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Upper extremity DVT|Upper extremity DVT|56|Male
Upper extremity DVT|Upper extremity DVT|56|Male
DVT, Phlegmasia Cerulea Dolens | Suction Thrombectomy | 48 | Female
DVT, Phlegmasia Cerulea Dolens | Suction Thrombectomy | 48 | Female
Pulmonary Embolism (PE), DVT | Transcatheter Thrombectomy, Stenting | 75 | Female
Pulmonary Embolism (PE), DVT | Transcatheter Thrombectomy, Stenting | 75 | Female
2016anesthesiaanesthesiologistBoston ScientificcardiaccathetersclotpreparedpulmonaryremarkablyrespiratorySIRstentssurgeon
DVT|IVC Filter Placement|29|Female
DVT|IVC Filter Placement|29|Female
DVT | Inferior Vena Cava Filter (IVC) | 65 | Male
DVT | Inferior Vena Cava Filter (IVC) | 65 | Male
2016apexArgon MedicalcavaleventuallyfilterforcepsgroinhooklooppatientpulledretrievalsheathSIRtechnique
Saddle PE (Submassive)|Thrombolysis (Catheter-directed)|38|Female
Saddle PE (Submassive)|Thrombolysis (Catheter-directed)|38|Female
Submassive PE|Peripheral Thrombolysis|66|Female
Submassive PE|Peripheral Thrombolysis|66|Female
Fully thrombosed IV, Filter|Thrombolysis, Filter Retrieval|61|Male
Fully thrombosed IV, Filter|Thrombolysis, Filter Retrieval|61|Male
DVT, IVC Filter Stuck | Balloon-assisted IVC Filter Retrieval, Stenting | 57 | Female
DVT, IVC Filter Stuck | Balloon-assisted IVC Filter Retrieval, Stenting | 57 | Female
2016Bard PVcableclotcompressedfilterfiltersflankinjectedirregularmarkmigratedpatientsheathSIRstentstentstrialultrasound
Mesenteric Venous Thrombosis|Mechanical Thrombectomy, Balloon Maceration|30|Female
Mesenteric Venous Thrombosis|Mechanical Thrombectomy, Balloon Maceration|30|Female
DVT, PE | Inferior Vena Cava Filter (IVC) | 75 | Male
DVT, PE | Inferior Vena Cava Filter (IVC) | 75 | Male
PE (Massive) ARVC Decompensation|Mechanical Thrombectomy|22|Male
PE (Massive) ARVC Decompensation|Mechanical Thrombectomy|22|Male
2016angioArgon MedicalarrhythmiasaspiratedcalibercathetersdecompensateddecompensationdeviceechohemodynamicallyhemoptysishypoxicinfiltrationInterventionsintubationlumbarlysedmassiveneurologicocclusivePenumbrapulmonarysegmentalsinusoidalSIRsystemicallythrombectomythrombogenicthrombusvenousventricleventricularvolume
Popliteal Artery Occlusion | Mechanical Thrombectomy, Balloon Angioplasty | 92 |Male
Popliteal Artery Occlusion | Mechanical Thrombectomy, Balloon Angioplasty | 92 |Male
2016angiomaxBoston ScientificclotemboliEV3lyseOscoroversizeprettySIRspiderstentingtibialwire
Aortofemoral, Common Femoral, Iliac Occlusion | Thrombectomy, Thrombolysis | 70 | Male
Aortofemoral, Common Femoral, Iliac Occlusion | Thrombectomy, Thrombolysis | 70 | Male
2016anastomosisanastomoticangiogramBoston ScientificdistaldistallyduplexiliaclysedocclusionprettyprofundaproximalreconstitutionSIR
Aortofemoral, Femorofemoral, Femoropopliteal Bypass Occlusion | Thrombolysis, Thrombectomy, Balloon Angioplasty | 66 | Male
Aortofemoral, Femorofemoral, Femoropopliteal Bypass Occlusion | Thrombolysis, Thrombectomy, Balloon Angioplasty | 66 | Male
2016AngiodynamicsanticoagulationBoston ScientificchronicallydistalgraftslimbsmultipleoccludedPatentprettyprofundaproximalSIRsurgicalthrombectomythrombolysisvascularvein
Bilateral Artery Occlusion (Popliteal, Peroneal) | Aspiration Thrombectomy, Angioplasty | 43 | Male
Bilateral Artery Occlusion (Popliteal, Peroneal) | Aspiration Thrombectomy, Angioplasty | 43 | Male

thrombosis. There're different flavors of radio, probably get to see another one

later from my colleague Dr. Saad. History and physical, 56-year-old male, who had recent diagnosis of small cell carcinoma, with some mediastinal adenopathy, and a small subsegmental PE. And he was initially started on Lovenox with transitioned to Warfarin.

Not sure how they did that, although there was a known diagnosis of malignancy. But that's how it is, when they go into the, not away from the main campuses, they go to the suburbs. People don't know the importance of having these people on, low

molecular weight heparin, who's a known candidate with cancer, and use DBT. He later presented with left upper extremity swelling, and severe pain. Physical examination showed that, he had swelling all the way from his shoulder, down up to his hands. And he had severe pain associated

with that, when he presented to the emergency department. And for some reason, a counsel was not sent to us initially. And his INR, at that time of admission in the emergency, was 3.1. And the Doppler evaluation was done at that time, which had shown upper extremity vein, you'll see the findings, upper extremity veins, Doppler was done. And for some reason, he was started on oral anticoagulants,

they're not sure why it was done that way. But Pradaxa was started, thinking that, okay, patient was on Warfarin, developed this possible venous thrombosis. So somebody decided in the ER, start him on Pradaxa, so he was already on Pradaxa. He did not improve. And this was the left axillary vein,

color Doppler ultrasound imaging, which shows some hyperechogenic material within the auxiliary vein. it was similar in the brachial vein as well. Is not a good color flow throughward, and it was not compressible. So all the findings consistent with deep venous thrombosis in the upper extremity. So based on the findings in ultrasound, and when the counsel came

through finally, with his symptoms not getting any better, we planned for doing a mechanical thrombectomy, to remove the clot burden. Since he was already on Pradaxa, with it's half life being anywhere between 17 and 21 hours, and we still don't have prax buying the antidote that, to reverse in these people right away, although it's available now, and

it's approved by FDA in October 2015. So we were in a bind, how are we gonna do lysis who's already on Pradaxa, with history of lung malignancy, and you don't know what's his status in the brain? We were a little bit reluctant, to kinda of do lytic infusion, or use a lot of lytic straight away. So it was not done on the initial

day. We stopped the Pradaxa, changed him to unfractionated heparin, while he was in the hospital. Then realized that he had some, kind of hit with some thrombocytopenia developing. He was changed to Argatroban. But once he came

to us, we did an angiogram through the left basilic vein, which was still patent, and a venogram was done. And initially, we did some mechanical aspiration thrombectomy with the CAT6, we didn't have CAT8 at that time. Like I said, we decided against lytic infusion catheter through the clot, because the effect of Pradaxa had not worn off.

This is the initial images. Here you can see access from the basilic vein. The initial angiogram showed that ready appearance, of the left basilic continuing as the axilla. And then the central veins were something like this. There's irregular eight years of filling defect within the vein. And then some irregularity

in this area, and a large filling defect in the left brachiocephalic vein. Here you can see the CAT6, going through the separator coming right here, We worked on for it for quite some time, without much improvement of

the appearance of the clot, in the central veins. You have to believe me, the actual CT sections did not show any mass lesion right here. There was some mediastinal adenopathy,

but there was none around the left brachiocephalic vein, to explain for this. So it was not just extrinsic compression causing this whole problem. It's cancer induced thrombosis, but he was symptomatic, so you're trying to help him

to relieve the clot burden. So once we did this on the first day, and Pradaxa was stopped there, we didn't do a lytic infusion. We were able to clear, most of the clot from the axillary region. And then at the end, only some part of the left brachiocephalic vein, and little bit in the subclavian vein

remained. Further work the next day, things seems to have gotten better. And at this point, he was off Pradaxa. We did an Angiojet pharmacal mechanical thrombectomy. At this point, since he was off Pradaxa for more than two days, we were a little bit more positive. And we did a little bit of lytic in a

pulse-spray fashion, with up to 68 milligrams here, and it cleared out more clot. And finally, this part in the left brachiocephalic vein, was very difficult to just suck out the Angiojet. We didn't have the ZelanteDVT at that time. So what we did was, we managed to use a cleaner, and hopefully because of the fact. that it was a little

bit soft. And although it didn't come out, with the help of Angiojet only, it kind of cleared, and the patient got better with that. And we were able to operate up completely. So now for the samp question. Which of the following is a finding in the setting of deep venous thrombosis?

Choice A, a non-compressible vein on ultrasound evaluation. Choice B, no detection of flow on color Doppler. Choice C, filling defect on direct venography. Choice D, presence of multiple enlarged

collateral veins. Choice E, is all of the above. Time starts here. [BLANK_AUDIO] Okay. everybody got it right, hurray, 100%. Okay, that

was a simple question. So little bit about the upper extremity DVT. Catheter-associated upper extremity DVT accounts for vast majority. So I'm talking here, only about the secondary forms of upper extremity DVT.

There is a primary form which you already know, it's a Paget-Schroetter. The secondary forms, it results mainly from indwelling central venous lines or portacads/g, and less frequently from pacemaker or defibrillator leads. Systematic screening however in these patients, reveal thrombosis in up to

two thirds of cancer patients, with central venous catheters. And patient-related risk factors include the presence of cancer, especially ovarian or lung adenocarcinoma, presence of distance metastases, and also a history of thrombosis or thrombophilia in these patients. Cancer

related upper extremity DVT, even in the absence of central venous catheter, it is usually the cause of secondary upper extremity DVT, because there are cancer-induced prothrombotic states or venous stasis, resulting either from venous compression, or from some kind of infiltration as the contributing factors.

