these number of patients, and then all these chimney grafts that have been placed in different vessels. Here's the patients with different number of branches. Our access you can see here, with the majority
being done through right axillary approach. The technical success was high, mortality rate was reasonable in this group of patients. With the strokes being listed there. One rupture, which is treated with a covered stent. The strokes, two were ischemic,
one hemorrhagic, and one mixed. When you compare the group to our initial group, more women, longer hospital stay, more of the patients had prior aortic interventions, and the mortality rate was higher. So in conclusion, we think that
this is technically feasible to do. That right side is just as safe as left side, and that potentially the right side is better for type III arches. Thank you very much.
- Thank you very much for the opportunity to speak carbon dioxide angiography, which is one of my favorite topics and today I will like to talk to you about the value of CO2 angiography for abdominal and pelvic trauma and why and how to use carbon dioxide angiography with massive bleeding and when to supplement CO2 with iodinated contrast.
Disclosures, none. The value of CO2 angiography, what are the advantages perhaps? Carbon dioxide is non-allergic and non-nephrotoxic contrast agent, meaning CO2 is the only proven safe contrast in patients with a contrast allergy and the renal failure.
Carbon dioxide is very highly soluble (20 to 30 times more soluble than oxygen). It's very low viscosity, which is a very unique physical property that you can take advantage of it in doing angiography and CO2 is 1/400 iodinated contrast in viscosity.
Because of low viscosity, now we can use smaller catheter, like a micro-catheter, coaxially to the angiogram using end hole catheter. You do not need five hole catheter such as Pigtail. Also, because of low viscosity, you can detect bleeding much more efficiently.
It demonstrates to the aneurysm and arteriovenous fistula. The other interesting part of the CO2 when you inject in the vessel the CO2 basically refluxes back so you can see the more central vessel. In other words, when you inject contrast, you see only forward vessel, whereas when you inject CO2,
you do a pass with not only peripheral vessels and also see more central vessels. So basically you see the vessels around the lesions and you can use unlimited volumes of CO2 if you separate two to three minutes because CO2 is exhaled by the respirations
so basically you can inject large volumes particularly when you have long prolonged procedures, and most importantly, CO2 is very inexpensive. Where there are basically two methods that will deliver CO2. One is the plastic bag system which you basically fill up with a CO2 tank three times and then empty three times
and keep the fourth time and then you connect to the delivery system and basically closest inject for DSA. The other devices, the CO2mmander with the angio assist, which I saw in the booth outside. That's FDA approved for CO2 injections and is very convenient to use.
It's called CO2mmander. So, most of the CO2 angios can be done with end hole catheter. So basically you eliminate the need for pigtail. You can use any of these cobra catheters, shepherd hook and the Simmons.
If you look at this image in the Levitor study with vascular model, when you inject end hole catheter when the CO2 exits from the tip of catheter, it forms very homogenous bolus, displaces the blood because you're imaging the blood vessel by displacing blood with contrast is mixed with blood, therefore as CO2
travels distally it maintains the CO2 density whereas contrast dilutes and lose the densities. So we recommend end hole catheter. So that means you can do an arteriogram with end hole catheter and then do a select arteriogram. You don't need to replace the pigtail
for selective injection following your aortographies. Here's the basic techniques: Now when you do CO2 angiogram, trauma patient, abdominal/pelvic traumas, start with CO2 aortography. You'll be surprised, you'll see many of those bleeding on aortogram, and also you can repeat, if necessary,
with CO2 at the multiple different levels like, celiac, renal, or aortic bifurcation but be sure to inject below diaphragm. Do not go above diaphragm, for example, thoracic aorta coronary, and brachial, and the subclavian if you inject CO2, you'll have some serious problems.
So stay below the diaphragm as an arterial contrast. Selective injection iodinated contrast for a road map. We like to do super selective arteriogram for embolization et cetera. Then use a contrast to get anomalies. Super selective injection with iodinated contrast
before embolization if there's no bleeding then repeat with CO2 because of low viscocity and also explosion of the gas you will often see the bleeding. That makes it more comfortable before embolization. Here is a splenic trauma patient.
CO2 is injected into the aorta at the level of the celiac access. Now you see the extra vascularization from the low polar spleen, then you catheterize celiac access of the veins. You microcatheter in the distal splenic arteries
and inject the contrast. Oops, there's no bleeding. Make you very uncomfortable for embolizations. We always like to see the actual vascularization before place particle or coils. At that time you can inject CO2 and you can see
actual vascularization and make you more comfortable before embolization. You can inject CO2, the selective injection like in here in a patient with the splenic trauma. The celiac injection of CO2 shows the growth, laceration splenic with extra vascularization with the gas.
There's multiple small, little collection. We call this Starry Night by Van Gogh. That means malpighian marginal sinus with stagnation with the CO2 gives multiple globular appearance of the stars called Starry Night.
You can see the early filling of the portal vein because of disruption of the intrasplenic microvascular structures. Now you see the splenic vein. Normally, you shouldn't see splenic vein while following CO2 injections.
This is a case of the liver traumas. Because the liver is a little more anterior the celiac that is coming off of the anterior aspect of the aorta, therefore, CO2 likes to go there because of buoyancy so we take advantage of buoyancy. Now you see the rupture here in this liver
with following the aortic injections then you inject contrast in the celiac axis to get road map so you can travel through this torus anatomy for embolizations for the road map for with contrast. This patient with elaston loss
with ruptured venal arteries, massive bleeding from many renal rupture with retro peritoneal bleeding with CO2 and aortic injection and then you inject contrast into renal artery and coil embolization but I think the stent is very dangerous in a patient with elaston loss.
We want to really separate the renal artery. Then you're basically at the mercy of the bleeding. So we like a very soft coil but basically coil the entire renal arteries. That was done. - Thank you very much.
- Time is over already? - Yeah. - Oh, OK. Let's finish up. Arteriogram and we inject CO2 contrast twice. Here's the final conclusions.
CO2 is a valuable imaging modality for abdominal and pelvic trauma. Start with CO2 aortography, if indicated. Repeat injections at multiple levels below diaphragm and selective injection road map with contrast. The last advice fo
t air contamination during the CO2 angiograms. Thank you.
- Thank you, Dr. Veith, for this kind invitation. Aberrant origin of the vertebral artery is the second most common aortic arch anomaly. It is more common in patients with thoracic aortic disease when compared to the general population. It's usually of no clinical significance,
except when encountered while treating cerebro-vascular disease or aortic arch pathology. And that's when critical decision-making to preserve its perfusion becomes necessary. This picture illustrates the most common
types of aortic arch anomalies. Led by bovine arch, isolated vertebral artery, and aberrant right side. In this study, it shows a significant correlation with thoracic aortic disease. We first should evaluate the origin
of the vertebral artery. On the right side of the screen you can see the most common type and it's when it's between the left subclavian and the left common carotid artery origin. This is an example of the left vertebral artery
aberrant associated with a mycotic aneurysm of the aortic arch. And this one is a right aberrant vertebral artery associated with a descending thoracic aneurysm and center retroesophageal location. We then look at the variation of
the vertebral artery and posterior circulation. Most commonly dominant left or hypoplasia of the right vertebral artery as shown in the picture. For termination in the posterior inferior cerebellar artery, or PICA.
Or occlusive lesion on the right side, which necessitates perfusion of the left side. This study shows that vertebral artery variations that could need perfusion is up to 30% of patients
with thoracic aortic disease. There are, unfortunately, minimal literature in the vascular, mostly case reports or series. And most of this says procedure data comes from the neurosurgical literature for occlusive disease that shows in this study,
for example, low morbidity, mortality. Complications include thoracic duct injury, recurrent laryngeal nerve, Horner's and CVAs. And they showed high patency rates. The SVS guidelines for left subclavian revasculatization, although low quality,
shows they indicated routine revascularization and they mention some of the indications for left vertebral artery revasculatization. And extrapolating from that, from those guidelines, we summarize the indications for vertebral artery
revascularization dominant ipsilateral left or hypoplastic right. Incomplete circle of Willis, or termination of the left in the PICA artery. Diseased or occluded contralateral vertebral artery.
Extensive aortic coverage or inability to evaluate the circle of Willis prior to intervention. Some technical tips, we use a routine supraclavicular incision. We identify the vertebral artery posterior-medial
location to the common carotid. We carefully preserve the recurrent laryngeal nerve or non-recurrent laryngeal nerve, which is common in aortic arch anomalies. Thoracic duct on the left side. Transpose it to the posterior surface
of the common carotid. And then clamp distal to the anastomosis and to avoid prolonged ischemia to the posterior circulation. This is a completion aortagram that shows patent left vertebral artery transposed
to the common carotid. And then one month follow-up shows that the left vertebral artery is patent with a complete repair of the aorta. So in our experience, we did six vertebral transpositions over
the last couple years, four on the left, two on the right. No perioperative complications. One lost follow-up. And up to 27 months of the patent vessels. In summary, aberrant vertebral artery is uncommon
finding, but associated with thoracic aortic disease. The origin and the course of the vertebral artery should be thoroughly evaluated prior to treatment. Revascularization should be considered in certain situations to avoid
posterior circulation ischemia. But more data is needed to establish guidelines. Thank you.
- So Beyond Vascular procedures, I guess we've conquered all the vascular procedures, now we're going to conquer the world, so let me take a little bit of time to say that these are my conflicts, while doing that, I think it's important that we encourage people to access the hybrid rooms,
It's much more important that the tar-verse done in the Hybrid Room, rather than moving on to the CAT labs, so we have some idea basically of what's going on. That certainly compresses the Hybrid Room availability, but you can't argue for more resources
if the Hybrid Room is running half-empty for example, the only way you get it is by opening this up and so things like laser lead extractions or tar-verse are predominantly still done basically in our hybrid rooms, and we try to make access for them. I don't need to go through this,
you've now think that Doctor Shirttail made a convincing argument for 3D imaging and 3D acquisition. I think the fundamental next revolution in surgery, Every subspecialty is the availability of 3D imaging in the operating room.
