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External Occlusion of IVC from Urothelial Carcinoma|Thrombolysis,Stent Placement|63|Male
External Occlusion of IVC from Urothelial Carcinoma|Thrombolysis,Stent Placement|63|Male
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Submassive PE | Pulmonary Emoblism Interactive Lecture
Submassive PE | Pulmonary Emoblism Interactive Lecture
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Pulmonary Ablation | Interventional Oncology
Pulmonary Ablation | Interventional Oncology
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Algorithm for Treatment | Pelvic Congestion Syndrome
Algorithm for Treatment | Pelvic Congestion Syndrome
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Systemic vs Catheter-based Thrombolysis | Management of Patients with Acute & Chronic PE
Systemic vs Catheter-based Thrombolysis | Management of Patients with Acute & Chronic PE
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Q&A Pulmonary Embolism | Management of Patients with Acute & Chronic PE
Q&A Pulmonary Embolism | Management of Patients with Acute & Chronic PE
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Treatment Options- CAS- Embolic Protection Device (EPD)- Proximal Protection | Carotid Interventions: CAE, CAS, & TCAR
Treatment Options- CAS- Embolic Protection Device (EPD)- Proximal Protection | Carotid Interventions: CAE, CAS, & TCAR
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Indirect Angiography | Interventional Oncology
Indirect Angiography | Interventional Oncology
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Cone Beam CT | Interventional Oncology
Cone Beam CT | Interventional Oncology
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Education Strategies to Reduce Human Errors | Looking for risk in all the Right Places: The Anatomy of Errors in Healthcare
Education Strategies to Reduce Human Errors | Looking for risk in all the Right Places: The Anatomy of Errors in Healthcare
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Percutaneous Mechanical Intervention | Management of Patients with Acute & Chronic PE
Percutaneous Mechanical Intervention | Management of Patients with Acute & Chronic PE
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Prospective CDT Trials | Pulmonary Emoblism Interactive Lecture
Prospective CDT Trials | Pulmonary Emoblism Interactive Lecture
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Treatment Options- CAS- Embolic Protection Device (EPD)- Distal Protection | Carotid Interventions: CAE, CAS, & TCAR
Treatment Options- CAS- Embolic Protection Device (EPD)- Distal Protection | Carotid Interventions: CAE, CAS, & TCAR
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Massive PE | Pulmonary Emoblism Interactive Lecture
Massive PE | Pulmonary Emoblism Interactive Lecture
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Ablative Radioembolization | Interventional Oncology
Ablative Radioembolization | Interventional Oncology
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Ultrasound-assisted Catheter-directed Thrombolysis | Management of Patients with Acute & Chronic PE
Ultrasound-assisted Catheter-directed Thrombolysis | Management of Patients with Acute & Chronic PE
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Ideal Stent Placement | TIPS & DIPS: State of the Art
Ideal Stent Placement | TIPS & DIPS: State of the Art
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TIPS: Techniques- CO2 Venography | TIPS & DIPS: State of the Art
TIPS: Techniques- CO2 Venography | TIPS & DIPS: State of the Art
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Where do we go from here for submassive PE | Pulmonary Emoblism Interactive Lecture
Where do we go from here for submassive PE | Pulmonary Emoblism Interactive Lecture
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Case 3 - Right iliac occlusion | Subintimal Recanalization | Complex Above Knee Cases with Re-entry Devices and Techniques
Case 3 - Right iliac occlusion | Subintimal Recanalization | Complex Above Knee Cases with Re-entry Devices and Techniques
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Treatment Case 2 | Pelvic Congestion Syndrome
Treatment Case 2 | Pelvic Congestion Syndrome
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CTEPH Studies | Management of Patients with Acute & Chronic PE
CTEPH Studies | Management of Patients with Acute & Chronic PE
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CT Imaging- Acute PE | Management of Patients with Acute & Chronic PE
CT Imaging- Acute PE | Management of Patients with Acute & Chronic PE
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Therapies for Acute PE | Management of Patients with Acute & Chronic PE
Therapies for Acute PE | Management of Patients with Acute & Chronic PE
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Treatment Options- TransCarotid Artery Revascularization- TCAR | Carotid Interventions: CAE, CAS, & TCAR
Treatment Options- TransCarotid Artery Revascularization- TCAR | Carotid Interventions: CAE, CAS, & TCAR
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The Case that Launched the Cornell PERT (PE Response Team) | Pulmonary Emoblism Interactive Lecture
The Case that Launched the Cornell PERT (PE Response Team) | Pulmonary Emoblism Interactive Lecture
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Case 1 - Non-healing heel wound, Rutherford Cat. 5, previous stroke | Recanalization, Atherectomy | Complex Above Knee Cases with Re-entry Devices and Techniques
Case 1 - Non-healing heel wound, Rutherford Cat. 5, previous stroke | Recanalization, Atherectomy | Complex Above Knee Cases with Re-entry Devices and Techniques
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Case- May Thurner Syndrome | Pelvic Congestion Syndrome
Case- May Thurner Syndrome | Pelvic Congestion Syndrome
arterycatheterizecausingchapterclassiccliniccommoncommon iliaccompressioncongestionendovascularevidenceextremitygonadalhugeiliaciliac veinimagingincompetenceincompetentMay Thurner Syndromeobstructionoccludedpelvicpressuresecondarystentsymptomstreatmentsvalvularvaricositiesvaricosityveinveinsvenavenous
Background on Interventional Oncology | Interventional Oncology
Background on Interventional Oncology | Interventional Oncology
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Bland Embolization | Interventional Oncology
Bland Embolization | Interventional Oncology
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Registry and Data | Management of Patients with Acute & Chronic PE
Registry and Data | Management of Patients with Acute & Chronic PE
arterycathetercatheter directedchaptercomplicationsdirectedechoheparinimprovementintermediateinterventionalmassiveNonepatientpatientsperfectpressurepulmonarypulmonary arteryratioreductionregistryriskseattlestrainstudiesstudysystolicthrombolysistpaunfractionated
Transcript