So early thrombus removal and restoration of the patency, it aims at reducing the risk of post-thrombotic syndrome in these patients. And catheter-based therapy is recommended for patients, with proximal upper extremity DVT of recent onset, and with severe symptoms, and in patients who have low risk of bleeding complications with a good functional status.

case, is another IVC filter theme case. So 48 year old female, two prior episodes of lower extremity DVT treated with anticoagulation. Also pertinent histroy. She had a history of Subarachnoid hemorrhage secondary

to rupture aneurysm, and she was treated with coil embolization. So she got another DVT, a third DVT and she was placed on anticoagulation although this time she started having severe menorrhagia and anemia, they held off for a while but then they wanted to do a hysterectomy. So they called us and said can you put in a filter before her surgery,

so we did, and uncomplicated filters, posted the last one but remember this was her third DVT so she developed a new post operative DVT in her right leg. An anticoagulation was felt should be held at the time. She had a filter in place so people were okay.

Her symptoms of right lower extremity, pain and swelling start getting worse. And we weren't notified at this point and time about this. We weren't involved in the decision making. But her symptoms got worse and then eventually got worse to where

she had a tense right leg, swollen bordering on phlegmasia, and her left leg was swollen and her whole external genitalia were engorged. Now we got called. And so these are coronal images from the CT,

obviously it fits with her exam, you see that there's clot in the caevar/g goes into her right iliac and femoral vein, the left is open here but there is clot in the left as well. And you can see clot extending above the filter.

And here just to show you the shear volume of clot from her axial CT in my study and in my iPhone. >> It could be more than 100 CCs or 200 CCs. >> Yeah and it's incredible clot vial, so basically and I think

you saw it in the coronal to allow for the second time. So the treatment plan, she had post up bleeding, she had anemia. The volume of thrombosis you just mentioned was quite significant. She had severe symptoms. We do tend toward catheter-directed lysis but with all the other

confounding issues, we decided to perform an AngioVac thrombectomy, and we had performed quite a few of these today, at the time of this case. The patient was very well informed, very educated.

The family was very involved and we had our multidisciplinary team, internal medicine, hematology. We worked with cardiothoracic surgery for these cases and IR. Driving in on the morning for this case, I have to put the gynecologist. The gynecologist calls me and says,

hey What are you doing? What are you doing on my patient? Are you taking, I think, some vacuum? Are you taking it in there?

Well it turns out his buddy from medical school was the original founder of the vortex catheter which was subsequently bought by [UNKNOWN]. He goes, call me when it's over. I said all right sure. So we had our team, cardiothoracic surgery,

anesthesiologist IR, intubated TEE, we did venous access. For those of you who've used the AngioVac, we put the 26 French Dry Seal sheath in the right internal jugular, the reinfusion cannula

which was 19 French in the left IJ and we used the left common femoral vein, you remember that vein was open for adjuvant procedures which we found to be pretty standard for the AngioVac cases. And here typical venogram, you can see here this is the AngioVac catheter coming through the sheath,

okay. We do a little puff of contrast, nothing's going, you could see the clot is above the filter and that's the injection From the left side and the right side and just as that CT showed and then here just more venography.

So when we've done these cases, if we can get the AngioVac, we clean out above the filter that's usually pretty standard and then sometimes we'll try and get the catheter just to go through the filter keeping the filter in. But when it doesn't we'll elect to take the filter out,

so we had a second IJ access that we had already had because we were possibly gonna do some AngioVac therapy through the jugular and so we decided let's take the filter out. So that through the other catheter in the IJ while the AngioVac device is on the whole time. And as I said sometimes in these cases you'll remove the filter

of which we had without any incidents. So here just showing some of the AngioVac, that's a cleaner going in the left iliac vein while the suction is on, and then here, so we've cleaned out the left Iliac vein now we're gonna go to the right side.

So here this was through that other catheter and you can see this is going really well, everything is great we went down into the leg. >> It's like a batting cage basically you pitch stuff at it and you hope that it will catch it.

>> Correct. Good point. And the suction is on the whole time and I have to say the IVC and iliac vein cases, these are not quick cases. You are in there for quick a while. There couldn't be some chronic clot in there by the time they present them and

you're in there for hours, but this thing is going about as well as honestly any of our cases had. But this is an M&M so of course you know that I can't continue. Okay so that is that, and then here. One of my partners and I were doing this case, we turned to each other,

we're like pretty happy. We were done in under an hour from everything. And then the anesthesiologist says is there something why her pressure's dropping? What's going on?

And we're like no. And just so you know this was our final, everything's looking great and this was our shot literally as we shot this, he's like, yeah, something's going on.

He pressure's dropping and then she basically developed hypotension, arrhythmia. She arrested, we did CPR on the table and he had the ECKO there and he's like, I see this big clot. It's in the RV. Decreased Contraction but you have to understand,

picture the situation, we had VV ECMO going on. Venovenous bypass, and we pulled the II out of the way, we're doing compressions, she's dying, he's said that. So we had catheters

still in place where we can try and get, we had the AngioVac out by this point and time and we shut actually pulmonary angiograms and we are trying to establish ulterior access for V-A ECMO during this process and you can imagine, you're doing compressions, getting ulterior access wasn't rapid but we were on her like that. >>

[SOUND] >> Very quickly. These are just pictures, he didn't see the clot anymore, it was like there and then it was gone, we shot preliminary angiograms,

couldn't see anything, there was nothing in the heart and the PA grams look pretty good, this was all done pretty rapidly. So we add on VA-ECMO, she RV function recovered very quickly, she

was weaned off ECMO in 2 days, however, she was brain dead. Continuous EG monitoring, status epilectipus, she was kept on meds and then she expired 24 days post op. So we had root cause analysis for this,

we met as a big team, we talked about everything. One, I think we have felt this too. When your AngioVac is on, you're like Zeke/g said. You're trying to hope that it's on and you're sucking clot out and

it's acting as your filter, and maybe that is some inadequate reassurance. I have to say, in many of the cases we've done, we have typically removed the filter at the beginning because it gets in the way. And with these retrievable filters,

we've had cases where we're trying to get the catheter through there, and it's a push. You're really twerking on the filter, and you could do more damage than good.

But we have successfully worked through the filter. The question is should we have placed a new IVC Filter after the retrieval especially when difficulty was encountered and when we knew we were gonna use a bunch of these adjuvant techniques. We did talk about that and actually, we talked about that.

>> So did you have a lot of time when the flow rates were dropping, when you were little to nothing, when you were stuck or- >> During the case, very little and a lot of those cases,

your perfusion is still say, no flow, okay, you're back, no flow, but this, like I said, it was the easiest AngioVac case I've ever done. >> I've learned a little bit and I do that last point on every case now, which is I put a four or five inch catheter in the artery.

Ahead of time in the opposite sides and just leave them there at the start of the case. We have converted ones imaginably/g. >> So that is exactly what we talked about with our heart surgeon, which was one, do we get an arterial access on all cases? You can talk to the company, they send out a person pretty much for every case, and we're probably gonna start doing what we are

doing that now. The other question is, you're doing venovenous bypassing. How quickly can you perfusion this if you have a second machine that would be ideal, most places won't have a second machine in IR but they'll have to rapidly convert from BV to VA

on the same machine so, that's my case. >> That was a really good follow on to the other case.

75 year old woman, 1 month after a spinal surgery she's admitted with perhaps submassive PE not necessarily treated as such, she

was on a floor/g. And she's got an occlusive clot on her right leg. Femoral all the way down. She's treated it with Heparin and IVC filter. I learnt about it five days later when we were consulted in the evening as to whether or not we might consider doing something for her PE directly.

She was having a little bit more hypertension and perhaps some right heart strain. So we get her into the ICU and agree to set her up for some transcathoder thrombectomy. You can see the coronal pictures showing you some of the clot. [BLANK_AUDIO]

Get in and she has very very elevated PA pressures quickly showing you just some of the pictures I guess the mouse doesn't work on this case cause I'm loaded from the back. So you can see the clot casting the truncus anterior, the upper lobe.

Wow, I think that's the mouse from the back. Whoever is running that you are doing well from backstage. [LAUGH] And also the interlobular artery on the left. So start thrombectimizing her with penumbra catheters and section thrombectomy, getting a little bit of stuff out.

She's deteriorating. Her respirator demands are increasing. The anesthesiologist was discussing increasing pressures and I stopped and started to look around the department for help because anesthesia was in another room. I called for respiratory support.

The MICU attendings coming in as well. And then thought that maybe we should put her on ECMO. So we are on IR suite. There were about nine or ten additional people who arrive at the time, cardiac anesthesiologist who was remarkably available as a second anesthesiologist in addition

to a case that was happening in another room and remarkably a CT surgeon is free. And the perfusion crew rolls in, and suddenly we have more than two IRs, a cardiac anesthesiologist, anesthesia resident, a respiratory

tech, a bunch of IR nurses, two IR techs, perfusion, MICU physicians and a whole bunch of other people in this case very quickly, which was stunning to me to sort of step back at a meta level. Then shortly after she's getting intubated,

she codes and we're starting to do CPR and the CT surgeon and I put her on venoarterial ECMO which I felt comfortable with from angio-vac/g cases. I don't think I would have been mentally prepared or even considered that had I not learned to use that in similar devices for those cases as well.