We have lead the way in that in vascular surgery, but you think how this could revolutionize urology, general surgery, neurosurgery, and so I think it's very important that we battle for imaging control. Don't give your administration the idea that
you're going to settle for a C-arm, that's the beginning of the end if you do that, this okay to augment use C-arms to augment your practice, but if you're a finishing fellow, you make sure you go to a place that's going to give you access to full hybrid room,
otherwise, you are the subservient imagers compared to radiologists and cardiologists. We need that access to this high quality room. And the new buzzword you're going to hear about is Multi Modality Imaging Suites, this combination of imaging suites that are
being put together, top left deserves with MR, we think MR is the cardiovascular imaging modality of the future, there's a whole group at NIH working at MR Guided Interventions which we're interested in, and the bottom right is the CT-scan in a hybrid op
in a hybrid room, this is actually from MD Anderson. And I think this is actually the Trauma Room of the future, makes no sense to me to take a patient from an emergency room to a CT scanner to an and-jure suite to an operator it's the most dangerous thing we do
with a trauma patient and I think this is actually a position statement from the Trauma Society we're involved in, talk about how important it is to co-localize this imaging, and I think the trauma room of the future is going to be an and-jure suite
down with a CT scanner built into it, and you need to be flexible. Now, the Empire Strikes Back in terms of cloud-based fusion in that Siemans actually just released a portable C-arm that does cone-beam CT. C-arm's basically a rapidly improving,
and I think a lot of these things are going to be available to you at reduced cost. So let me move on and basically just show a couple of examples. What you learn are techniques, then what you do is look for applications to apply this, and so we've been doing
translumbar embolization using fusion and imaging guidance, and this is a case of one of my partners, he'd done an ascending repair, and the patient came back three weeks later and said he had sudden-onset chest pain and the CT-scan showed that there was a
sutured line dehiscence which is a little alarming. I tried to embolize that endovascular, could not get to that tiny little orifice, and so we decided to watch it, it got worse, and bigger, over the course of a week, so clearly we had to go ahead and basically and fix this,
and we opted to use this, using a new guidance system and going directly parasternal. You can do fusion of blood vessels or bones, you can do it off anything you can see on flu-roid, here we actually fused off the sternal wires and this allows you to see if there's
respiratory motion, you can measure in the workstation the depth really to the target was almost four and a half centimeters straight back from the second sternal wire and that allowed us really using this image guidance system when you set up what's called the bullseye view,
you look straight down the barrel of a needle, and then the laser turns on and the undersurface of the hybrid room shows you where to stick the needle. This is something that we'd refined from doing localization of lung nodules
and I'll show you that next. And so this is the system using the C-star, we use the breast, and the localization needle, and we can actually basically advance that straight into that cavity, and you can see once you get in it,
we confirmed it by injecting into it, you can see the pseudo-aneurism, you can see the immediate stain of hematoma and then we simply embolize that directly. This is probably safer than going endovascular because that little neck protects about
the embolization from actually taking place, and you can see what the complete snan-ja-gram actually looked like, we had a pig tail in the aura so we could co-linearly check what was going on and we used docto-gramming make sure we don't have embolization.
This patient now basically about three months follow-up and this is a nice way to completely dissolve by avoiding really doing this. Let me give you another example, this actually one came from our transplant surgeon he wanted to put in a vas,
he said this patient is really sick, so well, by definition they're usually pretty sick, they say we need to make a small incision and target this and so what we did was we scanned the vas, that's the hardware device you're looking at here. These have to be
oriented with the inlet nozzle looking directly into the orifice of the mitro wall, and so we scanned the heart with, what you see is what you get with these devices, they're not deformed, we take a cell phone and implant it in your chest,
still going to look like a cell phone. And so what we did, image fusion was then used with two completely different data sets, it mimicking the procedure, and we lined this up basically with a mitro valve, we then used that same imaging guidance system
I was showing you, made a little incision really doing onto the apex of the heart, and to the eur-aph for the return cannula, and this is basically what it looked like, and you can actually check the efficacy of this by scanning the patient post operatively
and see whether or not you executed on this basically the same way, and so this was all basically developed basing off Lung Nodule Localization Techniques with that we've kind of fairly extensively published, use with men can base one of our thoracic surgeons
so I'd encourage you to look at other opportunities by which you can help other specialties, 'cause I think this 3D imaging is going to transform what our capabilities actually are. Thank you very much indeed for your attention.
- Thank you, and thank you Dr. Veith for the opportunity to present. So, acute aortic syndromes are difficult to treat and a challenge for any surgeon. In regionalization of care of acute aortic syndromes is now a topic of significant conversation. The thoughts are that you can move these patients
to an appropriate hospital infrastructure with surgical expertise and a team that's familiar with treating them. Higher volumes, better outcomes. It's a proven concept in trauma care. Logistics of time, distance, transfer mortality,
and cost are issues of concern. This is a study from the Nationwide Inpatient Sample which basically demonstrates the more volume, the lower mortality for ruptured abdominal aortic aneurysms. And this is a study from Clem Darling
and his Albany Group demonstrating that with their large practice, that if they could get patients transferred to their central hospital, that they had a higher incidence of EVAR with lower mortality. Basically, transfer equaled more EVARs and a
lower mortality for ruptured abdominal aortic aneurysms. Matt Mell looked at interfacility transfer mortality in patients with ruptured abdominal aortic aneurysms to try to see if actually, transfer improved mortality. The take home message was, operative transferred patients
did do better once they reached the institution of destination, however they had a significant mortality during transfer that basically negated that benefit. And transport time, interestingly did not affect mortality. So, regional aortic management, I think,
is something that is quite valuable. As mentioned, access to specialized centers decrease overall mortality and morbidity potentially. In transfer mortality a factor, transport time does not appear to be. So, we set up a rapid transport system
at Keck Medical Center. Basically predicated on 24/7 coverage, and we would transfer any patient within two hours to our institution that called our hotline. This is the number of transfers that we've had over the past three years.
About 250 acute aortic transfers at any given... On a year, about 20 to 30 a month. This is a study that we looked at, that transport process. 183 patients, this is early on in our experience. We did have two that expired en route. There's a listing of the various
pathologies that we treated. These patients were transferred from all over Southern California, including up to Central California, and we had one patient that came from Nevada. The overall mortality is listed here. Ruptured aortic aneurysms had the highest mortality.
We had a very, very good mortality with acute aortic dissections as you can see. We did a univariate and multivariate analysis to look at factors that might have affected transfer mortality and what we found was the SVS score greater than eight
had a very, very significant impact on overall mortality for patients that were transferred. What is a society for vascular surgery comorbidity score? It's basically an equation using cardiac pulmonary renal hypertension and age. The asterisks, cardiac, renal, and age
are important as I will show subsequently. So, Ben Starnes did a very elegant study that was just reported in the Journal of Vascular Surgery where he tried to create a preoperative risk score for prediction of mortality after ruptured abdominal aortic aneurysms.
He found four factors and did an ROC curve. Basically, age greater than 76, creatinine greater than two, blood pressure less than 70, or PH less than 7.2. As you can see, as those factors accumulated there was step-wise increased mortality up to 100% with four factors.
So, rapid transport to regional aortic centers does facilitate the care of acute aortic syndromes. Transfer mortality is a factor, however. Transport mode, time, distance are not associated with mortality. Decision making to deny and accept transfer is evolving
but I think renal status, age, physiologic insult are important factors that have been identified to determine whether transfer should be performed or not. Thank you very much.
- So I'm just going to talk a little bit about what's new in our practice with regard to first rib resection. In particular, we've instituted the use of a 30 degree laparoscopic camera at times to better visualize the structures. I will give you a little bit of a update
about our results and then I'll address very briefly some controversies. Dr. Gelbart and Chan from Hong Kong and UCLA have proposed and popularized the use of a 30 degree laparoscopic camera for a better visualization of the structures
and I'll show you some of those pictures. From 2007 on, we've done 125 of these procedures. We always do venography first including intervascular intervention to open up the vein, and then a transaxillary first rib resection, and only do post-operative venography if the vein reclots.
So this is a 19 year old woman who's case I'm going to use to illustrate our approach. She developed acute onset left arm swelling, duplex and venogram demonstrated a collusion of the subclavian axillary veins. Percutaneous mechanical thrombectomy
and then balloon angioplasty were performed with persistent narrowing at the thoracic outlet. So a day later, she was taken to the operating room, a small incision made in the axilla, we air interiorly to avoid injury to the long thoracic nerve.
As soon as you dissect down to the chest wall, you can identify and protect the vein very easily. I start with electrocautery on the peripheral margin of the rib, and use that to start both digital and Matson elevator dissection of the periosteum pleura
off the first rib, and then get around the anterior scalene muscle under direct visualization with a right angle and you can see that the vein and the artery are identified and easily protected. Here's the 30 degree laparoscopic image
of getting around the anterior scalene muscle and performing the electrocautery and you can see the pulsatile vein up here anterior and superficial to the anterior scalene muscle. Here is a right angle around the first rib to make sure there are no structures
including the pleura still attached to it. I always divide, or try to divide, the posterior aspect of the rib first because I feel like then I can manipulate the ribs superiorly and inferiorly, and get the rib shears more anterior for the anterior cut
because that's most important for decompressing the vein. Again, here's the 30 degree laparoscopic view of the rib shears performing first the posterior cut, there and then the anterior cut here. The portion of rib is removed, and you can see both the artery and the vein
are identified and you can confirm that their decompressed. We insufflate with water or saline, and then perform valsalva to make sure that they're hasn't been any pneumothorax, and then after putting a drain in,
I actually also turn the patient supine before extirpating them to make sure that there isn't a pneumothorax on chest x-ray. You can see the Jackson-Pratt drain in the left axilla. One month later, duplex shows a patent vein. So we've had pretty good success with this approach.