My case is a 63 year old man with past medical history of steady T3

High grade uroelial carcinoma and then he underwent right nephruoretectomy at 18 months ago. But recently he presented with worsening of the back pain and lower extremity swelling. This is the contrast MR imaging six days prior to procedure and the next image of MR there is a soft tissue dense/g in the aorta

and then there is a small size of an IVC is displaced down to here. Another image showing inferior to [INAUDIBLE] There is some another irregular mass, continue to inferior and then there is some [UNKNOWN] mass and this is [INAUDIBLE] Sort of on the IVC but still below this mess, there is some contrast in as

much but it definitely something on the IVC. [BLANK_AUDIO] And then he subsequent had progressive worsening in bilateral lower extremity swelling. Also he complained of some kind of tingling numbness that's why the private team requested CT angio to see if there is a peripheral artery damage or not, and this is the contract CT. There is a little bit of IVC here. It's very small. There is a soft tissue around the aorta and the post of IVC and then in this message continue down, this is your previous

surgical cleave that you wrapped in renal vein, still there is a soft tissue mass, This is another soft tissue mass around the empirial chuto/g surgical cleaves. This inferior vena cava and there is a little bit of an increasing size as some infiltration, it's hard to tell this is just thrombosis

so there's a little over less contrasting as much [BLANK_AUDIO] This is your coronary the contrast image, similar to the MR imaging, there is some extensive soft tissue mass around the surgical cleave, below the inferior vena cava there is some low density to the side [BLANK_AUDIO]

Now this is a shunt. Basically upon the clinical and imaging findings. which of the following would be the most appropriate diagnosis? A. Occlusion of the IVC from the exrinsic compression, primary to the tumor of IVC, tumor extension into the IVC, short

inflow of the unopacified blood, congenital absence of IVC with azygos continuation. It's a very easy questions. [BLANK_AUDIO] 52%. Okay the tumor extension into the IVC, I think is as just to based on clinical

history is we think that it is a recurrent urethral carcinoma, recurrent mass, just to exchange a compression that its hard to tell invasion into IVC or not, but is a temperature diagnosis over this kind of things and then sometimes is a primary carcinoma made into the It could have been a cover but it appears that the patient already had a [INAUDIBLE] 18 months.

I think is critically is just an [UNKNOWN] vwna cava I think it's just the best answer but it's possible diagnosis that it is [INAUDIBLE] tumor over inferior vena cava and sometimes the tumor extension into the IVC and the inflow of unopacified blood and is rarely has a congenital absence of inferior vena cava with azygos continuation. [BLANK_AUDIO] okay this is the second

same question based upon the clinical and imaging findings which of the following would be the most appropriate management step? Radio therapy, surgical resection of the tumor, anticoagulation, catheter-directed thrombolysis only, catheter directed from thrombolysis and stent placement.