We're doing this while somebody's doing CPR and her oxygenation is restored and remarkably she gets normal sinus rhythm back. There are the ECMO catheters and you can see that I lifted the leg of the filter, in advancing the venous catheter there as well,

and there it is just since we have lot of filters here. So went back to section thrombectomy now the things are a lot quieter, and the room had thinned out a bit, and added in some AngioJet, added a little more section thrombectomy, weren't necessarily getting anywhere. So flow is sluggish,

there is still some issues of stability, so I figured lets put some stents in. So here is one pulmonary stent, and there is another self expanding stent on the other side, one was a [UNKNOWN] the other one was

a wall stent, because that's just what was available in stock. Cleaned a little bit more and stopped. And this is a follow up CT which shows you that the stents are patent. Pretty much the majority of the remainder of her pulmonary artery's lysed on a subsequent CT as well. I've seen her now in follow up for three and a half months,

and she has no recollection of the atmo-period/g of time, she has absolutely no respiratory issues, and we're talking about her back pain and issues related to that.

So I put this up in part two because I've now done another recent case in which we took a look at somebody with who was on the verge between submassive and massive PE and something didn't feel quite right. And I've had enough cases over the years where you get ready to start the case and then they code before you're even you've been

into the pulmonary, I see some people nodding. How many people have had that case where they've coded while you're starting thrombectomy? That's more hands than not. And I think that situation is this part where they've been resuscitated and they're pouring fluids into them overtime,

and supporting that right ventricle until it finally cramps while you're starting to work. And this really sort of changed the tenure of it and as we're all gonna get involved in PE response team around, and we're essential front and center in deciding the responses and the calls for the

transfers and otherwise I think we need to be prepared for that tipping point and the inability to predict who's gonna flip from one into the other and really be prepared to place these people on ECMO which means just putting it into the Verbix whether it's in hybrid/g, or whether you're gonna put it into

IR. And be prepared it really just changes the entire scope of the case. That's what I brought. >> [APPLAUSE]

one case, kind of neat. 25 year woman with history of metastatic colon cancer

status post segmental resection with positive DVT on Doppler on post-op day one. And we saw the patient because they requested a filter placement. So patient had a wedge resection of the liver. And what happened was the liver, because of the missing liver segment, fall away and with it it pulls IVC with it and makes this area very tight. And that's our postulation why there are clots forming,

because when we did the venogram we didn't see a whole lot of flow pass this point, in addition to all the huge amount of thrombus in the IVC itself. So the filter was placed above all the clots. It was 5 o'clock, 5:30 or so, in the afternoon. So we just put the filter in there and

we re-thought our plan of action. So post-op day one, a filter was placed. Post-op day two, patient suffered cardiovascular decompensation with low cardiac output, which we think is due to the IVC thrombus which then decreased the venous return. And the patient was transferred to

the ICU. So we set the patient up for post-op day three, thrombectomy. So you can see here the liver has fallen away, and the filter was placed with the tip at the cavoatrial junction basically. [BLANK_AUDIO] So we decided to use the AngioVac device here. It's a large-bore aspiration thrombectomy system, mated to an

extracorporeal bypass circuit and reinfusion cannula. So you suck the blood out below, and then you re-diffuse the filtered blood in from above. And so you strip off

and suction both acute and chronic material. It goes through a filter, and the blood is returned into the body. And I quote, approved by the FDA to remove undesirable material during performance of extracorporeal bypass. [BLANK_AUDIO] So here it is, with the device in position, and we push it up to suck out blood. [BLANK_AUDIO] And then you can see, we attack the upper area as well.

[BLANK_AUDIO] So you just keep looking until you clear it all out like the venogram right here. So what do we do now? We know there's a kink in the IVC, so we took the IVC filter out cause there are no clots left. [BLANK_AUDIO] Looks pretty good.

[BLANK_AUDIO] So then we had to stent that IVC to keep it open, with a Z-stent. So we achieved great result, patient was fine, follow-up months later. And here's the clot that's inside, that was trapped. [BLANK_AUDIO] So another

>> So this is a case actually one of my colleagues, and one of my fellows loaned to me. This 65 year old man has history DVT, started coumadin, he had an option filter placed on 12/16, he had placed under, he had CO2 simply

because he had a little bit of decreased GFR, his filter was placed in good position. I'm sorry, it must have been 12/16/14 so the letter was sent nine months later which is typical for us if the patient doesn't present,

we typically actually, if we can track them down. We send a letter before then, came in for a clinic visit a week later, had a bilateral duplex ultrasound, that was negative, and the same had a filter

retrieval attempted so it's actually about ten months post placement. We snared, we tried to snare from above but the hook was embedded in the caval wall. The loop technique failed and one issue I have with the option filter which I think is a great filter but the problem with it is,

at the apex there's a lot of covered space, it doesn't go right up to a point like the tulip does right before it goes to the hook. It's got this relatively long. I kinda think of it as like the tip of a tipi,

where the fabric is kinda together so it's got this long sort of segment beneath the hook towards the legs that is difficult to get around. So what happens is you get around with your loop technique and then you just sorta drive that filter apex almost deeper into the caval wall.

So I tried it for a little bit of time we had an hour and twenty minutes of sedations and a significant amount of fluoro. My, you always blame the the fellow right? So my fellow kept telling me I just pull a little harder, just pull a little harder, and eventually I stopped simply because well my

wife keeps my balls at home in a jar so I stop at these things- >> [LAUGH] >> A lot faster than I really should. So this is the first retrieval you can see here this is the, is that showing for you guys? >> Yeah.

>> I mean is it showing? >> How big is the jar? >> How big is the jar. Thanks Stan [LAUGH] >> It's a bucket.

>> [LAUGH] >> So you can see here with the loop-snare technique again, you are kinda, I don't know how I can see this but hook is not inside the sheath at this point in time and again you just sort of driving everything a little bit deeper, so I stopped but

at the end the filter didn't exactly look like it had looked before. And right you end up at this sort of point of no return with this filter retrievals and, at that point in time you're just a little bit screwed so- >> It's like the Hunchback of Notre Dame. >> He does look like the Hunchback, that's the ray curve falling filter

retrieval. So that was in September and so the patient now is 15 months after placement, he didn't wanna come back we kept telling him to come back, let's try repeat retrieval and eventually [LAUGH] Thanks Mike. >> [LAUGH] >> Eventually the patient came back and was put under general anesthesia for what we knew was gonna be a pretty

aggressive retrieval. So we got, right neck and right groin access, the filter was really unchanged in appearance, cavogram was negative, you can see again the hook is really kind of outside the caval wall at this point.

So groin access from the groin was up to 26Fr, to the neck was 16Fr, and the idea then was to put a coaxial 18Fr sheath into the 16Fr. Here's your sheath kind of telescoping sheath system.

And then from above to inflate a compliant balloon to sort of protect from any distal emboli that we were a little bit concerned about. Now remember this filter now is 15 months old. So we tried some rat-tooth forceps from below we had to be sure, we had a couple of attempts and weren't unable to grab it right at sort of underneath the filter apex eventually grabbed it,

inverted it completely. In which one I close my eyes as Isran/g pulled harder than anybody I have ever seen pull anything in my life completely inverted the filter and pulled it back with the 18Fr sheath telescoping through the 26Fr and then pulled the whole system out.

They were no filter fragments at this point in time. Now one thing, so when we had the 26Fr sheath coming from the groin, we are kind of pushing it without the dilator in and ended up with this sort of channel into the IVC that of course our pigtail found during the first injection. That

ended up being clinically silent, what are you doing to me. And actually manual compression was enough to repair or to getting a metastasis in the right groin. One lesson learnt here we had two different types of red-tooth forceps both were from endoscopy. This was the disposable one and it broke,

and it broke relatively quickly and then we used one that is resterilizable that is much meatier and much beefier and that was the one that we ended up being able to get the filter out. This was the filter itself, there was a fair amount of intima. A lot of intima and cleaned up this is what the filter itself looked

like. All right. >> [APPLAUSE]

Second case, took a little bit more effort here. So it's a 38-year-old woman with acute shortness of breath, chest pain, sporadic light headedness with exhaustion.

She also had right calf pain and swelling, it turned out to be a DVT. This was all after 11 laparoscopic gastric bandings surgery one week ago. So a PE particle CT shows a [UNKNOWN] there extending into lumbar

and segmental vessels. Again focusing on the heart obvious left for a set of deviation, elevated RV to LV ratio. A patient in that criteria for a submassive PE, nobody was interested in systemic thrombolysis given the recent surgery.

So we decided to go do a catheter directed thrombolysis in this young woman. So initially, angiographic images show, just re demonstrate the thrombus seen on CT but you'll also see that there's more types of perfusion at the right lung base and left of her lung

zone. The PA pressure was elevated. We started thrombolysis with the catheter on the right side, and after 20 hours you'll note that there is improved perfusion at the right lung base. However there is a lot of central clot blood in there and the PA pressure

was not appreciably changed. So we kept on going with the catheter on the right side and at 42 hours, pretty similar appearance actually to the prior angiogram. And the PA pressure was not appreciably changed. At 60 hours though we started to see marked improvement in that central thrombus and the PA pressure started correspondingly improved.

84 hours the central clot thrombus has essentially got there's a little bit of segmental thrombus in the right of the lobe. The PA pressure was getting towards normal. So we swung the catheter over to left side, and again they're considering continuing thrombolysis.

We saw here that the central clot and [INAUDIBLE] clot that side was also essentially resolved more or less homogeneous perfusion of the left lung. So PA pressure was better patient was feeling much better we stopped at that point. She was discharged home on seventh day and therapeutic Lovenox.