23 patients have requires post operative reintervention, but no operative venous reconstruction or bypass has been performed, and 123 out of 125 axillosubclavian veins have been patent by duplex at last follow-up. A brief comment on controversies,
first of all, the surgical approach we continue to believe that a transaxillary approach is cosmetically preferable and just as effective as a paraclavicular or anterior approach, and we have started being more cautious
about postoperative anticoagulation. So we've had three patients in that series that had to go back to the operating room for washout of hematoma, one patient who actually needed a VATS to treat a hemathorax,
and so in recent times we've been more cautious. In fact 39 patients have been discharged only with oral antiplatelet therapy without any plan for definitive therapeutic anticoagulation and those patients have all done very well. Obviously that's contraindicated in some cases
of a preoperative PE, or hematology insistence, or documented hypercoagulability and we've also kind of included that, the incidence of postop thrombosis of the vein requiring reintervention, but a lot of patients we think can be discharged
on just antiplatelets. So again, our approach to this is a transaxillary first rib resection after a venogram and a vascular intervention. We think this cosmetically advantageous. Surgical venous reconstruction has not been required
in any case, and we've incorporated the use of a 30 degree laparoscopic camera for better intraoperative visualization, thanks.
- Thank you. Here are my disclosures. Our preferred method for zone one TAVR has evolved to a carotid/carotid transposition and left subclavian retro-sandwich. The technique begins with a low transverse collar incision. The incision is deepened through the platysma
and subplatysmal flaps are then elevated. The dissection is continued along the anterior border of the sternocleidomastoid entering the carotid sheath anteromedial to the jugular vein. The common carotid artery is exposed
and controlled with a vessel loop. (mumbling) The exposure's repeated for the left common carotid artery and extended as far proximal to the omohyoid muscle as possible. A retropharyngeal plane is created using blunt dissection
along the anterior border of the cervical vertebra. A tunneling clamp is then utilized to preserve the plane with umbilical tape. Additional vessel loops are placed in the distal and mid right common carotid artery and the patient is systemically anticoagulated.
The proximal and distal vessel loops are tightened and a transverse arteriotomy is created between the middle and distal vessel loops. A flexible shunt is inserted and initially secured with the proximal and middle vessel loops. (whistling)
It is then advanced beyond the proximal vessel loop and secured into that position. The left common carotid artery is then clamped proximally and distally, suture ligated, clipped and then transected. (mumbling)
The proximal end is then brought through the retropharyngeal tunnel. - [Surgeon] It's found to have (mumbles). - An end-to-side carotid anastomosis is then created between the proximal and middle vessel loops. If preferred the right carotid arteriotomy
can be made ovoid with scissors or a punch to provide a better shape match with the recipient vessel. The complete anastomosis is back-bled and carefully flushed out the distal right carotid arteriotomy.
Flow is then restored to the left carotid artery, I mean to the right carotid artery or to the left carotid artery by tightening the middle vessel loop and loosening the proximal vessel loop. The shunt can then be removed
and the right common carotid artery safely clamped distal to the transposition. The distal arteriotomy is then closed in standard fashion and flow is restored to the right common carotid artery. This technique avoids a prosthetic graft
and the retropharyngeal space while maintaining flow in at least one carotid system at all times. Once, and here's a view of the vessels, once hemostasis is assured the platysma is reapproximated with a running suture followed by a subcuticular stitch
for an excellent cosmetic result. Our preferred method for left subclavian preservation is the retro-sandwich technique which involves deploying an initial endograft just distal to the left subclavian followed by both proximal aortic extension
and a left subclavian covered stent in parallel fashion. We prefer this configuration because it provides a second source of cerebral blood flow independent of the innominate artery
and maintains ready access to the renovisceral vessels if further aortic intervention is required in the future. Thank you.
- Thank you. No relevant disclosures to this presentation. The means to the end is removing Uremic toxins. That's what we want to do. That's what this is all about. We don't really know all the Uremic toxins and how they inter-relate, but there are a bunch
of compounds that have been identified. Urea obviously being one of them, although not necessarily being a particularly toxic compound. It's a small molecular weight marker of Uremia, which is convenient to use
if not clinically meaningful. We've developed, or Frank Gotch and Sargent developed this dimensionless concept of the Kt/V, an index of the body volume water space, which has been cleared fully of Urea and this index has been the standard for comparing dosing of dialysis for about 30 years now.
Since the National Cooperative Dialysis Study in the 80's. And the most recent iteration of this study has been the HEMO study in 2002, I believe this was published. Where they compared a high dose of Kt/V of 1.71 versus standard dose Kt/V of 1.3 and looked at patient outcomes and they were
concluding that the higher dose of dialysis wasn't beneficial. But this 1.3 was certainly better than we were seeing in the old days of 0.9 out of the NKDS studies, so 1.3 or that range has been accepted as the target dose
for dialysis and KDOQI guidelines now suggest that we strive to achieve a single pool Kt/V of 1.4, so we have a little cushion with a minimum delivery of 1.2, and that has been adopted now by CMS and the payers.
That's in our conditions for coverage that we achieve or we strive for a Kt/V 1.2 and now we have this quality incentive program, which might relate a little bit to the question earlier about saving access as we get penalized or incentivized
for doing certain things, and right in our penalty methodology in the top categories Kt/V, if we don't hit that target we get dinged up to 2% of the total payment for dialysis on that.
So it's something that's being identified, monitored, and if you like ... Not negatively incentivized. It's not a reward. It's a penalty for failing to achieve. And also you can go to dialysiscompare.gov now.
You login your unit. Here's my little unit in Hockessin. We got four stars. A nearby unit got three stars. They're really just as good as us, but somebody thinks those stars mean something,
and one of the components in those stars is hitting your Kt/V target, so if I want to get stars and not be seen as a poor performing unit, I need to hit these performance parameters, so that's why the Kt/V is the holy grail for Nephrologist. We need to get that number.
It's a very simple concept. Mathematically, you've got two items in the numerator and one in the denominator, and you want to maximize that parameter. Number one we can dispense with the volume of distribution
of Urea is pretty much determined by the patient. It's total body of water times the fraction. It varies a lot depending on the age, weight, gender, obesity, etc. You can put it in the calculator and same qx metal to deliver that number for you.
But we can't really change that, unless somebody has an amputation, or a large amount of weight loss or gain, then it changes. Time we have complete control over. We can dialyze theoretically as long as we want and in the U.S. we sort of like
to believe four hours has been adopted as a standard. There are some recommendations that wouldn't do that. Patient acceptance of that is variable. I can sit in front of a patient and tell them they need four and half hours, and they may look at me askance,
because they know they don't want it, and if you look at dialysis times in different countries, you can see certain countries like Germany, typically dialyzes closer to three hours. Typical dialysis time in the United States is more like... Did I say three hours?
I meant five hours. And typical dialysis time in the United States is about three and a half hours. There are also resource limitations and cost involved in that. So the third variable is the one we have
the most control over, which is the clearance of Urea. And that's depending on the dialyze of the blood, in the blood, out. the dialyze of that... capacity of that filter to remove the solute of interest, Urea in this case in a dialysate flow,
and there are specs for each kidney. Here is a Optiflux F160 at a blood flow of 300 and a dialysate flow of 500. It predicts we should get a Urea clearance of 271 mL per minute, or conversely a larger kidney, an F180 had a blood flow of 500, a dialysate flow of 800.
We should get a Urea clearance of 412. Obviously, none of these are perfect clearances. The maximum theoretical clearance would be that of the blood speed, but it's impossible to clear it 100% of the blood. So when your asked as a surgeon or a provincialist
to make a functional access what your Nephrologist is really asking for in a customer service world is give me a fistula that flows 150% higher. 150% of my intended pump speed and we're good to go. Need a little cushion on that as well.
And here's how it translates into action. Here's an example on a calculator. Here's a patient, who's a 70 kilogram female, dialysis time three and a half hours, 210 minutes. Her Kt/V calculates at 1.77. All good.
Same parameters three and a half hours, 120 kilogram, 40 year old male. His Kt/V is 0.96, clearly below the target. You're not going to get that guy's clearance with those parameters. If you goose him up to 500 mL per minute
on a minute on a bigger kidney and you achieve a clearance of 410, then the same male with the same treatment parameters will get 1.45, so you've met their target. If you want to do better than targets just put him on four hours and you only get 1.66,
so these are very easily definable, measurable, predictable quantities that you can achieve. And then you've got limiting factors. What is the pump speed? Well, hemolysis through needles is really an overstated concern.
This arterial negative pressure alarm won't let you go below 250 on this machine and if-- 300 is it Debbie? 250, 300 and at that point it will cut off, so you won't be able to drive the negative pressure that high,
and so you've got parameters for each needle, which are fairly fixed, a little latitude in it, but with 17-gauge needle you can go up to 300 and so on. With a 14-gauge needle you can go up to 500 or more, and it's a pretty si le higher flow.
And here's a case where you've got a 2 millimeter radial artery, a small fistula. The access flow measures at 450. You can dialyze at a blood speed of 300 with a 17-gauge needle and you're good to go. Where as you got a huge brachial artery here.
This access flow is greater than 2000. You can run the blood speed at whatever you want. And you can use a needle size of 14-gauge. You can put whatever needle size you want in this fistula. So the point is that one size doesn't fit all. Dialysis dose, and dialysis needles,
and dialysis fistulas need to be scaled to the size of the patient. You got a neonate. You got Shaquille O'Neal. Somewhere in between is our patient. Thank you.
- I will be talking about new KDOQI guidelines. I know many of you have heard about KDOQI guidelines being revised for the past maybe over a year or maybe two. Yes, it is being done, and it is going slow only because it's being done in a very different way. It's more than an update.