[BLANK_AUDIO] Okay most of the people answer [BLANK_AUDIO] I think this patient has acute occlusion of IVC by recurrent mass.Catheter directed thrombolysis only doesn't relieve the extrinsic compression of IVC recurrent mass, so additional stent placement needed to keep IVC open and that patient is not a good candidate for surgical

resection of the extensive recurrent mass. Radio therapy has made the size of the chromatin mass but there's a I think I don't know about radiotherapy but it takes some time to relieve the patient's symptoms or if the patient's symptom is getting worse, and that's why the catheter directed thrombolysis and stent placement could be the best three month option,to relieve the symptoms of this patient.

And then we accessed both popiteal veins and we placed the catheter just over the IVC occlusion and then we infused 0.5 miligram per hour and then we keep them overnight And this is, venogram much better because there's a patient with acute thrombolysis and then [UNKNOWN] do well with just tPA infusion overnight but there is

some little residual, some thrombosis also there is some right here common iliac narrowing, and then we start with the angiojet device and then this is thrombolysis, some blood clots there but most of the blood is clear. And then also we [UNKNOWN] we did venogram.

There is some tight narrowing or under such [UNKNOWN] and then we made diameter and then about 17 millimeters over the anterior vena cava And then we noticed there is some [UNKNOWN] of the post iliac vein and then we placed a 60 millimeter Wallstent post iliac vein and then we [UNKNOWN] and then we placed a 20 millimeter Wallstent along the surgical cleave and then we

open up to 80 millimeter balloon. And then there is some residual blood clot on the right common femoral vein And then we use a Cleaner device. And then just to [INAUDIBLE AUDIO] assemblage blood clot. This is the final imaging.

And then as a very widely [UNKNOWN], and a good floor. And the stent usually widely opened. They tried to revisit the procedure. Somewhat over this patient is a 63-year-old, and then they [INAUDIBLE

AUDIO] the arterial crashed lumbar. And then it's causing [UNKNOWN] over inferior vena cava by the occluded mass. And then cuts addictive/g thrombolisis, incentive/g placement/g was possibly/g done.

And then his symptom have resolved after procedure. And then six months follow-up. And then he had no recurrence of leg swelling.

much more controversial so you it was pretty clear that we have to rescue

massive PD patients from death but with these statistics what are we supposed to do with sub massive PE well are we supposed to prevent mortality it's gonna be hard to do if the mortality is only 2 to 3% because you're trying to really

improvements of a very low statistic are you trying to reduce the rate of hemodynamic deterioration that's a possibility what about long-term disability if you remove clot upfront

will these patients do better six months one year or two years down the road frankly we don't know the answer to any of this and the reason is that the pytho trial made things quite difficult for us to interpret the pytho trial was the

trial that was going to answer all uncertainty this was a trial where it took some massive PD patients in that high-risk intermediate category and randomized them to receive a bolus of tenecteplase which is similar to TPA but

is not the same versus anticoagulation alone what did it show well it showed there was no difference in death between tenecteplase and placebo so they actually gave a placebo drug so that no it was a double blinded

study now if you look at the next line though a lot more patients decompensated if they receive the placebo than that's not to place this is not a bad thing you know it's not it's not great when you have to intubate somebody or initiate

pressors so if you can avoid that outcome that's it that's a pretty good thing so maybe it is the right thing to give systemic thrombolysis in the setting of sub massive PE problem was this the bleeding you look down here

there was an eleven percent rate of major bleeding in the tenecteplase arm there was a two percent rate of intracranial hemorrhage so now we've got this therapeutic window that's hard to interpret so we seem to be improving

outcomes from an efficacy standpoint but then we're also increasing the rate of bleeding so basically what we've sort of coalesced around is that systemic thrombolysis has a questionable risk benefit profile because the rate of

bleeding and the rate of really serious bleeding is makes us nervous so is that an opportunity for catheter director thrombolysis and I'll call this the poster child for Catherine throwing license if this is how it worked every

time we might have a homerun so this is gentleman looked terrible well still in the sub massive category but breathing at 35 times a minute hypoxic had his main PA systolic pressure of 60