She was [INAUDIBLE] outside institution but was asymptomatic on a 60-day follow up with us in our clinic. I just wanted to briefly contrast our technique with those in the published literature. So flow-directed CDT seems effective in our institutional experience but I think a valid question at this point is can we do better?

For example what is the optimal catheter to use and what is the appropriate thrombolytic dose and duration? Focusing on the catheter so ULTIMA and SEATTLE II both use ultrasound assisted thrombolysis. It's an attracted device, ultrasound disaggregates uncross-linked fibrin fibrous. Increases

permeability to clot thrombolysis and it's also FDA approved for medication. But I think it's important at this point if we ever get the benefit of USAT over conventional CDT has not been established in clinical trials. There was however, a prospective randomized controlled trial of USAT versus conventional CDT for acute iliofemoral DVT.

Half of the patients had EkoS placed and turned on and others had the head tuned off. And so essentially functioned as the infusion catheter is affixed to this regiment. And they saw no difference in primary or secondary end points. For example, thrombus load reduction, need for adjunctive angioplasty

or stenting, incidents of complications, three month patency and incidents of post thrombotic syndrome. Now, granted this trial was power to see a 50% difference. And it's possible that if they enrolled more patients. There was seen a difference,

but the obviously felt like that was unlikely given the similarity between the groups. Why do I think this is irrelevant? So, in DVT the transducers are typically embedded in the clot. In PE lesion/g in a my experience, I think it's difficult to achieve that,

I think the majority ensure the transducers are often remote from thrombus, for example in a different lobe entirely or proximal adjacent to the thrombus. And given that the effect of ultrasound is local if no benefit was demonstrated in the DVT thrombolysis then it isn't clear to me

at this point if there is a benefit for a PE. There may well be a benefit but it just is a value driven measure in our institution. We have not yet adopted in the USAT in our practice. Secondly I just wanted to briefly touch on thrombolytic dose and duration.

So ULTIMA and SEATTLE II fixed those therapies and duration, lasting less than recorded 24 hours. And I think an unresolved question is there an advantage to longer thrombolysis so anecdotally I feel like reducing reductions in PA pressure and thrombus burden with continued CDT after 24 hours.

This may be impart attributable to heparin catch up as patients who are on heparin will have an improved thrombus burden and PA pressure over time although I think it's important to note that in SEATTLE II they saw that same PA pressure the end of USAT, and that transgressing echo 24 hours after the procedure.

So it is possible that we get a more accelerated PA pressure reduction with continuing CDT over 24 hours. But there are clear disadvantages to longer thrombolysis for example length and ICU statements which is gonna be a very important factor in adoption of CDT ICU stay time and hospital time for example. There's probably an increase bleeding risk at this time there's

no clinical benefit to accelerated PA pressure reduction. We recently enrolled in the PERFECT registry and comparing our results to others in the published literature may help me to share light on

of breath at rest. Her symptoms, she quantified as being moderate to severe. She told us she had a little bit of baseline asthma.

This was quite different. She actually had some new right leg swelling, and had been driving from Florida back up to New England. She did have her own history of DVT, but was not on anticoagulants. Other pertinent history, she didn't have any chest pain. She had no fever.

Her past medical history was otherwise positive for hyperlipidemia, and some orthopedic issues primarily. And you can see the rest of the, she was on baby aspirin, that was about it. And then some medications for her orthopedic issues. The timing's important here, so I want you to look at everything.

It's at 7:30 when she was first seen. You can see she's a bit tachycardic. She's 95% on Room Air though. And she's got a good blood pressure. She actually was not in a lot of distress. Her LABS were essentially

negative. But I will point out that, both the troponin and BNP were abnormal in her cardiac profile. She got an EKG perform, and I'd love to give you guys enough time to analyze this, but I'll just cut through the chase quick, and say that, she basically showed some sinus tach. A little bit of right access deviation, and a little bit of ST elevation.

It's a little bit unclear, we did not have an Ovkg. So initially, she was seen by the ER, and the Critical care team. CT of the chest was ordered, of course. She actually had consultation with both VIR and Cardiothoracic surgery, which is sort of our standard protocol.

CT findings, I want everyone to take a look at, pretty clear though if you, I'm gonna come over and try to get this. >> No, it's fine. >> Is it on there? >> Yeah. >> Oh, I'm sorry. So I'll just point out. I think everyone can see the large filling defect.

Here's some axial images that are through the ventricles. Again, I think the findings are pretty clear there. So based upon this clinical scenario, and the imaging findings, which of these is false or incorrect, if you wanna roll

the same question? [BLANK_AUDIO] I'm just gonna read these, they're kinda long. So the patient has clinically significant acute PE, and should be treated with anticoagulation.

Remember which one is false. Patient does not meet the definition of massive PE based on hemodynamic criteria. The patient meets the less common definition of submassive PE, based on obstruction over 75% of the right pulmonary artery.

D, the patient meets the most common definition of submassive PE, based on hemodynamic EKG, lab and CT findings. Or the real tough one, so you gotta think about it, none of these are false. I think we can open the polling. [BLANK_AUDIO]

And I'm gonna do a little bit different, I'm gonna try to go over the answers at the end. But you can show me answer now, it's fine, it's not gotta matter. We're gonna talk about each of these. Each of these is designed to sort of teach a certain point. So the

fact, if we get them wrong, that's good, okay. Looks like most people did pretty well on that. Can you go back to the slides please? So this is real clinical care, and this is what happens with these patients. So over the next five hours, I have the vitals. What I wanna

point out is the difference, that the patient starts out at 7:30 on Room Air. And by the time we're getting toward midnight, we're seeing the patient has progressed to a non-rebreather mask, and then basically on CPAP at the end. So this is happening relatively abruptly. And they have been starting an anticoagulation. Basically,

blood pressure is still maintained. Those are probably the important points there. An echo was obtained. And again, in the interest of time, I'll just show you that the reading was a limited study. But there were suggestions of right ventricular volume overload, and there was actually dilation, and reduced function in the left

ventricle. Those are probably the key findings. Based on the current scenario. Now this one is which one is correct. You can go ahead and show that polling.

>> You got the same question? >> Yeah, I wanna put the next. Yeah, I'll just read this quick. So continued anticoagulation and monitoring is recommended, thrombolysis should never be performed, unless there's hemodynamic compromise. Peripheral thrombolysis

may be performed in such cases. Catheter based thrombolysis, rather than peripheral thrombolysis, should always be performed for this case like this. Or emergent surgical embolectomy, rather than peripheral, or catheter thrombolysis should be performed in cases like this. So let's just roll that poll.

[BLANK_AUDIO] Okay, and we could show the answer. So, sounds like most people are on track there. I'm gonna kinda go through these now, and talk about them a little bit. And the main focus of my talk is gonna be, sort of differentiating massive and submassive PE. These are basically gonna be based on the guide lines. And I

suggest everybody familiarize themselves with these, and they are changing periodically, they're updated every few years. Which one is false. I think people did pretty well here. The one that was false was, this one about the less common definition of submassive PE. Submassive PE is really based on right heart strain, not the

volume of clot seen on PE, although it can be dramatic. And therefore, that was the one that was incorrect. Volume of clot burden has not been predictive of mortality. And that's been shown in a large metanalysis. Just some of the other answers.

Large clot burden, the standard of care is anticoagulation. I don't think anybody would argue with that. Patient with the massive PE criteria, you really need hemodynamic compromise, which our patient did not have at that time. And these are the criteria.

You really have to have a pressure under 90, or sustained blood pressure drop of 40 for 15 minutes, or require basically CPR blood pressure support. Submassive PE is essentially defined, that which produces right heart strain, without producing systemic hemodynamic compromise. That's kind of the key.

And a right heart strain, can be evidenced by many of the findings that we saw, including EKG, echo, CT, or cardiac levels of the blood that we'll talk about. EKG abnormalities, they're talked about a lot, but they're actually fairly non-specific.

And that's one of the problems with them. People talk about the classic pattern which is the S1Q3T3, but it's really seen in less than 20% of cases. In this case, we did have many of the findings, and it was suggestive. But again, EKGs are not specific enough to really

diagnose that. CT really is actually quite good. And again, in this large metanalysis is actually shown to also correlate with mortality, both from PE and all-cause. So CT is very useful. Although again,

the thrombus load is not really predictive of mortality. That's important to keep in mind. But it is associated with adverse clinical outcomes. So you can take that into account, when you're deciding on some of these submassive cases, whether you progress to more aggressive

treatment. Clearly in this case, if we look at the diameters of the right, and left ventricle, and the measurements are there, there was no doubt that this was actually right heart strain. The humoral markers are a little bit like the EKG. And that they're not extremely specific, because as we'll talk about here,

BNP can be elevated, anytime there's any condition stretching the RV. And troponin is really elevated by anything that causes myocardial ischemia. However, in the setting of submassive PE, they are associated with right heart strain,

clinically significant right heart strain. So that's important to keep in mind, they can be useful. Over the next five hours, the patient got more hypoxic, the vital signs got worse. So we have a patient that's declining. The echo, as we talked about, confirmed right heart strain.

This is just to add up something, to orient you a little bit, showing the dilation of the RV, compared to left V. EKG really is the gold standard. Although I have to say, there're some papers on MR now, that are pretty good,

where you actually can get some of these also. The big thing really is diameter, and hypokinesis, or a kinesis actually, which was present in this case. I didn't show you the video to save some time. The next question which again, I think people did pretty well on.