It's going to be more of an overhaul for the entire KDOQI guidelines. We in KDOQI have looked at access as a solitary problem like we talked about grafts, catheters, fistulas for access, but actually it sort of turns out
that access is part of a bigger problem. Fits into a big ESKD lifeline of a patient. Instated distal patients come in many varieties. It can affect any age, and they have a lot of other problems so once you have chronic renal failure, renal replacement mortality fits in
only when it becomes Stage IV or Stage V. And renal replacement mortality is not just access, it is PD access, it's hemo access, it is transplant. So these things, we need to see how they fit in in a given person. So the new KDOQI guidelines concentrates more
on individualizing care. For example, here the young Darien was an 11 year old with a prune belly syndrome. Now he has failed PD. Then there's another person here who is Lydia who is about 36 or 40 year old lady
with a insulin dependent diabetes. Already has bad vascular pedicle. Lost both legs. Needs access. Now both these patient though they need access, it's not the same.
It's different. For example, if you think of Darien, he was in PD but he has failed PD. We would love to get him transplanted. Unfortunately he's got terrible social situation so we can't get him transplanted.
So he needs hemo. Now if he needs hemo, we need to find an access that lasts for a long time because he's got many years ahead of him. On the other hand we have Lydia, who has got significant vascular disease.
With her obesity and existing infectious status, probably PD won't be a good option for her. So she needs hemo, and she's obviously not a transplant candidate. So how are we going to plan for hemo? So these are things which we are to more concentrate
and individualize when we look at patients, and the new guidelines concentrate more on these sort of aspects. Doing right access for right patient, right time, and for right reasons. And we go about planning this keeping the patient first
then a life plan ESKD lifeline for the patient, and what access we are looking at, and what are the needs of the patient? Now this is also different because it has been done more scientifically. We actually have a evidence review team.
We just poured over pretty much 1500 individual articles. Recent articles. And we have looked through about 4000 abstracts and other articles. And this data is correlated through a workgroup. There a lot of new chapters.
Chapter specific surgery like peri-operative, intra-operative, post-operative, cat issues, managing complication issues. And we started off with the coming up with the Scope of Work. The evidence review team took the Scope of Work
and tried to get all the articles and sift through the articles and came up and rated the evidence using a certain rating system which is very scientific. The workgroup then kind of evaluated the whole system, and then came up with what is clinically relevant.
It's one thing for statisticians to say how strong evidence this is, but it's another thing how it is looked upon by the clinicians. So then we kind of put this into a document. Document went through internal and external review process.
This is the process we have tried to do it. Dr. Lok has been the Chair of the group. Myself and Dr. Yevzlin are the Vice-Chairs. We have incredible workgroup which has done most of the work. And here are the workgroup members.
We comprised of nephrologist, transplant surgeons, vascular surgeons, Allied Health personnel, pediatric nephrologist so it's a multi interventional radiologist and interventional nephrologist. This is a multi disciplinary group which has gone through this process.
Timothy Wilt from Minnesota was the head of the Evidence Review Team, who has worked on the evidence building. And now for the editorial sections we have Dr. Huber, Lee, and Dr. Lok taking care of it. So where are we today?
We have pretty much gone through the first part of it. We are at the place where we are ready for the Internal Review and External Review. So many of you probably will get a chance to look through it when it comes for the External Review and would love
to have your comments on this document. Essentially, we are looking at access in the context of end stage renal disease, and that is new. And obviously we have gone through and done a very scientific review, a very scientific methodology to try
to evaluate the evidence and try to come up with guidelines. Thank you.
- Thank you very much for the kind introduction, and I'd like to thank the organizers, especially Frank Veith for getting back to this outstanding and very important conference. My duty is now to talk about the acute status of carotid artery stenting is acute occlusion an issue? Here are my disclosures.
Probably you might be aware, for sure you're aware about pore size and probably smaller pore size, the small material load might be a predisposing factor for enhanced thrombogenicity in these dual layer stents, as you're probably quite familiar with the CGUARD, Roadsaver and GORE, I will focus my talk a little bit
on the Roadsaver stent, since I have the most experience with the Roadsaver stent from the early beginning when this device was on the market in Europe. If you go back a little bit and look at the early publications of CGUARD, Roadsaver and GORE stent, then acute occlusion the early reports show that
very clearly safety, especially at 30 days in terms of major cardiac and cerebrovascular events. They are very, very safe, 0% in all these early publications deal with these stents. But you're probably aware of this publication, released end of last year, where a German group in Hamburg
deals with carotid artery stenosis during acute stroke treatment. They used the dual layer stent, the Roadsaver stent or the Casper stent in 20 cases, in the same time period from 2011 to 2016, they used also the Wallstent and the VIVEXX stent,
in 27 cases in total and there was a major difference, in terms of acute stent occlusion, and for the Roadsaver or Casper stent, it was 45%, they also had an explanation for that, potential explanations probably due to the increase of thrombogenic material due to the dual layer
insufficient preparation with antiplatelet medication, higher patient counts in the patients who occluded, smaller stent diameters, and the patients were not administered PTA, meaning Bridging during acute stroke patient treatment, but it was highlighted that all patients received ASA of 500mg intravenously
during the procedure. But there are some questions coming up. What is a small stent diameter? Post-dilatation at what diameter, once the stent was implanted? What about wall apposition of the stent?
Correct stent deployment with the Vicis maneuver performed or not and was the ACT adjusted during the procedure, meaning did they perform an adequate heparinization? These are open questions and I would like to share our experience from Flensburg,
so we have treated nearly 200 patients with the Roadsaver stent from 2015 until now. In 42 patients, we used this stent exclusively for acute stroke treatment and never, ever observed in both groups, in the symptomatic and asymptomatic group and in the group of acute stroke treatment,
we never observed an acute occlusion. How can we explain this kind of difference that neither acute occlusion occurred in our patient group? Probably there are some options how we can avoid stent thrombosis, how we can minimize this. For emergency treatment, probably this might be related
to bridging therapies, though in Germany a lot of patients who received acute stroke treatment are on bridging therapy since the way to the hospital is sometimes rather long, there probably might be a predisposing factor to re-avoid stent thrombosis and so-called tandem lesions if the stent placement is needed.
But we also take care of antiplatelet medication peri-procedurally, and we do this with ASA, as the Hamburg group did and at one day, we always start, in all emergency patients with clopidogrel loading dose after positive CT where we could exclude any bleeding and post-procedurally we go
for dual anti-platelet therapy for at least six months, meaning clopidogrel and ASA, and this is something probably of utmost importance. It's quite the same for elective patients, I think you're quite familiar with this, and I want to highlight the post-procedural clopidogrel
might be the key of success for six months combined with ASA life-long. Stent preparation is also an issue, at least 7 or 8 diameters we have to choose for the correct lengths we have to perform adequate stent deployment and adequate post-dilatation
for at least 5mm. In a lot of trials the Roadsaver concept has been proven, and this is due to the adequate preparation of the stent and ongoing platelet preparation, and this was also highlight in the meta-analysis with the death and stroke rate of .02% in all cases.
Roadsaver study is performed now planned, I am a member of the steering committee. In 2000 patients, so far 132 patients have been included and I want to rise up once again the question, is acute occlusion and issue? No, I don't think so, since you keep antiplatelet medication
in mind and be aware of adequate stent sizing. I highly appreciated your attention, thank you very much.
- Thank you very much and I would like to thank Dr. Veit for the kind invitation, this is really great meeting. Those are my disclosures. Percutaneous EVAR has been first reported in the late 1990's. However, for many reasons it has not been embraced
by the vascular community, despite the fact that it has been shown that the procedure can be done under local anesthesia and it decreases OR time, time to ambulation, wound complication and length of stay. There are three landmark papers which actually change this trend and make PEVAR more popular.
All of these three papers concluded that failure or observed failure of PEVAR are observed and addressed in the OR which is a key issue. And there was no late failures. Another paper which is really very prominent
is a prospective randomize study that's reported by Endologix and published in 2014. Which revealed that PEVAR closure of the arteriotomy is not inferior to open cut down. Basically, this paper also made it possible for the FDA to approve the device, the ProGlide device,
for closure of large bore arteriotomies, up to 26 in the arterial system and 29 in the venous system. We introduced percutaneous access first policy in our institution 2012. And recently we analyzed our results of 272 elective EVAR performed during the 2012 to 2016.
And we attempted PEVAR in 206 cases. And were successful in 92% of cases. But the question was what happened with the patient that failed PEVAR? And what we found that was significantly higher thrombosis, vessel thrombosis,
as well as blood loss, more than 500 cc in the failed PEVAR group. Similarly, there was longer operative time and post-operative length of stay was significantly longer. However, in this relatively small group of patients who we scheduled for cut-down due to different reasons,
we found that actually there was no difference between the PEVAR and the cut-down, failed PEVAR and cut-down in the terms of blood loss, thrombosis of the vessel, operative time and post-operative length of stay. So what are the predictors of ProGlide failure?
Small vessel calcification, particularly anterior wall calcification, prior cut-down and scarring of the groin, high femoral bifurcation and use of large bore sheaths, as well as morbid obesity. So how can we avoid failures?
I think that the key issue is access. So we recommend that all access now or we demand from our fellow that when we're going to do the operation with them, cut-down during fluoroscopy on the ultra-sound guidance, using micropuncture kits and access angiogram is actually mandatory.
But what happened when there is a lack of hemostasis once we've deployed two PEVARs? Number one, we try not to use more than three ProGlide on each side. Once the three ProGlide failed we use the angioseal. There's a new technique that we can have body wire
and deployed angioseal and still have an access. We also developed a technique that we pack the access site routinely with gelfoam and thrombin. And also we use so-called pull and clamp technique, shown here. Basically what it is, we pull the string of the ProGlide
and clamp it on the skin level. This is actually a very very very good technique. So in conclusion, PEVAR first approach strategy successful in more than 90% of cases, reduced operative time and postoperative length of stay, the failure occurred more commonly when the PEVAR
was completed outside of IFU, and there was no differences in outcome between failed PEVAR and planned femoral cut-down. Thank you.