millimeters of mercury you look over here and there's this large clot in the right upper lobe go to the left side and then there's all this clot in the left lower lobe as well so what do we do we put in bilateral infusion catheters this

can be an E Coast catheter it can be a standard catheter these areyou nafeez catheters have side holes starting from here and ending it's hard to see but there's another radiopaque marker somewhere down there on this side there

and somewhere over there and between those markers you have multiple side holes and those are put up inside the clot so you're dripping TPA at a rate of about 0.5 to 1 milligram per hour and you're getting it directly into the

clock that's the theory and so after 20 to 24 hours of that you know you're given 20 to 24 milligram of TPA that's compared to 50 or a hundred that you get was sitting with systemic thrombolysis you get something

that looks like this where the pulmonary arteries look pristine the PA still the systolic pressures come down the patient feels great now the skeptic would look at this and say well if you just tried some heparin and you just infuse saline

would you have the same result and frankly if you were to conduct the experiment you might find something interesting or not interesting but we never have conducted that experiment but you know I'll tell you a little bit

about the ultimate trial if I have time I don't want to go to overtime though

blasian it's well tolerated and folks with advanced pulmonary disease there's a prospective trial that showed that

there are pulmonary function does not really change after an ablation but the important part here is a lot of these folks who are not candidates for surgical resection have bad hearts a bad coronary disease and bad lungs to where

a lot of times that's actually their biggest risk not their small little lung cancer and you can see these two lines here the this is someone who dr. du Puy studied ablation and what happens if you recur and how your survival matches that

and turns out that if you recur and in if you don't actually a lot of times this file is very similar because these folks are such high risk for mortality outside or even their cancer so patient selection is really important for this

where do we use it primary metastatic lesions essentially once we feel that someone is not a good surgical candidate and they have maintained pulmonary function they have a reasonable chance for surviving a long

time we'll convert them to being an ablation candidate here's an example of a young woman who had a metastatic colorectal met that was treated with SPRT and it continued to grow and was avid so you can see the little nodule

and then the lower lobe and we paste the placement prone and we'd Vance a cryo plugs in this case of microwave probe into it and you turn off about three to five minutes and it's usually sufficient to burn it it cavitate s-- afterwards

which is expected but if you follow it over time the lesion looks like this and you say okay fine did it even work but if you do a PET scan you'll see that there's no actually activity in there and that's usually pretty definitive for

those small lesions like that about three centimeters is the most that will treat in a lot of the most attic patients but you can certainly go a little bit larger here's her follow-up actually two years

that had no recurrence so what do you do when you have something like this so this is encasing the entire left upper lobe this patient underwent radiation therapy had a low area of residual activity we followed it and it turns out

that ended up being positive on a biopsy for additional cancer so now we're playing cleanup which is that Salvage I mentioned earlier we actually fuse the PET scan with the on table procedural CT so we know which part of all that

consolidated lung to target we place our probes and this is what looks like afterwards it's a big hole this is what happens when you microwave a blade previously radiated tissue having said that this

was a young patient who had no other options and this is the only side of disease this is probably an okay complication for that patient to undergo so if you follow up with a PET scan three months later there's no residual

activity and that patient actually never recurred at that site so what about

typical symptoms if you want to hit the play on this I think this is one we've probably already seen but it's it's the the algorithm that I go through for treatment so we do my renal vena Graham

there we go it's classic definitely has reflux and so next I will selectively catheterize the gonadal vein and here you see very large pelvic varicosities and so my standard is to actually treat the varicose veins with a sclerostin

much like I would sclerosis a varicose vein in the leg and there's a few reasons that I do that and so here's how I do it I'll put an occlusion blown up you see the picture on the left of the screen has an occlusion balloon it's the

same occlusion balloon we use for a tips procedure and I'll temporarily block the gonadal vein and fill up the system or the varicosities with contrast so that I get a sense for the volume of sclerosis and I would use then the picture on the

right is a venogram after I've injected the sclerostin so I've evaluated the volume and then I've replaced all that contrast by forcing it through the system to drain out the pelvic veins and filling the varicosities with

soldier column I do that because I believe and there's no data to prove it that it helps prevent superficial phlebitis in those varicosities so if we're just gonna block off the gonna dull vein then we have stagnant blood in

all the pelvic varicosities and stating that blood wants to clot and when blood clots on its own it'll stretch and expand the vein and cause pain and so in my own personal experience that has created a little bit worse post