I don't wanna say it's a trick question, but it does make you think, and we'll talk about the answers. The one that was correct is that, peripheral thrombolysis may be performed. It's not mandated, you don't have to do it. And I'm gonna talk about the guidelines, that they're actually very soft on thrombolysis.

So when going through each of these, the patient clearly at this point was still submassive. And the guidelines recommend anticoagulation, not routine thrombolytics, unless you have a protocol. But they are advocated in certain situations. And those certain situations are, that you have a low risk of bleeding, or the initial course or clinical course after anticoagulation, suggests

hypotension or risk of developing it. And it was felt in this case, that this patient was progressing this way. So this is the correct answer for this. Regarding pulmonary artery catheter directed therapy, which is probably what people would rather hear about than this clinical side,

the recommendations are pretty limited if you really read this closely, not because people don't believe in it, because there aren't good randomized-controlled trials to prove it, and they're

very clear about that. Essentially if you're gonna give the lytic, they actually recommend a short two hour infusion, rather than infusing into the main PA. The guidelines recommend, catheter assisted removal for patients with massive PE, and contraindications, failed thrombolysis, or thrombus likely to cause death, all right?.

Now just so we don't all feel bad, surgical embolectomy is in the same boat, because there's not really good randomized trials. And if you look at the recommendations on surgical pulmonary embolectomy, they're actually the same. They recommend contraindications,

failed thrombolysis or thrombus likely to cause death. Now I don't know if you're psychic or how you really know that, cuz if it's that imminent, you're probably in trouble. But that is the guidelines, and that's what you need to be familiar

with. Just a little side on pulmonary embolectomy, we actually have a couple good surgeons. Certain cases are somewhat recommended. So if you have a large right heart burden, that's potentially a case where they do better at, okay.

And the mortality rate has been coming down. So we're fortunate to have a couple of young, impressive surgeons that are available for this. This is just such an example. Just wanted to show you this large burden in the right heart. We decided that we'd send that person to surgery, and they actually

took the smaller stuff out of the left. Just to close it out now, the therapy for the current patient. I just have to show it quick. The patient actually continued to go downhill very rapidly in that last hour.

The TEE confirmed the TTE. She did start to drop her blood pressure. Thus as we talked, she went into the massive category. Basically did the usual. We accessed and went up. In the interest of time, I'll go quickly.

Multimode treatment, we dropped the pressure from about 60, down to about a mean of around 35 or so. We left an infusion catheter in for a few hours. Came back later, her mean pressure was even lower, put a filter in.

She actually got extubated the following day, and believe it or not, went home. So this is to summarize, the guidelines are all evidence based. I suggest everybody really know them, cuz they are right now the key to managing the patients.

I think a pulmonary embolism response team is key, with an algorithm at your institution. I think case by case variation is not good. Your institution needs to manage these, based on the signs that we had. And if you do that, and plan ahead, you will save time, and take good care of patients.

So, I'll leave it at that.

[INAUDIBLE] case. If the entire IVC is thrombosed we may need to do a thrombolysis and after thrombolysis in this case the thrombose only was limited

into the filter, and then the filter was retrieved. So again if the filter bearing IVC thrombosis is it because of the filter or is it from the disease process, maybe the filter is doing its job and then DVT thrombus is coming from the legs so overall it's like chicken egg so no one knows the exact answer, but Dr. Core/g actually mentioned

about the IVC filters may increase the DVT, and the IVC thrombose rates. So that's one of the reasons that actually retrieve those

So 57 year old, same stuff we've been talking about.

Edema 6 days 8 duration, [SOUND] ER ultrasound [UNKNOWN] Thrombolysis. Here is the CT and as you can see there is clot in the [UNKNOWN] Right there, and there is clot in the [UNKNOWN] For catheter directed lesions I usually don't put the filters in, but in this case

we put a filter in. So everything went fine, filter placed and patient underwent uneventful lysis, [UNKNOWN] Patient evaluated

three months and six months for filter removal, but filter was not removed due to 'irregular IVC in the venogram' and I saw the venogram myself, also and I said, okay. So finally this was a trial patient, and trial patients are my

babies. So I said I'm gonna bring the patient back I'm gonna do this myself, so I brought the patient back in eight months to remove the filter, I should have scheduled the patient on the day that I wasn't there, but anyway nevertheless, so here's what it looks like and this is

what they were calling irregular filter, irregular IVC. This isn't clearly an inflow, and it's above the filter anyway. Anyway let's talk beyond that, so normal filter. We grabbed it and we pulled a little bit and here they come.

And I advanced the sheaths and I pulled a little bit more it still didn't come. So I called Mark Johnson. I said Mark come in the middle of a case and I this is not coming. >> Can you hear the sound of this. >> And he said that oh come on,

why don't you twist the sheathes as you advance it, and sometimes it has a cutting to the action and it can cut through these stuff and cut through. >> [INAUDIBLE] >> He just said no, those of you who you don't believe me that's his cellphone number call

him. Okay? >> [LAUGH] >> You will see the deaths hand and I did call him. [SOUND] There we go, there we go. So I listened to him, he has grey hair, he knows more than I do so,

and he doesn't have accent. >> [LAUGH] >> So it still didn't come and then the filter looked funny, it looked like that so I went down and I injected most of it and said, this doesn't look really good and I have done everything I can so at this point I called Zeeve/g

I said Zeeve/g Mark told me to twist and I twist it and this thing didn't come out and I'm sort of stuck in the keyboard is not included, he goes, well two things [SOUND] Okay. >> What I think I said. >> Yeah he said two things. Number one you never listen to Matt Johnson,

and number two we did a meth analysis in the JVIR and it turns out that whenever you get into this sort of situation you have to put a balloon in there, have you heard of a balloon? I said yeah we just saw one in the aorta of an esophagus so we can certainly do that. So we went ahead and put a balloon in there, and so post ballooning

this is what it looks like. So obviously the cable is twisted so this filter was in the [UNKNOWN] In the wall, and I listened to my Mark Johnson and twisted this thing, the whole cable twisted, so I cannot understand-

>> Do you remember which direction you twisted it? >> Clockwise or counterclockwise? >>He said to twist it like he used to do when he was 18 like that, but I didn't.

I actually went in one direction all the time and the whole thing just got twisted, what can I tell you? He was on the phone, I didn't see what he was saying. >> I cannot recall this conversation. >> [LAUGH]

>> I would tell you, this is actually true unlike everything else that you've said, and that is that working on filters in a long time in animals, and I was working on one filter and a retrieval device that was very aggressive and I couldn't get the filter out so I did twist it and I managed to twist it 720 degrees, and then I had a sheath from below and I injected from

below and the cable was completely occluded as you might expect cuz the filter was there and twisted then I let it up 720 degrees and it would look like it was normal afterward that's true so- >> I think maybe that's what you need to do. >> Well you didn't tell me that when I called you.

>> [LAUGH] >> You didn't turn it enough. >> So at this point I was a little discouraged so I called my date and I said Mike what can I do? And he said two things. Number one, by the way he was coming back from Japan and he was

in the airplane, but you can always reach him by the way and I didn't put his cell phone number up there, he said three things. One, you never listen to Mark Johnson, and number two you never listen to Zeeve/g and what did they teach you? When in doubt, put a stent in there.

And then I heard somebody in the background say, sir you can't be talking we're flying, so he hung up. So I put a stent in there. Anyway move on, and so this is what happened. And so we put a stent in there and of course the stent migrated,

I didn't misplace it the stent migrated by itself. >> [LAUGH] >> Looks like a tornado stent, is that what you placed? >> Yeah yeah I mean it sort of watermelon seeded out there just for the effect of it, and so it was really the stent's fault.

And so note that this area is compressed, so obviously the operator during the deployment noticed something was wrong and they were trying to adjust that stent and the top of the stent was open as they said earlier that the ends of the stent are not

very friendly, the ends were probably in the wall and as the operator was pulling this thing compressed and then they deploy and sort of ended up like this. So at this point I got involved and so we said okay well, Jake says when in doubt stent, so let's just put another stent

in there, so let's this time just make sure we've done it properly. So we went ahead and put another stent in there, and landed properly now we've got a stentment/g from there all the way down to there so about this segment is inside the other stent that we opened up, and the filter is beginning to look like a Matt Johnson filter now so sort of opening up a little bit.

And it looks okay, we've got our flow back and so after all that excitement we did okay at this point we were so- >> So now you are taking the filter out right? >> Yeah actually at this point I was thinking,

how I'm I going to take this filter out and I was thinking about how to take this filter out and then those other things and so this is how we took the filter out, this is the rest of it. You really don't expect me to sort of show something dumb and just simple, stop right there,

no this continues. Six days after this procedure, patient presented to ER with 2 day history of worsening left flank, and as we mentioned earlier on, these are trial

patients. Anybody does anything in the hospital to trial patient, they have to tell me so they called me and they said the patient had left flank pain and I was really, really, really, worried.

What I was thinking that something bad may have happened, so CT was done, and this is the CT. This is what I thought would happen. The patient was anti-coagulated by the way. And in fact it did happen.

So we got two layers of stents in here. This is Matt's/g filter, and so we have a fluid around the kidney, congested kidney, no outflow, maybe maybe not some clot in here. So I really did wanna call Mike and say Mike I'm sending this patient out so we decided that well we have to fix this,

we can't just let it go and when in doubt go hit stent. And so here is our attempt. [BLANK AUDIO] So as you can see I have a zeeve/g sheath in there, by the way that's a zeeve/g sheath as sort of angular,

and I was so hoping I could get in there just slide right by that thing and [SOUND] I am feeling so good now, is that all right? >> I thought you were going to stick the kidney?