- I'd like to share with you our experience using tools to improve outcomes. These are my disclosures. So first of all we need to define the anatomy well using CTA and MRA and with using multiple reformats and 3D reconstructions. So then we can use 3D fusion with a DSA or with a flouro
or in this case as I showed in my presentation before you can use a DSA fused with a CT phase, they were required before. And also you can use the Integrated Registration like this, when you can use very helpful for the RF wire
because you can see where the RF wire starts and the snare ends. We can also use this for the arterial system. I can see a high grade stenosis in the Common iliac and you can use the 3D to define for your 3D roadmapping you can use on the table,
or you can use two methods to define the artery. Usually you can use the yellow outline to define the anatomy or the green to define the center. And then it's a simple case, 50 minutes, 50 minutes of ccs of contrast,
very simple, straightforward. Another everybody knows about the you know we can use a small amount of contrast to define the whole anatomy of one leg. However one thing that is relatively new is to use a 3D
in order to map, to show you the way out so you can do in this case here multiple segmental synosis, the drug-eluting-balloon angioplasty using the 3D roadmap as a reference. Also about this case using radial fre--
radial access to peripheral. Using a fusion of image you can see the outline of the artery. You can see where the high grade stenosis is with a minimum amount of contrast. You only use contrast when you are about
to do your angiogram or your angioplasty and after. And that but all everything else you use only the guide wires and cathers are advanced only used in image guidance without any contrast at all. We also been doing as I showed before the simultaneous injection.
So here I have two catheters, one coming from above, one coming from below to define this intravenous occlusion. Very helpful during through the and after the 3D it can be helpful. Like in this case when you can see this orange line is where
the RF wire is going to be advanced. As you can see the breathing, during the breathing cycle the pleura is on the way of the RF wire track. Pretty dangerous stuff. So this case what we did we asked the anesthesiologist
to have the patient in respiratory breath holding inspiration. We're able to hyperextend the lungs, cross with the RF wire without any complication. So very useful. And also you can use this outline yellow lines here
to define anatomy can help you to define where you need to put the stents. Make sure you're covering everything and having better outcomes at the end of the case without overexposure of radiation. And also at the end you can use the same volt of metric
reconstruction to check where you are, to placement of the stent and if you'd covered all the lesion that you had. The Cone beam CT can be used for also for the 3D model fusion. As you can see that you can use in it with fluoro as I
mentioned before you can do the three views in order to make sure that the vessels are aligned. And those are they follow when you rotate the table. And then you can have a pretty good outcome at the end of the day at of the case. In that case that potentially could be very catastrophic
close to the Supra aortic vessels. What about this case of a very dramatic, symptomatic varicose veins. We didn't know and didn't even know where to start in this case. We're trying to find our way through here trying to
understand what we needed to do. I thought we need to recanalize this with this. Did a 3D recan-- a spin and we saw ours totally off. This is the RFY totally interior and the snare as a target was posterior in the ASGUS.
Totally different, different plans. Eventually we found where we needed to be. We fused with the CAT scan, CT phase before, found the right spot and then were able to use
Integrated registration for the careful recanalization above the strip-- interiorly from the Supraaortic vessels. As you can see that's the beginning, that's the end. And also these was important to show us where we working.
We working a very small space between the sternal and the Supraaortic vessels using the RF wire. And this the only technology would allowed us to do this type of thing. Basically we created a percutaneous in the vascular stent bypass graft.
You can you see you use a curved RF wire to be able to go back to the snare. And that once we snare out is just conventional angioplasty recanalized with covered stents and pretty good outcome. On a year and a half follow-up remarkable improvement in this patient's symptoms.
Another patient with a large graft in the large swelling thigh, maybe graft on the right thigh with associated occlusion of the iliac veins and inclusion of the IVC and occlusion of the filter. So we did here is that we fused the maps of the arterial
phase and the venous phase and then we reconstruct in a 3D model. And doing that we're able to really understand the beginning of the problem and the end of the problem above the filter and the correlation with the arteries. So as you can see,
the these was very tortuous segments. We need to cross with the RF wire close to the iliac veins and then to the External iliac artery close to the Common iliac artery. But eventually we were able to help find a track. Very successfully,
very safe and then it's just convention technique. We reconstructed with covered stents. This is predisposed, pretty good outcome. As you can see this is the CT before, that's the CT after the swelling's totally gone
and the stents are widely open. So in conclusion these techniques can help a reduction of radiation exposure, volume of contrast media, lower complication, lower procedure time.
In other words can offer higher value in patient care. Thank you.
- Dear Chairman, Ladies and Gentlemen, Thank you Doctor Veith. It's a privilege to be here. So, the story is going to be about Negative Pressure Wound Non-Excisional Treatment from Prosthetic Graft Infection, and to show you that the good results are durable. Nothing to disclose.
Case demonstration: sixty-two year old male with fem-fem crossover PTFE bypass graft, Key infection in the right groin. What we did: open the groin to make the debridement and we see the silergy treat, because the graft is infected with the microbiology specimen
and when identified, the Enterococcus faecalis, Staphylococcus epidermidis. We assess the anastomosis in the graft was good so we decided to put foam, black foam for irrigation, for local installation of antiseptics. This our intention-to treat protocol
at the University hospital, Zurich. Multi-staged Negative Pressure for the Wound Therapy, that's meets vascular graft infection, when we open the wound and we assess the graft, and the vessel anastomosis, if they are at risk or not. If they are not at risk, then we preserve the graft.
If they are at risk and the parts there at risk, we remove these parts and make a local reconstruction. And this is known as Szilagyi and Samson classification, are mainly validated from the peripheral surgery. And it is implemented in 2016 guidelines of American Heart Association.
But what about intracavitary abdominal and thoracic infection? Then other case, sixty-one year old male with intracavitary abdominal infection after EVAR, as you can see, the enhancement behind the aortic wall. What we are doing in that situation,
We're going directly to the procedure that's just making some punctures, CT guided. When we get the specimen microbiological, then start with treatment according to the microbiology findings, and then we downgrade the infection.
You can see the more air in the aneurism, but less infection periaortic, then we schedule the procedure, opening the aneurysm sac, making the complete removal of the thrombus, removing of the infected part of the aneurysm, as Doctor Maelyna said, we try to preserve the graft.
That exactly what we are doing with the white foam and then putting the black foam making the Biofilm breakdown with local installation of antiseptics. In some of these cases we hope it is going to work, and, as you see, after one month
we did not have a good response. The tissue was uneager, so we decided to make the removal of the graft, but, of course, after downgrading of this infection. So, we looked at our data, because from 2012 all the patients with
Prostetic Graft infection we include in the prospective observational cohort, known VASGRA, when we are working into disciplinary with infectious disease specialist, microbiologists, radiologist and surgical pathologist. The study included two group of patients,
One, retrospective, 93 patient from 1999 to 2012, when we started the VASGRA study. And 88 patient from April 2012 to Seventeen within this register. Definitions. Baseline, end of the surgical treatment and outcome end,
the end of microbiological therapy. In total, 181 patient extracavitary, 35, most of them in the groin. Intracavitary abdominal, 102. Intracavitary thoracic, 44. If we are looking in these two groups,
straight with Negative Pressure Wound Therapy and, no, without Negative Pressure Wound Therapy, there is no difference between the groups in the male gender, obesity, comorbidity index, use of endovascular graft in the type Samson classification,
according to classification. The only difference was the ratio of hospitalization. And the most important slide, when we show that we have the trend to faster cure with vascular graft infection in patients with Negative Pressure Wound Therapy
If we want to see exactly in the data we make uni variant, multi variant analysis, as in the initial was the intracavitary abdominal. Initial baseline. We compared all these to these data. Intracavitary abdominal with no Pressure Wound Therapy
and total graft excision. And what we found, that Endovascular indexoperation is not in favor for faster time of cure, but extracavitary Negative Pressure Wound Therapy shows excellent results in sense of preserving and not treating the graft infection.
Having these results faster to cure, we looked for the all cause mortality and the vascular graft infection mortality up to two years, and we did not have found any difference. What is the strength of this study, in total we have two years follow of 87 patients.
So, to conclude, dear Chairman, Ladies and Gentlemen, Explant after downgrading giving better results. Instillation for biofilm breakdown, low mortality, good quality of life and, of course, Endovascular vascular graft infection lower time to heal. Thank you very much for your attention.
- Thank you Mr. Chairman. Ladies and gentleman, first of all, I would like to thank Dr. Veith for the honor of the podium. Fenestrated and branched stent graft are becoming a widespread use in the treatment of thoracoabdominal
and pararenal aortic aneurysms. Nevertheless, the risk of reinterventions during the follow-up of these procedures is not negligible. The Mayo Clinic group has recently proposed this classification for endoleaks
after FEVAR and BEVAR, that takes into account all the potential sources of aneurysm sac reperfusion after stent graft implant. If we look at the published data, the reported reintervention rate ranges between three and 25% of cases.
So this is still an open issue. We started our experience with fenestrated and branched stent grafts in January 2016, with 29 patients treated so far, for thoracoabdominal and pararenal/juxtarenal aortic aneurysms. We report an elective mortality rate of 7.7%.
That is significantly higher in urgent settings. We had two cases of transient paraparesis and both of them recovered, and two cases of complete paraplegia after urgent procedures, and both of them died. This is the surveillance protocol we applied
to the 25 patients that survived the first operation. As you can see here, we used to do a CT scan prior to discharge, and then again at three and 12 months after the intervention, and yearly thereafter, and according to our experience
there is no room for ultrasound examination in the follow-up of these procedures. We report five reinterventions according for 20% of cases. All of them were due to endoleaks and were fixed with bridging stent relining,
or embolization in case of type II, with no complications, no mortality. I'm going to show you a couple of cases from our series. A 66 years old man, a very complex surgical history. In 2005 he underwent open repair of descending thoracic aneurysm.
In 2009, a surgical debranching of visceral vessels followed by TEVAR for a type III thoracoabdominal aortic aneurysms. In 2016, the implant of a tube fenestrated stent-graft to fix a distal type I endoleak. And two years later the patient was readmitted
for a type II endoleak with aneurysm growth of more than one centimeter. This is the preoperative CT scan, and you see now the type II endoleak that comes from a left gastric artery that independently arises from the aneurysm sac.