procedural symptoms for patients compared to the patients that I use so TRADOC all to actually treat the varicosities so that's what I start out with and then since I'm kind of an old-fashioned guy I still go with the

coils and so I coiled the whole going a ttle vein and you can use sort of whatever you want you know that's the simplest thing for me are using nester coiours coils and and fill it up some people use the long detachable shaping

coils kind of an expensive way to do it if it saves you radiation then then that's that's one of the reasons to do it but the point is in in the venous system you have to be able to and I show this slide because you can see a

collateral vein or at least a branch there a confluence point that we've coiled off too if you do not treat the entire length there's a there's a lot higher chance for recurrence and veins have a way to find their way around if

they can communicate back up then patient gets recurrent symptoms and that can happen in about ten percent of cases so in order to prevent that you treat the whole gun out of vein and that's sort of why I think some people like to

use liquid sclerosis because then they will be able to sort of profuse all those branch points that would have a chance for recurrence case number two

a little bit more systemic versus catheter directed thrombolysis so once you've decided that a patient needs TPA what are the differences here well if

you give patients systemic TPA you're gonna give them a much more rapid delivery this is for those patients who have high-risk PE they're the ones who are coding for those patients you give them 200 milligrams of IV usually you

get 50 first and then another 150 over a very short time period they have a very high risk of bleeding as a result of that a catheter is much slower you're gonna infuse one milligram maybe which is what I think most people do

over several hours maybe a few maybe a day so it's slower targeted versus non targeted well catheter is much more targeted you're gonna give Pete you're gonna give the TPA right into the

pulmonary arteries that's the whole point in our in our thought process as a result you give a lot less drug so when you give a patient based off of some of the trials 24 milligrams of TPA over a 24-hour period that's a lot less than

200 milligrams in a 10 minute period and then the bleeding risk is very different for these patients catheter based treatments have a high bleeding risk but it's possibly lower than the initial bleeding risk of patients getting

systemic TPA so I wanted to go through a

happy to take any questions or in

ultrasound we don't usually use contrast but one of the procedures were doing for the treatment management of a pulmonary embolism is the ultrasound assisted Rumble Isis do we need contrast so for the thrombolysis is the catheter itself

so you still need to give contrast two to do the procedure but while the catheter is running you don't need to give any contrast four for that is that what you're we don't usually use contrast for ultrasound but

all right when you're treating how will you know that it sliced the clot is less what you frequently do is check the pressures so that catheter allows you to check the pressure and so once you start a patient so you do a pulmonary

angiogram which requires contrast and you put the ultrasound assisted thrombolysis catheter in the eCos catheter then after 24 hours or 12 hours you can measure a pressure directly through that catheter and if the

patient's pressure is reduced you don't have to give them anymore injections yeah and if we are using ultrasound for treatment is it possible to do it for diagnostic purposes No so not for non the prominent artists for

diagnostic imaging unless you're doing an echocardiogram which is technically ultrasound in the heart but for treatment otherwise you need you will need to inject some dye oh thank you

hi I'm Katrina I'm NGH I have one more question okay for your patients with chronic PE do most of them begin with acute PE or if they very separate sort of presentations that's that's a great question so all of them

had acute PE because you can't have chronic without acute but a lot of them are not ever caught so you'll have these patients who had PE that was silent that maybe one day they woke up and had a little bit of chest pain and then it

went away couple days later they thought they had a bronchitis or a cold and then you find out five years later that they had a huge PE that didn't affect them so badly and then they have these chronic findings they usually show up to their

family practice doctor again with hey I just can't walk as far as I can I have a little heaviness they rule them out from a heart attack but it turns out that they have CTF so you you all of them had a Q PE but it takes a lot of time and

effort to find out whether they truly have chronic PE so it's usually in a delayed fashion thank you all right well thank you guys again appreciate it [Applause]

of these issues filters are generally still use or were used up until a few years ago or five years ago almost exclusively and then between five years and a decade ago there was this new concept of proximal protection or flow

reversal that came about and so this is the scenario where you don't actually cross the lesion but you place a couple balloons one in the external carotid artery one in the common carotid artery and you stop any blood flow that's going

through the internal carotid artery overall so if there's no blood flowing up there then when you cross the lesion without any blood flow there's nothing nowhere for it to go the debris that that is and then you can angioplasty and