>> I cut that's actually not a bad idea. But we got through, we got through that and as you can see there is a very little room right there but surprising to say that here's what things look like as same as CT, [INAUDIBLE] Felling the effects sitting in there, and I was thinking that at some point we're going to have to come

back and embolize other variance there right, for pelvic congestion. And so the first stent went in, these stents I tell you stand no chance against two layers of compressed wall stents against the wall.

It's just pull filter right there, this is, I stand no chance with that. >> Migrated again yeah. >> Yeah what can I tell you. So we decided that oh, this needs a second layer of stents, and so the second layer of stents was put in and this guy,

by the way these two stents, I will not mention the manufacturer and all that, I picked them because of the engineering sort of information we had that they have the largest radial force and compression resistance of any nitinol stents, and these are the two that we selected and

double layered and that- >> They're also unlabeled for this indication. >> Yes absolutely. It does say it in the IFU by the way oh I'm sorry the name is right on that so having said that let's move on.

So we ballooned it and then this is what we've got. We re-establish antegrade flow and as you note this is what's the date in here okay, it's 7/25/2014. And this [UNKNOWN] Looks okay,

so let's give you follow ups. Let's flank pain result in a few hours, no change in kidney function at all, serial duplex ultrasound confirm continue with patency last follow up was a month ago, and everything is amazingly open, and she's doing great

with all that hardware in there, and group planning and taking match filter out one of these days. Thank you.

be able to hear it. So this first case is a young woman who had undergone what is quickly becoming a very popular bariatric procedure in the United States, a sleeve gastrectomy. This was done recently, three weeks earlier.

And she has been unwell for the last 48 hours with sort of a gastroenteritis type of symptoms and presents to the ER with diffused abdominal pain, vomiting, and diarrhea. I won't show you her detailed labs, suffice to say lactate was normal, white blood count was normal,

as was amylase. So being a good ER they did what all ERs do. They immediately put her into the scanners and did a contrast-enhanced CT. I think they did that before they examined her. So she has a completely impacted Mesenteric Venous System with fresh

clot that is distending the veins and it's extending up to and including all of her portal system. So these are the salient causes of the Mesenteric Venous Thrombosis and let's say parenthetically she was subsequently found to have a hypercoagulable state, and she was dehydrated by virtue of her recovery from her recent surgery.

So historically the treatment is systemic anticoagulation, and then if peritoneal signs develop, this mandates typically an exploratory laparotomy. These are very, very challenging cases to do surgically.

All of our GI surgeons involved in this case were not at all really wanting to go in and do a thrombectomy. So a newer approach is to create a TIPS. This is a TIPS in a person with a normal liver, non-cirrhotic liver and then using that TIPS as a conduit to create outflow cuz you

need outflow, you need inflow [COUGH] To do catheter directed therapy. So this was our initial portal venous access as you can imagine it was very difficult to know when we were in because if you inject too much contrast you'll kind of obscure things, and if you don't inject enough contrast,

you can't really be sure. It's not like you're doing a DVT case where you've got the beautiful venogram with the contrast perfectly opacified and a long sausage of clot. This is always [INAUDIBLE] Sort of this snagle-tooth appearance of contrast.

So that was signs that we were in and then it was simply a matter of getting down and again with a looped wire confirming that we were coursing down through the main portal vein and into the SMV. From that point, we did a venogram again to confirm that we were in the Mesenteric Venous System. We then went ahead and did a conventional TIPS with a stent graft.

And then at this point, and this is something that other members of the audience here might have a different approach. We tend to use the androgen in this setting. There is a black box warning for use in the pulmonary arteries and certainly if you're doing anything that is going to be close to the SA node, you need to be very,

very careful for [UNKNOWN] Arrhythmias. So our approach is to activate the device for no more than 20 seconds at a time, monitor the heart rate, make sure the heart rate returns to baseline and of course have atropine standing by.

And that's actually been a very successful approach not just in TIPS, but in the pulmonary arteries. I know that's not the experience that some others have had. This was a very hard to manage clot, so we had to supplement that with balloon meseration, and then even the over-the-wire percutaneous

thrombectomy device which is, for those of you who aren't familiar with that, it's sort of a rotating basket that spins at about 3,000 RPMs, and it's inserted and delivered over an 025 wire. This is a Nitrex wire that the device is being used in. You can see we're making some progress

here but it's by no means a great looking appearance. We've got a little bit of flow now trickling through the splenic vein but even our TIPS, our fresh TIPS created within this normal liver is accumulating some clot within it and you do have to be careful with these kind of devices and the chain link fence,

they can become entrapped. So you have to be very careful as you're monitoring your delivery. So once we'd established some slow flow through from the SMV through the portal vein, we then did again something that would be considered controversial.

As we said this woman had a sleeve gastorectomy three weeks earlier. She has morbid obesity. It's going to be very difficult to determine if she is having oozing from her surgical bed. So this obviously involved big conversation with intensive care, with GI surgery, hepatobiliary surgery,

us and so forth. So the consensus of that was we were going to be monitoring her very, very closely but [INAUDIBLE] Overnight. And this is what came out of that. This was the next day. We did do some touch up angioplasty with these images and we did

have this area where we had some refractory thrombus just at the root of the main portal vein and as we worked on that some more again with a variety of thrombectomy devices, this was the best we could get. But the flow through here on a DSA venogram was so robust as you'll

see some examples that Riyadh will show where if you're having good flow, just the patient's own intrinsic lytic system, their own intrinsic plasma can take care of this. So we decided at this point to stop and she did well.

The rest of her recovery was uneventful. She was eating by the next day. She was discharged the following day. This is six months later. Everything is wide open and a year out she had symptom-free. She had been worked up and was found to have a hypercoagulable syndrome,

so she's gonna be on lifelong anticoagulation. She's also on Lactulose, just sort of prophylactically. She doesn't have any discernible systemic encephalopathy issues, but she was to be coming back for occlusion of her TIPS. She's so happy with the outcome she's kinda worried if we occlute

her TIPS something bad will happen. So she's subsequently moved to Texas. So if any of you are from Texas, there's a patient from Philadelphia who needs to TIPS embolization.

She's not coming back to Philly for that. She's said that. So that was just an example of using the TIPS as a conduit both to approach clot and to get outflow and because the clot volume is so massive, a combination of mechanical and pharmacological techniques is typically required.

Any questions before Scott shows the case? >> [INAUDIBLE] Exactly. >> [INAUDIBLE] >> Yes, you could have just gotten trans-hepatic access into the portal vein percutaneously, you could have gone transjugularly and gone in temporarily but,

I think the conventional wisdom of folks who have done this for acute Mesenteric Venous Thrombosis, is that you need to have that outflow of the TIPS. You're trying to create continuity of a vascular system and having that outflow through the TIPS enables the clot to be bathed with your

lytic, and endogenous plasma and so on. That's the rationale. >> [INAUDIBLE] And I agree with Tim, I'd put the TIPS in, and the idea is you wanna raise the flow. [INAUDIBLE]

How long do you [INAUDIBLE] >> Well that's a very good question. The largest series in the literature is from Asia, I think there's six or eight cases. It's really limited to case reports so we don't have a lot of data.

But empirically you kinda wait for that early thrombogenic period to subside, and you wait until the patients is successfully anticoagulated and has gone a period of weeks symptom free. So we were prepared to embolize her when we saw her back at six months. She was so happy and she was very, very ill at the time and she

sort of felt like she dodged a bullet as it were and so we started those discussions at six months and then a year later, we resumed those discussions and she subsequently left the area. But I think within the first few weeks you wanna make sure the patient's

anticoagulated that residual clot. There had been interval improvement in her TIPS ultrasound as well. So that segment of the main portal vein was completely open and free of clot. Yes. >> [INAUDIBLE] In this scenarios you hear a lot [INAUDIBLE] Make these

decisions and not really [UNKNOWN] >> Yes definitely. The thing about TPA, circulating TPA is half life of four to six minutes. But the problem in venous lyces/g is that the clot volume is so high

you get absorption of TPA to the surface of the clot. So you accumulate a systemic lytic state by having still active TPA that's not necessarily circulating but it's bound to clot. And that's why you'll see a big steep rise in bleeding complications with venous thrombolysis in days two three and so on. So we were prepared to do an overnight thrombolysis in her accepting

that there was gonna be potential for a systemic bleeding state and therefore bleeding from the sleeve gastrectomy. We were following her [UNKNOWN] Not that they would have been expected to do anything which they didn't overnight. But we did it more as kind of a medical legal thing so that we could never something did happen,

well the Fibrinogen must have dropped and you never followed it. So we were following those at four hour intervals. Yes, one last question and then we do wanna get on, got some amazing cases for you to see so.

>> So we have something similar to this where we have [INAUDIBLE] I'm not sure cuz [INAUDIBLE] In this scenario you have [UNKNOWN] >> We do now. We didn't at the time we did this case. I think that would be another very interesting approach.

There's more than one way to get to the finish line. You do have to give up wire access for that device, and we like knowing that we were over the wire the whole time. We knew exactly where we were but definitely that's another great option.

All right so, do you wanna share your, one more.

So this is a gentleman, 75 year old male, presented outside hospital with a PE and DVT,

had OptEase placed three months prior. They attempted the retrieval at the outside hospital, and we got a call saying we're sending this patient to lights and sirens. [BLANK_AUDIO] [LAUGH] What the heck is that?