This is the endoleak route that starts from a branch of the hepatic artery with retrograde flow into the left gastric artery, and then into the aneurysm sac. We approached this case from below through the fenestration for the SMA and the celiac trunk,
and here on the left side you see the superselective catheterization of the branch of the hepatic artery, and on the right side the microcatheter that has reached the nidus of the endoleak. We then embolized with onyx the endoleak
and the feeding vessel, and this is the nice final result in two different angiographic projections. Another case, a 76 years old man. In 2008, open repair for a AAA and right common iliac aneurysm.
Eight years later, the implant of a T-branch stent graft for a recurrent type IV thoracoabdominal aneurysm. And one year later, the patient was admitted again for a type IIIc endoleak, plus aneurysm of the left common iliac artery. This is the CT scan of this patient.
You will see here the endoleak at the level of the left renal branch here, and the aneurysm of the left common iliac just below the stent graft. We first treated the iliac aneurysm implanting an iliac branched device on the left side,
so preserving the left hypogastric artery. And in the same operation, from a bowl, we catheterized the left renal branch and fixed the endoleak that you see on the left side, with a total stent relining, with a nice final result on the right side.
And this is the CT scan follow-up one year after the reintervention. No endoleak at the level of the left renal branch, and nice exclusion of the left common iliac aneurysm. In conclusion, ladies and gentlemen, the risk of type I endoleak after FEVAR and BEVAR
is very low when the repair is planning with an adequate proximal sealing zone as we heard before from Professor Verhoeven. Much of reinterventions are due to type II and III endoleaks that can be treated by embolization or stent reinforcement. Last, but not least, the strict follow-up program
with CT scan is of paramount importance after these procedures. I thank you very much for your attention.
- [Narrator] Good morning everyone. Again, thank you Dr. Veith for inviting me for this legendary meeting. I just love your meeting, thank you very much. Here you have my disclosures, I have said that the T-Branch device from Cook is not commercialized in the US
but it is in South America, now it's in Europe. Our presentation today is based in our article published German Vascular Therapy last year in August, Advanced technical considerations for implanting the T-branch off the shelf.
Branches stent-graft to treat Thoracoabdominal Aneurysms. I'm sure most of you already know this device. It's a off the shelf device from Cook. It has 202 millimeters in length. The proximal stent is 34 millimeters, the distal stent is 18 millimeters.
Of course, it has also four downward branch, so you have to adapt the anatomy of your patient and then to use this device in many situations. Here is a simple example, you can use this device in perirenal or superrenal aneurysms type 4. Just cutting one or two of the proximal stents.
Just be aware to (mumbles) the device in the (mumbles). So you can avoid the migration of the device. That's a good way to diminish the risks of paraplegia for you patient. The same way you can now cut the distal portion one or two stents, so and in cases you have
a previous device, you can pipe one in the leak, is we can show in cases, maxes lights, you can use this device. Also, the second component to anybody of the device, the bifurcated component can be cut. You can cut the proximal stents, you can cut
the distal stents, you can make that straight graft. So just like that, use it in many circumstances. And this is one of the maneuvers we use very often. We call that device driven by the sheath because you do a through and through wire and then you put that set the nose of our device
inside the sheath that come from the arm. So it helps by the avoid your device to touch the aort wall or even devices previously inserted. And also allow you to rotate the device to a correct position. Another maneuver is snare-ride technique that
we have already described in the Journal Endovascular Therapy last year. It's a very simple way so we can bring from the femoral access, we can bring the snare inside the one artery and that snare can capture a wire come from the arm, so we can
hold the position inside the target vessel. Here, an example that you can see all those maneuvers. This patient has a previous I-stent surgery and then the device that is probably the false lumen all the vessels come from this true lumen, which is secluded like capsule decortication.
They have minimal aortic communication. They've going to seen more details in the next slides. So here you can see the case that is a communication close to the celiac track and then is stuck. And then you have another communication, the intrarenal aort are very thin.
So here is a draw, you can see the first challenge was could we move a sheath, 12 branch sheath across the (mumbles) in the thin aorta and put that in the thin aorta, so without that, we could not do the case. We start the case doing that and as you can see,
we see that it was possible to do that, so we continue in the case. Following are challenges you will face was would we be able to cross this aort, very thin channel and to go there, to put the device here, and then to put the t-branch device to
all the branches from this true lumen. So here is our study, our plan was if you cross that communication, we put a t-branch here and used the celiac branch to TAAAs. Left renal artery, the celiac branch, the mysentary to branch the celiac artery, the left renal branch
to the mysentary artery and then right renal branch to right renal branch. So, that proves to be feasible. We could graft that communication and that adversary straight device to start the (cuts off). So here you see that the things
happened exactly as we planned it. The celiac was done by the SMA branch, the SMA done by the left renal, and the right renal by the right renal. At that point, we consider the game over. (cuts off) who could try the
celiac branch to the left renal. The angle was not preferable, so we come from the femoral artery in have access to left renal and open (mumbles) there and the diverse that wire should be put inside the left renal. Here you see the maneuver completed.
We advanced and hold the stent so we can have this branch also done. Here, you have a closed view of the left renal branch done by the celiac branch of the device. And now we have the final result of the branch done. How the bifurcate the device of completely
excluding the false movement of this complex dissection. So to illustrate this presentation, I bring you the control, one week control of this patient and could we fold the breasts where (mumbles) did it in the dissection, totally excluded from the circulation.
So, in conclusion ladies and gentlemen, I would say that the use of the branched stent-grafts in the treatment of Thoracoabdominal use is proven feasible, safe, and the off-the-shelf multibranched t-branch can be used in both urgent and elective scenarios.
Employing adjunctive maneuvers can increase the anatomic suitability of rience, these techniques have increased the applicability to 80 percent of the cases, included dissections of the small lumen.
I want to thank you all for your kind attention. Thank you, again, Frank for accepting my talk recorded. And I'm very pleased to answer questions by email or WhatsApp as you can see, this is live. Thank you very much.
- (speaks French) liver surgeon I perform hepatobiliary surgery and liver transplantation. Maybe I don't belong here, I so probably more rested than anybody in the room here. But today I will present about liver surgery and hepatectomy. I work at The Royal Free where I have the honor and pleasure to have seen Krassi. We are in the
little island in the North Sea. There is many things going wrong there including Brexit but, the guys uh, we have a major advantage. The NHS favors centralization. Centralization look there: London is bigger than New York Uh, eight million, 50 million greater London
and we drain about six millions of people with our HPB center. In the center we perform about 2,000 operations, of major surgery. In five years, half of them are liver surgery. And most of them have uh, benign, malignant tumor. A very small percentage have benign tumor.
I count here for complications uh, and mortality look there, 3.1% of only the malignant because the benign are young people and we perform a different strategy, they have no mortality. Today Hepatic Hemangioma, look there it is uh, 1898 is a key year. Not only the first description
of the lady that died after bleeding out in an autopsy but also, Hermann Pfannenstiel uh, Professor Pfannenstiel. I will introduce you to him. He described the first operation. Now, we're talking of congenital malformations, they uh, lesions occur in the liver and they may grow,
but only 20% they grow. They have a chaotic network of vessels and they have fibrotic, fibrotic development within it. I introduce you Hermann Pfannenstiel, he was a gynecologist, famous, famous, important incision that we still use today.
Remember him, we'll talk to him later. Microscopically, the microscopic is our well-circumscribed lesion, they're compressible. Important you see down there that they compress the liver that is normal close to it. This has an implication because if you operate,
you fill find a blood duct or a vessel and it will bleed or leak by. Microscopically, they are ectatic blood vessels and they are fed by arteries. This is also an important point, for therapy. Separated by fibrous septa, this is also important
because they become harder and they become bigger. And they have distorted blood vessels. They're more frequent uh, benign tumor. Prevalence up to 7%, they have non-neoplastic this must be clear, they are non-cancer. The proliferation of endothelial cells, women
have more and particularly pregnant women, more pregnancy or contraceptive. We divide them in cavernous and capillary and we'll have a word on that. Symptomatic being half of the cases, multiple in 10%, they rarely bleed and they rarely rupture.
Capillary Hemangiomas cells small, I show you an MRI here. The differential with HCC liver cancer is most important. They both are theorized but they continue to appear on late face. They are asymptomatic please, do not touch them, they do no harm.
And so we will not speak of them. We speak only of the cavernous hemangioma. And here, the cavernous hemangioma bleeds Oh my God, no, it's not true. There are 83 reports of bleeding since the report of Hermann Pfannenstiel. Uh, 97 cases, adenomas bleed more frequently.
Frequently, in the past they were confused. Hemangioma and adenoma, adenoma does bleed. There are only true cases, 46 in the literature. Size is not important and they are very rare in elderly people.
This is what we see when they are giant cavernous hemangiomas, they're serious, they are rather easy to diagnose. Diagnostic criteria, uh, look up typical for uh, cavernous hemangioma. How do you point here? Yep, you stop. If you then see that you have
an atypical hemangioma, you jump over to an MRI. MRI is too nowadays, diagnostic and uh, the important thing is you stop. Once you have the diagnosis with MRI, you stop, do nothing yet, do not follow, bye-bye. Treatment modalities surgery: Selective TAE, Radiotherapy, Medication: two classes,
Propranolol, to decrease the hyper circulation. Bevacizumab as a class of drugs of inhibitors of inferior growths and endories, eventually are cold. This is seminal paper, about 35 years ago "Do not treat asymptomatic patients." This is a key: do not bother with hemangioma.
If you do have the algorithm, you look at complaints that can present incidentally when they have complained, not complained, no treatment of abdominal pain. Unrelated to no treatment, we have to eventually make sure that the pain is not related to the cavernous hemangioma. If there is other futures
like compression giant, you can do surgery. If you have a doubt in diagnosis, today rare with MRI, then you can perform a biopsy. The surgical indication then remain progress, severe, disabling symptoms. Diagnostic uncertainty nowadays not the case, with MRI.