or stent and then ultimately place your stent and then get out and then aspirate all of that column of stagnant blood before you deflate the balloons and take your device out so step-by-step I'll walk through this a couple times because

it's a little confusing at least it was for me the first time I was doing this but common carotid artery clamping just like they do in surgery right I showed you the pictures of the surgical into our directa me they do the vessel loops

around the common carotid approximately the eca and the ICA and then actually of clamping each of those sites before they open up the vessel and then they in a sequential organized reproducible manner uncle Dee clamp or unclamp each of those

sites in the reverse order similar to this balloon this is an endovascular clamping if you will so you place this common carotid balloon that's that bottom circle there you inflate you you have that clamping that occurs right

so what happens then is that you've taken off the antegrade blood flow in that common carotid artery on that side you have retrograde blood flow that's coming through from the controller circulation and you have reverse blood

flow from the ECA the external carotid artery from the contralateral side that can retrograde fill the distal common carotid stump and go up the ica ultimately then you can suspend the antegrade blood flow up the common

carotid artery as I said and then you clamp or balloon occlude the external carotid artery so now if you include the external carotid artery that second circle now you have this dark red column of blood up the distal common carotid

artery all the way up the internal carotid artery up until you get the Circle of Willis Circle of Willis allows cross filling a blood on the contralateral side so the patient doesn't undergo stroke because they've

got an intact circulation and they're able to tolerate this for a period of time now you can generally do these with patients awake and assess their ability to tolerate this if they don't tolerate this because of incomplete circle or

incomplete circulation intracranial injury really well then you can you can actually condition the patient to tolerate this or do this fairly quickly because once the balloons are inflated you can move fairly quickly and be done

or do this in stepwise fashion if you do this in combination with two balloons up you have this cessation of blood flow in in the internal carotid artery you do your angioplasty or stenting and post angioplasty if need be and then you

aspirate your your sheath that whole stagnant column of blood you aspirate that with 320 CC syringes so all that blood that's in there and you can check out what you see in the filter but after that point you've taken all that blood

that was sitting there stagnant and then you deflate the balloons you deflate them in stepwise order so this is what happens you get your o 35 stiff wire up into the external carotid artery once it's in the external cart or you do not

want to engage with the lesion itself you take your diagnostic catheter up into the external carotid artery once you're up there you take your stiff wire right so an amp lats wire placed somewhere in the distal external carotid

artery once that's in there you get your sheath in place and then you get your moment devices a nine French device overall and it has to come up and place this with two markers the proximal or sorry that distal markers in the

proximal external carotid artery that's what this picture shows here the proximal markers in the common carotid artery so there's nothing that's touched that lesion so far in any of the images that I've shown and then that's the moma

device that's one of these particular devices that does proximal protection and and from there you inflate the balloon in the external carotid artery you do a little angiographic test to make sure that there's no branch

proximal branch vessels of the external carotid artery that are filling that balloon is inflated now in this picture once you've done that you can inflate the common carotid artery once you've done that now you can take an O on four

wire of your choice cross the lesion because there's no blood flow going so even if you liberated plaque or debris it's not going to go anywhere it's just gonna sit there stagnant and then with that cross do angioplasty this is what

it looks like in real life you have a balloon approximately you have a balloon distally contrast has been injected it's just sitting there stagnant because there's nowhere for it to go okay once the balloons are inflated you've

temporarily suspends this suspended any blood flow within this vasculature and then as long as you confirm that there's no blood flow then you go ahead and proceed with the intervention you can actually check pressures we do a lot of

pressure side sheath pressure measurements the first part of this is what the aortic pressure and common carotid artery pressures are from our sheath then we've inflated our balloons and the fact that there's even any

waveform is actually representative of the back pressure we're getting and there's actually no more antegrade flow in the common carotid artery once you've put this in position then you can stent this once the stent is in place and you

think you like everything you can post dilated and then once you've post dilated then you deflate your balloon right so you deflate your all this debris that's shown in this third picture is sitting there stagnant

you deflate the external carotid artery balloon first and then your common carotid artery and prior to deflating either the balloons you've aspirated the blood flow 320 CC syringes as I said we filter the contents of the third syringe

to see if there's any debris if there's debris and that third filter and that third syringe that we actually continue to ask for eight more until we have a clean syringe but there's no filter debris out because