>> I'll let it speak for itself. >> Equatorial. >> [LAUGH] >> Equatorial. >> That is a 300 O14 wire, a support catheter, a nine French sheath in the right groin, and a severely turned up-tease

on its head. [SOUND] [LAUGH] So we're thinking, how are we gonna get this out? What do we approach first? He said, lets try the wire first in the jugular approach. Took the wire, pulled it and I don't know if you can really appreciate it here, but this filter's free floating, not attached in any way

whatsoever. And when you pull the wire, it's basically tying a slipknot inside the filter. So there's no way that that wire thing was gonna work. And as you can see the other end of the wire is coming out the

sheath at the groin. Literally they had hooked up a [UNKNOWN] to the sheath side arm, taped like a garden hose, the wire, put in the ambulance. So we've got left groin access, put in the 18 French sheath

and said, maybe forceps will help us get a little bit better control. Turn it around and it's really not this massive metal which is exactly what it became. It's not doing any better for us. So then we thought, okay,

let's snare it from the top, and see if we can pull it in that way. Wasn't working and it became clear to us that the only way we're gonna be able to do this is to get a 26 French Dry Seal on the right groin, forceps while pulling simultaneously from the top to elongate it

as much as possible. So that's what we did, pulled hard, pulled hard. By the way, the way we got this in is we had the foreign body wire in and then we put her in wire and side-by-side and the foreign body wire

was->> You were gonna stretch it out. That's what you're- >> Exactly. Elongating the whole thing. And so we had the foreign body wires coming out external to this Dry Seal, and then out own wire inside of that.

The main finding here is the massively extended bladder. >> Oh, that's why it's an extreme case. >> [LAUGH] >> I totally get it. >> That is the lesson. >> That is a big bladder.

>> The M&M here is [INAUDIBLE] We got the filter out but it was still attached to the wire here. So what we did is we put our pull string ready at the right groin, pulled the whole thing out. And there it is. >> Where is the balloon?

>> [LAUGH] >> The balloon, there is a support catheter. And perhaps the most amazing thing is that this catheter was pristine. >> [INAUDIBLE] >> Pristine.>> Ready for another filter. [LAUGH] >> Great, thank you very much.

approach to pulmonary embolism.

This is a guy 22-year-old who has ARVC, which is arrhythmogenic right ventricular cardiomyopathy. Which is a bad condition whereby you get fibrosis and fat infiltration of your right ventricle, and essentially it becomes this very flabby,

very enlarged, very thrombogenic as well as very arrhythmogenic right ventricle. So this guy he was systemically unwell, but he presented with an acute decompensation where he got ventricular tarchycardia storm. And that's where you just are in V tacky constantly. He had an

ASCDA and this was shocking him 20 times a day when he presented. Very hypoxic guy as well, he was on Rumer/g he was done at 88% really was quite difficult to improve. Lucky or unlucky as well as all that he developed massive hemoptysis. This was so bad that he needed intubation to prevent a spill over

from presumably it was a right sided hemoptysis based on his chest X ray. As soon as he got intubated of course the usual thing that happened is, he decompensated further from a cardio respiratory point of view. And that's where we got urgently consulted.

So he was rushed for a CT, you can see he'd already been interbated at this time. His right ventricle looks terrible, his right artrium was a large volume thrombus or venous and in his lumbar and segmental both sides,

but predominantly on the right side he had a moderate volume thrombus there. So we restratified this gentleman as a massive presentation given the fact that he was hemodynamically compromised, and previously arrested with [UNKNOWN].

And then came up with our decision making algorithm. So this is a gentleman who was hemoptysizing massive hemoptysis requiring intubation, but the gentleman who had a large volume thrombosis in his lungs.

Eventually a decision was reached between everyone that he could not be lysed so we proceeded with mechanical thrombectomy. Obviously there are a couple of different options you can use there I felt that in my hands using a large caliber device such as the flowtreiver the Inari or the angio vac and a guy who is having recurrent arrhythmias would not be terrifically safe.

I didn't feel I'd be able to get it around to get the thrombus without him arresting again, so I decided to use a low profile device. So we came in from the neck as we do most of our interventions in pulmonary arteries from the neck. Came round you can see this occlusive thrombus here within the [INAUDIBLE] lumbar

artery, and then I used a device called cleaner. Which is rotation sinusoidal 035, 344 depending on which one you use. We use the 7 French device you can see here on the echo this is in the right main PA. Echo is very handy for monitoring of this main PA interventions so

you really get live real time updates that can be pretty helpful, particularly for doing aspirational thrombectomy that can tell you what your end point is and where you're gonna stop. So chopped up some of the clot with that you here you can see it on the angio view at it working in the area of [INAUDIBLE] thrombus. And then aspirated the thrombus that we had hopefully broken up

using the indigo device from panumbra. We use the cath six here for some reason we'd run out of catheters at the time, otherwise it would have put that. So this was 6 French aspiration device and we got out a descent amount of thrombus over the course of about an hour, or so he began

to stabilize he was never terrific to be honest but he stabilized somewhat. So he wasn't having anymore arrhythmias, no further shocks to his AACD and we were able to bring him up stairs. So success I think it's difficult to quantify how much good we actually

did, because two days later after he had some neurologic signs of improvement he proceeded to have ECMO. And then he went on to have a heart transplant for his AACD 30 days later and actually this is about a year ago, he's been doing very well, we pulled out the filter,

we placed at the time nine months and he's been doing great. So I think overall the procedural success, certainly a patient success is debatable to how much we contributed to his overall success.

And those are two of the cases. Thanks.

>> Okay. So, very old man with a cold left leg. History of heart disease and A-fib. [BLANK_AUDIO] So, what do you do? Heparin?

>> Yes. >> Back to hospice? >> [LAUGH] >> It's a problem right? Yeah no one's exactly chopping it the bit to treat this 92 year old guy right?

[LAUGH] Then again you can't leave it right? >> [INAUDIBLE] >> He's an ambulating guy so right. >> [INAUDIBLE].

>> Exactly so I mean I'm not sure there's much of a choice, right? You pretty much have to treat that. So here is the angiogram. So this one, unlike the last one, looks embolic, right. So approach for embolic.

>> [INAUDIBLE] >> Same thing. Penumbra. >> Would you try a Penumbra? >> Right. We try not to lyse them. Exactly. Absolutely. All right.

And there it is. This is a CAT 6 and actually we are using that separator thing here. The separator kinda looks like the burr of a Diamondback device almost. And it's funny that sometimes it's actually hard to get that thing to exit

the catheter. You kind of have to push it a little bit. But you can be pretty aggressive like Dan said. The wire's very floppy. Similar to the catheter, you can pretty much be pretty aggressive with that thing and not cause

a whole lot of damage. >> When you introduce the catheter, are you introducing it over like a standard wire that you have. And so you take the wire out and put the macerator in. >> Right.

>> Okay. >> So in this case, since he doesn't have any disease above that's of significance, you can pretty much take that thing over an 035. I mean I've done this, I don't have a huge experience with the Indigo, but as far as I can tell,

the way to do it is you bury in the clot so that when you turn on, there's nothing coming back, which just minimal. And then you wait. And you let it do its thing. Like a couple minutes.

And then at some point, I think if it doesn't progress, then you break out and separator or a wire or something and you kinda open up some flow in the distal end and then it's start sucking again and you try to retrieve that.

But what you ought to be careful of is once the flow opens up, it's gonna suck a lot of blood. So you wanna be ready to turn that thing off anytime you have too much blood loss. So after doing some of that, looks like we had some residual clot

in the AT. On this guy we actually knew that the PT was his primary run off vessel. So we weren't too concerned about that and obviously something like this we're just trying to get something that is okay and get him off the table right?

Tried the Indigo in the PT but didn't have much luck. I think we might have downsized, a different catheter probably. So I did my Spider thing again and obviously I wouldn't be showing this case if it hadn't worked right? So again deploy the Spider below and pull back,

and I think here we're stenting it right through the six French guide. And you can actually inject around it of course cause you have a tube at the back of that. >> How do you size your Spider for something like this? >> I like to oversize it for this kind of thing.

>> Even in the tibial vessels?. >> Yeah, this is probably a four. I think you have less chance of losing emboli around the top of it if you oversize it. >> You don't think there's in-folding? I mean. >> If you go really big I think so yeah. [BLANK_AUDIO]

But I don't know this I mean. >> Nitro on the table? >> Lots of Nitro. Pulled that back right into the guide, pulled out all sorts of junk. And in this case this worked nicely. So the run off is open so that point we get out

as soon as possible, as quickly as possible and move on. And that's the kind of case I would do obviously with Angiomax running, as opposed to heparin, and in my experience it's far superior.

Okay next case 70 year old male history of bilateral fem distal

bypasses, has an occlusion on the left side, and this guy is severely ischemic. So he's got like motor deficit, and some level of paralysis. He's pretty far gone.

Sensorimotor deficit, let's call it 2C. But anyway somewhere around there, right. So the question here is do you go straight to surgery? Which I think is a legitimate option. Unfortunately, in my experience surgeons don't like that option and they want everything lysed

regardless. So here is the angiogram and he's not only thrombosis fem distal bypass, but also the common femoral and the iliac above that right so that explains why. And I think we actually knew this going into it cause we get duplex ultrasound on all these patients.

We usually don't get CT or MR but we'll have usually have enough time to get at least a duplex. We have a pretty good idea what's going on already. Cause duplex is pretty good for looking for acute occlusions. And there is minimal reconstitution of some branches down here. So how would you approach this?

Obviously mechanical right >> Yeah I mean for [INAUDIBLE] >> You got to get something open right? >> Exactly. >> Exactly. So that's what we did. And that's an A-Jet, I guess.