Consumptive coagulopathy or Kasabach-Merritt syndrome is a serious, we will see when you perform human transplants. Spontaneous rupture with bleeding as an emergency. Rapid growth in 25%. This is a paper that shows that the size of the cavernous hemangioma is here,
and you can see that operation has been performed for larger size, however, look that even in non-symptomatic or partially asymptomatic patients, you can reach sizes up to 15 centimeters. And this a review of the literature from a Chinese group where they revised a thousand to a hundred cases,
no mortality in the series and enucleation versus the anatomic resection is better. Less complications, less blood less, less time of surgery, and less hospital stay. So please, in this case of surgery, we do enucleation. I was asked by my society the HPBA to speak
about transplantation for liver tumor. You can that an indication is unresectable disease, severe symptoms and mass occupying effects. Pre-cancerous behavior is not for hemangioma only for adenoma differential diagnosis with HCC. And you have to be attentive that you avoid
liver insufficiency during your resection. So, in conclusion, for benign lesions, hemangioma technically is the only indication. And now the systematic review that shows around several emothing United States UNOS and the ELTR Several, several benign tumors but if you break down
for type of tumors you see that most of them are Polycystic disease or partly cavernous hemangioma are very low. 77 in Europe, out of 97,000 operation of transplantation. So, let's get an old paper. The pioneer of transplantation again, extremely low,
one out of 3,200. An extremely low percentage. It's my personal experience I was working at Essen, Germany. Almost a thousand transplants we performed. Unfortunately most of them I did and we never transplanted one hemangioma, my experience for transplantation is zero because it should not be done.
So, my advice for hemangioma. Biopsy not advised, see a liver surgeon in a serious center, diagnosis is done my MRI, observe doubt symptoms and observe. Let the patient beg you for surgery, if significant increase in size and symptoms, we can do surgery. Embolization is possible.
Sometimes it's harmful. The role of the surgeon is to confirm the diagnosis, differentiate it from cancer, exclude causes of other symptoms and avoid unnecessary surgery that's the main thing. Surgery for severe symptoms of Kasabach-Merritt. Only for complicated symptomatic lesions, or where the
diagnosis is uncertain. Ladies and gentleman, I will conclude with a couple of questions. If you have a daughter or son with a liver tumor, would you go to a center or a competent surgeon or to a gynecologist. Professor Pfannenstiel for instance or another doctor. If your car has a problem,
would you go to a good mechanic once for all, or to a small shop for 20-40 times. It is a matter of experience and a matter of costs. And with this, I am ready for your questions. - [Audience Member #1] When have you personally operated on these lesions?
- [Speaker] I am. And the experience that I have in the past I seemed young but I practiced for many years. When I started 25-30 years ago, we were operating many of these because we were not so certain. Then MRI came, and MRI basically made the diagnosis so easy and straight-forward and we started observing
patients. We still do operate today, but they are very large tumors and when I do personally, I avoid the androbolization before because you have more skylotec reaction, just (grainy sound effect) to peel it away from the normal parenchymal.
This is our experience. - [Audience] Thank you. - [Speaker] Thank you very much, yes? - [Audience Member #2] Yes, one question. When you operate, and with all of the experience you have, what are the complications of
(mumbles) - [Speaker] The main, so first of all, there has been also an evolution in the type of operation we don't do anymore the resections where you have some bi-leaks. If you operate correctly, it's bleeding and one infection not one born. If you have to watch bi-leak is the one
that you have to watch and that's because the tissue is pushed away and you may miss something during the enucleation.
- Lymphatic, so it's fun, actually, not to talk on venous interventions for once. And, naturally, the two systems are very different. But, on the other hand, they're also related in several ways and I will come back to that later. I have no disclosures, maybe only my gratitude to this man, Dr. Maxim Itkin,
who actually got me started in the field, and was gracious enough to supply me some of his material. And who is also responsible for making our lives way easier over the last years. Because in former times, we needed to do, to visualize the lymphatic system,
we needed to do pedal lymphangiography and that was very, very cumbersome. It took a long time and was very painful for the patient. And he introduced the ultrasound guided intranodal lymphangiography,
and that's fairly easy for most of us. With ultrasound you find a lymph node in the groin, you puncture that and you can control the needle position with contrast enhanced ultrasound and once you establish that position, you might do a MR lymphangiography.
Thereby showing, in this case, a beautiful, normal anatomy of the thoracic duct. I need to say, the variations in lymphatics are extreme. So, you can also visualize, naturally, the pathology, like for example, pulmonary lymphatic perfusion syndrome.
What's going on there. Normally, lymph courses up through thoracic duct, but in this case, you kind of have a reflux in the bronchial tree and lymph leakage. And you can image that again, beautifully with MR, which you can show extensive leakage
of lymph in the lung parenchyma. So you can treat that. How can you treat that? By embolization of the thoracic duct. But first we need to get into there, and that's not a very easy thing to do.
But now, again, with access to a lymph node in the groin, you can push lipiodol, and then visualize the cisterna chyli and access that transcutaneously with a 21/22 gauge needle and then push up a O-18 wire high up in the thoracic duct.
First you deploy some coils to prevent any leakage of glue inside the venous system, and then by microcatheter, you infuse glue all the way down, embolizing the thoracic duct. So, complete different group of lymphatic disorders is oriented in the liver and hepatic lymphatic disorders.
And maybe not everybody knows that, but 80% of the flow in the thoracic duct is caused by the liver and by the intestine. And many times in lymphatic disorders, there needs to be a combination of two factors. One factor is a venous variation of a,
sorry, an anatomical variation in lymph vessels and the other one is that we have an increase in lymph flow. And in the liver, that can be caused by a congestion of the liver, for example, cirrhosis, or a right side, that's congested heart failure.
What happens then is you increase the flow, the lymph flow, tremendously and if you also have a variation like in this case, when the vessels do not directly course towards the cisterna chyli, but in very close contact to the abdomen,
then you can have leakage of the lymph and leakage of proteins, which is a serious problem. So, what is then, to do next? You can access the lymph vessels in the liver by percutaneous access in the periportal space,
and induce some contrast and then later, visualize that one back, visualize that with dye that you can see with an endoscopy, thereby proving your diagnosis, and then, in a similar way,
you can induce lipiodol again with glue, embolizing the lymph vessels in the liver, treating the problem. In summary, popularity of lymphatic interventions really increased over the last years mainly because novel imaging,
novel interventional techniques, new approaches, and we all gained more experience. If you would like, I would guess that, we are at a phase where we were at venous, like 10, 15 years ago. If we are a little bit positive,
then the future is very bright. And within 10, 15 years, we find new indications and probably have much more to tell you. Thank you for your attention.
- Thank you. I have two talks because Dr. Gaverde, I understand, is not well, so we- - [Man] Thank you very much. - We just merged the two talks. All right, it's a little joke. For today's talk we used fusion technology
to merge two talks on fusion technology. Hopefully the rest of the talk will be a little better than that. (laughs) I think we all know from doing endovascular aortic interventions
that you can be fooled by the 2D image and here's a real life view of how that can be an issue. I don't think I need to convince anyone in this room that 3D fusion imaging is essential for complex aortic work. Studies have clearly shown it decreases radiation,
it decreases fluoro time, and decreases contrast use, and I'll just point out that these data are derived from the standard mechanical based systems. And I'll be talking about a cloud-based system that's an alternative that has some advantages. So these traditional mechanical based 3D fusion images,
as I mentioned, do have some limitations. First of all, most of them require manual registration which can be cumbersome and time consuming. Think one big issue is the hardware based tracking system that they use. So they track the table rather than the patient
and certainly, as the table moves, and you move against the table, the patient is going to move relative to the table, and those images become unreliable. And then finally, the holy grail of all 3D fusion imaging is the distortion of pre-operative anatomy
by the wires and hardware that are introduced during the course of your procedure. And one thing I'd like to discuss is the possibility that deep machine learning might lead to a solution to these issues. How does 3D fusion, image-based 3D fusion work?
Well, you start, of course with your pre-operative CT dataset and then you create digitally reconstructed radiographs, which are derived from the pre-op CTA and these are images that resemble the fluoro image. And then tracking is done based on the identification
of two or more vertebral bodies and an automated algorithm matches the most appropriate DRR to the live fluoro image. Sounds like a lot of gobbledygook but let me explain how that works. So here is the AI machine learning,
matching what it recognizes as the vertebral bodies from the pre-operative CT scan to the fluoro image. And again, you get the CT plus the fluoro and then you can see the overlay with the green. And here's another version of that or view of that.
You can see the AI machine learning, identifying the vertebral bodies and then on your right you can see the fusion image. So just, once again, the AI recognizes the bony anatomy and it's going to register the CT with the fluoro image. It tracks the patient, not the table.
And the other thing that's really important is that it recognizes the postural change that the patient undergoes between the posture during the CT scan, versus the posture on the OR table usually, or often, under general anesthesia. And here is an image of the final overlay.
And you can see the visceral and renal arteries with orange circles to identify them. You can remove those, you can remove any of those if you like. This is the workflow. First thing you do is to upload the CT scan to the cloud.
Then, when you're ready to perform the procedure, that is downloaded onto the medical grade PC that's in your OR next to your fluoro screen, and as soon as you just step on the fluoro pedal, the CYDAR overlay appears next to your, or on top of your fluoro image,
next to your regular live fluoro image. And every time you move the table, the computer learning recognizes that the images change, and in a couple of seconds, it replaces with a new overlay based on the obliquity or table position that you have. There are some additional advantages
to cloud-based technology over mechanical technology. First of all, of course, or hardware type technology. Excuse me. You can upgrade it in real time as opposed to needing intermittent hardware upgrades. Works with any fluoro equipment, including a C-arm,
so you don't have to match your 3D imaging to the brand of your fluoro imaging. And there's enhanced accuracy compared to mechanical registration systems as imaging. So what are the clinical applications that this can be utilized for?