that might tell us that there's a lot of debris in this particular column of blood because we don't want to liberate any of that so when do you not want to use this well what if the disease that you're dealing with extends past the

common carotid past the internal carotid into the common carotid this device has to pass through that lesion before it gets into the external carotid artery so this isn't a good device for that or if that eca is occluded so you can't park

that kampf balloon that distal balloon to balloon sheath distally into the external carotid artery so that might not be good either if the patient can't tolerate it as I mentioned that's something that we assess for and you

want to have someone who's got some experience with this is a case that it takes a quite a bit of kind of movement and coordination with with the physician technologists or and co-operators that

to talk about is indirect angiography this is kind of a neat trick to suggest to your intervention list as a problem solver we were asked to ablate this lesion and it looked kind of funny this patient had a resection for HCC they

thought this was a recurrence so we bring the comb beam CT and we do an angio and it doesn't enhance so this is an image here of indirect port ography so what you can do is an SMA run and see at which point along the

run do you pacify the portal vein and you just set up your cone beam CT for that time so you just repeat your injection and now your pacifying the entire portal vein even though you haven't selected it and what to show

well this was a portal aneurysm after resection with a little bit of clot in it the patient went on some aspirin and it resolved in three months so back to our first patient what do you do for someone who has HCC that's invading the

heart this patient underwent 2y 90s bland embolization microwave ablation chemotherapy and SBRT and he's an eight-year survivor so it's one of those things where certainly with the correct patient selection you can find the right

things to do for someone I think that usually our best results come from our interdisciplinary consensus in terms of trying to use the unique advantages that individual therapies have and IO is just one of those but this is an important

lesson to our whole group that you know a lot of times you get your best results when you use things like a team approach so in summary there are applications to IO prior to surgery to make people surgical candidates there are definitive

treatments ie your cancer will be treated definitively with curative intent a lot of times we can save when people have tried cure intent and weren't able to and obviously to palliate folks to try to buy them time

and quality of life thermal ablation is safe and effective for small lesions but it's limited by the adjacent anatomy y9t is not an ischemic therapy it's an ablative therapy you're putting small ablative radioactive particles within

the lesion and just using the blood supply as a conduit for your brachytherapy and you can use this as a new admin application to make people safer surgical candidates when you apply to the entire ride a panic globe

thanks everyone appreciate it [Applause] [Music]

know we're running a bit short on time so I want to briefly just touch about

some techniques with comb beam CT which are very helpful to us there are a lot of reasons why you should use comb beam CT it gives us the the most extensive anatomic understanding of vascular territories and the implications for

that with oncology are extremely valuable because of things like margin like we discussed here's an example of a patient who had a high AF P and their bloodstream which tells us that they have a cancer in her liver we can't see

it on the CT there but if you do a cone beam CT it stands up quite nicely why because you're giving levels of contrast that if you were to give them through a peripheral IV it would be toxic to the patient but when you're infusing into a

segment the body tolerates at the problem so patient preparation anxa lysis is key you have them exhale above three seconds prior to that there's a lot of change to how we're doing this people who are introducing radial access

power injection anywhere from about 50 to even sometimes thirty to a hundred percent contrast depends on what phase you're imaging we have a Animoto power injector that allows us to slide what contrast concentration we like a lot of

times people just rely on 30% and do their whole the case with that some people do a hundred percent image quality this is what it looks like when someone's breathing this is very difficult to tell if there's complete

lesion enhancement so if you do your comb beam CT know it looks like this this is trying to coach the patient and try to get them to hold still and then this is the patient after coaching which looks like this so you can tell that you

have a missing portion of the lesion and you have to treat into another segment what about when you're doing an angio and you do a cone beam CT NIT looks like this this is what insufficient counts looks like on comb beam so when you see

these sort of Shell station lines that are going all over the screen you have to raise dose usually in larger patients but this is you know you either slow down the acquisition speed of your comb beam or

you raise dose this is what it looks like after we gave it a higher dose protocol it really changes everything those lines are still there but they're much smaller how do you know if you have enhancement or a narrow artifact you can

repeat with non-contrast CT and give the patient glucagon and you can find the small very these small arteries that pick off the left that commonly profuse the stomach the right gastric artery you can use your comb beam CT to find

non-target evaluation even when your angio doesn't suggest it so this is a patient they have recurrent HCC we didn't angio from here those arteries down there where those coils were looked funny even though the patient was