We checked that. I guess we took this into the bypass and into the profunda and he got some flow into those branches. Some residual clot there so we stuck a catheter and lysed it. Again just regular Multi Sidehold Infusion. The most common I use I think is the 50 centimeter. [BLANK_AUDIO]

Brought him back and everything looks pretty good. He has a proximal anastomotic stricture. We ended up dilating there and got a nice result and distally at the PT, that actually looks really nice. So there we go and I guess my question on him is, is that the only, is that small lesion at the proximal anastomosis or the inciting event? Its hard to imagine but we couldn't

find anything else. Any questions?

Okay, next case. 60 year old male, history of multiple vascular surgical procedures, he had aortobifem, a couple of fem-fems,

a couple of fem-pops on both sides and had multiple thrombectomies performed. But never thrombolysis. This is an amazing case. This guy had actually extensive vascular history but never had an angiogram. I don't know why went for all this.

But I think it was actually Hopkins. I know, amazing. So he presents with very little information first of all, and cold legs with right more so than left but obviously it's thrombosed, something centrally.

We They did come with an outside CT luckily but unfortunately not much else. So we really didn't have much idea about his surgical history. And this can be challenging obviously. This looks similar to the other case but it's a different case but it's a different case. But that proximal end looks pretty similar.

This case of course both limbs are thrombosed. And I think in In this case you can make a pretty strong argument for surgical thrombectomy probably, right? This guy has an aortobifem, both of them are down,

there's a fem-fem below that. So one of this probably chronically down cause you've got a fem-fem So there he's got a couple of fem-fems there. All right, brilliant And then as you go down he's got like three

grafts on the right and a couple on the left. This is totally absurd right? Yeah. [LAUGH] So what do you access?

>> [LAUGH] >> Any ideas? >> [INAUDIBLE] >> Send him away, exactly. >> Stick the fem-fem. >> How do you know which one is the bad fem-fem? Palpation?

>> Yeah, well with ultrasound you can often see what's more acute. >> Right. >> Right? So the echogenic one is probably more chronic right?

So that's what we did. We ultrasounded, got an idea which fem-fem is more acute and stuck it. Oh wait, sorry. I've one thing before the CT scan. So as you it go it down,

you can see that obviously he's got all these grafts that are all occluded apart from this one here that looks it comes up a profunda and it goes down. And this thing is actually patent and then comes then and touches down the AT. So that's the amazing thing about vein grafts. When you get a good vein graft,

those things are really good. And this thing stays open despite this incredibly poor inflow. So yeah. We stuck the fem-fem. This is the angiogram. But we stuck the fem-fem here going in this direction.

And I'm not sure why we went in that direction, probably because his right leg was worse. This was easy so it's not clearly acute. We were able to catheterize the aorta easily, do an angiogram and you see that obviously the aortobifem limbs are both down.

And I'm assuming the left is the down chronically and this fem-fem was placed at some point. And then you see a lot of collaterals reconstituting the profunda, and then here is the proximal anastomosis of his vein graft of a profunda branch. It's pretty amazing. And that looks actually pretty good

And the AT is up below that. What was interesting about this guy is that he didn't seem to have a lot of pain. It was out of proportion with his vascular findings. I don't know if that was just from multiple surgeries maybe.

So in this guy, we lysed. And I had nothing to do with the fact that it was 4:30 in the afternoon. So we stuck a catheter in there, one of those long Uni-Fuse catheters. I tend not to use Ekos in the arterial system,

and yeah we've discussed thrombolysis I guess, right? Came back, looks pretty good, right? So this limb is all opened up. I mean thrombolysis works great.

If it weren't for thrombolysis, we couldn't do any of this stuff, right? So this is open, this is open. It's got some strictures here, but all in all pretty good apart from the outflow on the right.

So obviously now we're gonna redirect our access down the right leg and see what's going on, right? So we get into the profunda branches and get the A Jet out and start buzzing around a little bit, trying to find the connection to that bypass.

We end up ballooning here. And then that kinda opens things up and now we can see this branch which gives off that bypass. And in the interim what's funny is we've started filling some of these old fem pops, which look all degraded.

I mean I considered embolizing that. That doesn't look so good, right? >> [LAUGH] >> And on this side, this all looks pretty good, apart from

one little dislembles/g that we had which is very annoying. So we went after that and I think we might have used A-Jet or aspiration, I'm not sure but it ended up here. So as you can see this is open here and now it's occluded the distal anastomisis. So we went back down with a Spider, and I did my swat spider thrombectomy

trick, which is where I deploy a Spider below the lesion and then pull it back. And sometimes this works and you can actually pull out. And this is one of those cases that I actually pulled this out and got lucky, and he has a patent AT below that.

So we ballooned the distal anastomosis, got a decent result that reconstitutes peroneal, I think that is. And then we did end up actually getting access going in the other direction to work on the left side. So it's fairly a lengthy case.

And we haven't seen him since, so who knows what happened to him. >> Back at Hopkins. >> Back to Hopkins for some more surgery. And here is the seg and non-invasives. This is pre and post, so pretty much what you'd expect right? [BLANK_AUDIO]

Okay, questions? >> [INAUDIBLE] >> I think he was on anti-coagulation. Yeah. But I'm not entirely sure. But that's a good question. Like how do you treat these? I prefer not to give anticoagulation if possible and just go with antiplatelet.

But sometimes, a lot of patients guys who come back every year and get lysed get the same stupid ex-fem or whatever lysis and stuff. They end up basically being on anticoagulation and dual antiplatelet and they still come back so yeah.

case there is a 43-year-old had a two day history of abrupt onset pain and numbness in his right leg. He also was started on heparin and his symptoms resolved before we were called. He has an interesting past medical history of a lupus anticoagulant,

he also had a PE many years ago for which he was put on lifelong Coumadin. It's unclear exactly why, and he had recently stopped it of his own accord. Then he's also hypertensive,

hypercholesteromic. On exam he has no pedal pulses in his right leg. So this is interesting because we don't really know what exactly is going on for he does have some risk factors atherosclerosis or he could have in-situ thrombosis you could have a paradoxical embolus with his history of venous thromboembolism perhaps he has a right collect shunt, does he have a conventional embolus.

So actually the vascular surgeons and the arterios/g recall concurminently/g the vascular surgeons ordered a CT, it's a little bit hard to make this out but here's just a baloney pop showing that this is open. Also, there's no inflow or outflow disease, so the iliacs are clean.

This isn't emboli from the iliacs. Here you can see a filling defect in the baloney pop. Distally, only the peroneal is open in the right leg. Also there is a small filling defect in the the left which doesn't project well here on the image. But too there's bilateral emboli, so there's some sort of proximal source

[BLANK_AUDIO] So again what would be the treatment? Optionally I could just anti coagulated he is asymptomatic at this point, do you want to do some catheter directed thing and I think an important issue in these sort instances is what is the proper workup to find the source

of the emboli? So there is a big difference between how sensitive TTE and TEE are then there are also some of our diagnostic cogs will take cardiac MR as far as superior to either of those we also need to look for right collect shunt. So Dan what do you think about this? >> Typically we get echo and CTA and typically they are both negative and then you sort of lice it and move on.

>> [LAUGH] >> Hope for the best, that's my experience with that stuff. >> Yes I found it could be universally maybe TE is the way to go, I don't know probably too invasive, the acute setting. MR doesn't seem infusable if it's a patient with acute limb ischemia I guess this patient was probably asymptomatic,

so finding those embolic sources is not easy. >> And availability of MR is not great to explain. >> Yeah, I'd echo again, I've never actually found a source, but despite always looking for one. So we decided to go to angiography to try and open this up.

So here we know from the CT there is no in flow disease, SFA is open, here is this clot or embolus in the baloney pop extending into the AT, on this right side image you can see that the peroneal is reconstituted. So we again tried to use the Indigo system real to remove that large clot that was in the distal pop and proximal AT but as we knew

from the CT there was clot distal in the AT as well and then here you can see the reconstitution of the peroneal artery I guess this brings up the point of what is our goal? So are we gonna, or what are we satisfied with? Should we just try and open up the peroneals, if the patient has single

vessel runoff, should we try and get all the clot out, and what strategies would people employ to do that. So we've got the big piece out of the top but there still no inline flow to the foot, Dan what would you consider doing next? >> I would probably go after lowest hanging fruit here and try

to get at least one vessel open maybe in the peroneal, it's hard to know how hard that thrombus is and it could be easier to clear out or not. So I would probably try to get it wired down and see how difficult it was to pass and then maybe do aspiration thrombactomy there

as well. >> That's my thought as well I guess you can try to get the ET open but I don't I think you are gonna have much success if you don't have distal target and so if you are literally seeing nothing to reconstitute distally it's gonna be a herculean fete to open up the AT so given this appearance we know peroneal is open below so we just have to somehow span this

junction here. So we did exactly that we did some additional Indigo with an angio plastic balloon then when we were done we have reasonable inline flow to the foot and he did well afterwards. >> So you ballooned it as well. >> Yeah and

so after we did the Indigo we had trickle of flow but it sort of had disappearance but worse and we that angioplastic/g balloon might help improve the flow. >> And it did? >> Mm-hm >> With no additional backward/g effects so I mean yeah should we use this there is a protection device of something perhaps

curiously, or maybe expectedly we didn't find the source in this patient either. So he had a TTE in which they saw a right-to-left shunt. They called the right-to-left shunt on the TTEs then we got exited, maybe we actually have a source here. And they did a TEE and they said no,

in fact there is no shunt and there's no neural thrombus. So we don't have a source for this and what's the problem if there's anti-coagulation. Some other physician had determined he needed to be on life long coumadin for his thromboembolic disease so we just put him back.

>> He was right.

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