Fluoroscopy guided endovascular procedures in the lower thorax, abdomen, and pelvis, so that includes EVAR and FEVAR, mid distal TEVAR. At present, we do need two vertebral bodies and that does limit the use in TEVAR. And then angioplasty stenting and embolization
of common iliac, proximal external and proximal internal iliac artery. Anything where you can acquire a vertebral body image. So here, just a couple of examples of some additional non EVAR/FEVAR/TEVAR applications. This is, these are some cases
of internal iliac embolization, aortoiliac occlusion crossing, standard EVAR, complex EVAR. And I think then, that the final thing that I'd like to talk about is the use with C-arm, which is think is really, extremely important.
Has the potential to make a very big difference. All of us in our larger OR suites, know that we are short on hybrid availability, and yet it's difficult to get our institutions to build us another hybrid room. But if you could use a high quality 3D fusion imaging
with a high quality C-arm, you really expand your endovascular capability within the operating room in a much less expensive way. And then if you look at another set of circumstances where people don't have a hybrid room at all, but do want to be able to offer standard EVAR
to their patients, and perhaps maybe even basic FEVAR, if there is such a thing, and we could use good quality imaging to do that in the absence of an actual hybrid room. That would be extremely valuable to be able to extend good quality care
to patients in under-served areas. So I just was mentioning that we can use this and Tara Mastracci was talking yesterday about how happy she is with her new room where she has the use of CYDAR and an excellent C-arm and she feels that she is able to essentially run two rooms,
two hybrid rooms at once, using the full hybrid room and the C-arm hybrid room. Here's just one case of Dr. Goverde's. A vascular case that he did on a mobile C-arm with aortoiliac occlusive disease and he places kissing stents
using a CYDAR EV and a C-arm. And he used five mils of iodinated contrast. So let's talk about a little bit of data. This is out of Blain Demorell and Tara Mastrachi's group. And this is use of fusion technology in EVAR. And what they found was that the use of fusion imaging
reduced air kerma and DSA runs in standard EVAR. We also looked at our experience recently in EVAR and FEVAR and we compared our results. Pre-availability of image based fusion CT and post image based fusion CT. And just to clarify,
we did have the mechanical product that Phillip's offers, but we abandoned it after using it a half dozen times. So it's really no image fusion versus image fusion to be completely fair. We excluded patients that were urgent/emergent, parallel endographs, and IBEs.
And we looked at radiation exposure, contrast use, fluoro time, and procedure time. The demographics in the two groups were identical. We saw a statistically significant decrease in radiation dose using image based fusion CT. Statistically a significant reduction in fluoro time.
A reduction in contrast volume that looks significant, but was not. I'm guessing because of numbers. And a significantly different reduction in procedure time. So, in conclusion, image based 3D fusion CT decreases radiation exposure, fluoro time,
and procedure time. It does enable 3D overlays in all X-Ray sets, including mobile C-arm, expanding our capabilities for endovascular work. And image based 3D fusion CT has the potential to reduce costs
and improve clinical outcomes. Thank you.
- So I'm going to be talking about allografts for peripheral graft infections. This is a femoral artery that's been replaced after a closure device infection and complication, and we've bypassed to the SFA and profunda femoris. These are my disclosures. So peripheral arterial infectious processes,
well the etiology either is primary or secondary. Primary can be from bacteremic states and seeding of ulcerated plaque or thrombus. Secondary reasons for infections can be the vast usage of percutaneous closure devices that really have flooded the market these days.
Prosthetic graft infections after either a bypass or patch in the femoral artery. So early onset infections usually are from break in sterility. Secondary infections can be from either wound breakdowns or late seeding of the prosthetic graft.
The presentation for these patients can be relatively minor such as cellulitis or draining sinus, or much more dramatic, such as sepsis or pseudoaneurysm or mycotic aneurysm. On the CT scan we can see infected mycotic aneurysm after infected closure device and bleeding complications.
The treatment is broad in range. Ligation is obviously one option, but it leads to a very high risk of major limb amputation. So ideally some form of reconstruction, either extra-anatomic through clean planes,
antibiotic graft as we heard from the previous speaker, the use of autologous replacement with deep vein, or we become big proponents of the use of cryopreserved arterial allografts for reconstruction. And much of this stems from our work from about 10 years ago, where we looked
at the use of aortic cryopreserved grafts for aortic graft infections. This was published about 10 years ago but we looked at a small series of patients with aortic infections. You can see the CT scan of an infected stent graft
and associated aneurysm. And then the intraoperative photo after we've resected the stent graft and replaced that segment of the aorta with a cryopreserved aortic segment. So using that as a springboard,
we then decided to look at the outcomes using these types of conduits, arterial conduits, for peripheral arterial reconstructions in contaminated or infected surgical fields. So retrospective review at our tertiary care center, we looked at roughly 60 patients over a 15-year period
and excluded any aortic-based reconstructions. So these are all peripheral reconstructions. Mean follow-up was 28 months. As you would expect, the distribution of treatment zones were primarily in the lower extremities, so 51 cases.
As you can see, there's a list of all the different types of cases that we treated. But then there were a few upper extremity visceral and then carotid. I've shown this slide before at this meeting in the past, with a carotid patch infection
that was treated after it had a blow-out, and it's obviously a infected aneurysm, and this was treated with resection and a cryopreserved arterial segment. Looking at our outcomes, the 30-day outcome showed a mortality rate of 9%.
The 30-day conduit-related complication rate was surprisingly low at 14%. We had four patients that had bleeding complications, four patients with recurrent infectious complications. All eight of those patients required a return back to the operating room for correction.
The late conduit-related complication rate was only 16%. As listed here, you can see there's only one case of reinfection, three cases of graft thrombosis, surprisingly only one major limb amputation, two pseudoaneurysms and one late bleeding complication.
And graphically depicted, you can see here, this area here is looking at the less than 30 days, this is primarily when the complications occur. When you get to six months, fewer complications, and then beyond six months, the primary complications that we would see are either thrombosis of the graft
or the development of late pseudoaneurysms, again relatively low. So in summary, I think peripheral arterial infectious complications can be treated with a cryopreserved arterial allografts. The advantage is it's a single stage operation,
maintains in-line flow, there's a low incidence of repeat infection. I think it's also important to mention that the majority of these patients had adjunctive muscle flap coverage to cover the large soft tissue defect
at the time of the operation. So I think that this is a valuable alternative conduit in a setting of peripheral arterial infections. Thank you.
- Thank you very much. After these beautiful two presentations a 4D ultrasound, it might look very old-fashioned to you. These are my disclosures. Last year, I presented on 4D ultrasound and the way how it can assess wall stress. Now, we know that from a biomechanical point,
it's clear that an aneurysm will rupture when the mechanical stress exceeds the local strength. So, it's important to know something about the state of the aortic wall, the mechanical properties and the stress that's all combined in the wall.
And that could be a better predictor for growth and potential rupture of the aneurysm. It has been performed peak wall stress analysis, using finite element analysis based on CT scan. Now, there has been a test looking at CT scans with and without rupture and given indication
what wall stress could predict in growth and rupture. Unfortunately, there has been no longitudinal studies to validate this system because of the limitations in radiation and nephrotoxic contrast. So, we thought that we could overcome these problems and building the possibilities for longitudinal studies
to do this similar assessment using ultrasound. As you can see here in this diagram in CT scan, mechanical properties and the wall thickness is fixed data based on the literature. Whereas with 3D ultrasound, you can get these mechanical properties from patient-specific imaging
that could give a more patient-specific mechanical AA model. We're still performing a longitudinal study. We started almost four years ago. We're following 320 patients, and every time when they come in surveillance, we perform a 3D ultrasound. I presented last year that we are able to,
with 3D ultrasound, we get adequate anatomy and the geometry is comparable to CT scan, and we get adequate wall stressors and mechanical parameters if we compare it with CT scan. Now, there are still some limitations in 3D ultrasound and that's the limited field of view and the cumbersome procedure and time-consuming procedures
to perform all the segmentation. So last year, we worked on increased field of view and automatic segmentation. As you can see, this is a single image where the aneurysm fits perfectly well in the field of view. But, when the aneurysm is larger, it will not fit
in a single view and you need multi-perspective imaging with multiple images that should be fused and so create one image in all. First, we perform the segmentation of the proximal and distal segment, and that's a segmentation algorithm that is
based on a well-established active deformable contour that was published in 1988 by Kass. Now, this is actually what we're doing. We're taking the proximal segment of the aneurysm. We're taking the distal segment. We perform the segmentation based on the algorithms,
and when we have the two images, we do a registration, sort of a merging of these imaging, first based on the central line. And then afterwards, there is an optimalisation of these images so that they finally perfectly fit on each other.
Once we've done that, we merge these data and we get the merged ultrasound data of a much larger field of view. And after that, we perform the final segmentation, as you can see here. By doing that, we have an increased field of view and we have an automatic segmentation system
that makes the procedure's analysis much and much less time-consuming. We validate it with CT scan and you can see that on the geometry, we have on the single assessment and the multi assessments, we have good similarity images. We also performed a verification on wall stress
and you can see that with these merged images, compared to CT scan, we get very good wall stress assessment compared to CT scan. Now, this is our view to the future. We believe that in a couple of years, we have all the algorithms aligned so that we can perform
a 3D ultrasound of the aorta, and we can see that based on the mechanical parameters that aneurysm is safe, or is maybe at risk, or as you see, when it's red, there is indication for surgery. This is where we want to go.
I give you a short sneak preview that we performed. We started the analysis of a longitudinal study and we're looking at if we could predict growth and rupture. As you can see on the left side, you see that we're looking at the wall stresses. There is no increase in wall stress in the patient
before the aneurysm ruptures. On the other side, there is a clear change in the stiffness of the aneurysm before it ruptures. So, it might be that wall stress is not a predictor for growth and rupture, but that mechanical parameters, like aneurysm stiffness, is a much better predictor.
But we hope to present on that more solid data next year. Thank you very much.
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