quote-unquote coiled off we did a comb beam CT and that little squiggly C shape structures that duodenum that's contrast going in it this would be probably a lethal event for the patient or certainly would require surgery if you

treated that much with y9t reposition the catheter deeper towards the lesion and you can repeat your comb beam CT and see that you don't have an hands minh sometimes you have these little accessory left gastric artery this is

where we really need your help you know a lot of times everyone's focused and I think the more eyes the better for these kind of things but we're looking for these little tiny vessels that sometimes hop out of the liver and back into the

stomach or up into the esophagus there's a very very small right gastric artery in this picture here this patient post hepatectomy that rides along the inferior surface of the liver it's a little curly cube so and this is a small

esophageal branch so when you do comb beam TT this is what the stomach looks like when it enhances and this is what the esophagus looks like when it enhances you can do non contrast comb beam CTS to confirm ablation so you have

a lesion this is the comb beam CT for enhancement you treat with your embolic and this is a post to determine that you've had completely shin coverage and you can see how that correlates a response so the last thing we're going

strategies so some things that we have

in place right now our peer review Grand Rounds CPOE this is one of my one of my favorite process improvements is is making the right thing the easiest thing and you do that through standardization of processes so that's standard work so

that's your order sets that's the things pop-ups although you don't want to get into pop-up fatigue but pop-ups help our providers for little gentle reminders to guide them to what's right for the patient and to cover everything that we

need we need to cover to ensure the safety of our patient so recently in the fall of last year we had a TPA administration err that occurred it involved a 69 year old patient who two weeks prior had had some stenting in her

right SFA she presented to our clinic when our clinics with some heaviness in her leg and some pain and when she was looked at from an ultrasound standpoint it was determined that her stents were from Bost so she was immediately taken

to the cath lab and it was after angiography did indeed show that there was clot inside these stents they did start catheter directed thrombolysis in the cath lab they also did started concurrent heparin often oftentimes done

with CDT what's usual for our institution is that we have templates that pull in the active problem list for a patient in this case the active problem list or a templated HMP was not used had they

used the template at agent p they would have found that the second active problem on this patients list was a cerebral aneurysm so some physicians will tell you some ir docs will tell you that's an absolute

contra contraindication for TPA however the SI r actually lists it as a relative contraindication so usually we're used to when you when you start a final Isis case you know you're gonna be coming in every 24 hours to check in

that patient in this case we started the the CDT on a Thursday the intent was to bring her back on Monday the heparin many ir nurses will know that we will run it at a low rate usually 500 units an hour and we keep the patient sub-sub

therapeutic on their PTT although current literature will show you that concurrent heparin can also be nurse managed keeping the patient therapeutic in their PTT which is what was done in this case so what ended up the the

course progression of this patient was that so remember we started on Thursday on Saturday she regained her distal pulses in her right leg no imaging Sunday she lost her DP pulse it was thought that it was part of a piece of

that clot that was in the the stent had embolized distally so they made the decision with the performing physicians they consulted him to increase the TPA that was at one milligram an hour to 2 milligrams by Sunday afternoon the

patient had an altered mental status she went to the CT scan which showed a large cerebral hemorrhage they ain't we intubated to protect her airway and by Monday we were compassionately excavating her because

she me became bred brain-dead so in the law there's something that's called the but for argument so the argument can be made that this patient would not have died but for the TPA that we gave her in a condition that she should not have had

TPA for namely that aneurysm so this shows how standard work can be very important in our care of our patients and how standard work drives us down the right way making the easiest thing the safest thing so since that time

we've had a process improvement group that we've established an order set specifically for use and thrombolysis from a peripheral standpoint and then also put together a guideline that was not in place so it's some of that Swiss

cheese that just kind of we didn't have a care set we didn't have a guideline you know we didn't use our template so all those holes lined up and we ended up with a very serious patient safety event so global human air reduction strategies

oops sorry let's go back these are listed in a weaker two stronger and some of what we're using in that case is some checklists so we developed a checklist that needs to be done to cover the

absolute contraindications as well as the relative and it's embedded in the Ulta place order that the physician has to review that checklist for those contraindications and also there to receive a phone call from pharmacy

just to double-check and make sure that they have indeed done that that it's not somebody just checking it off so we have a verbal backup sorry so the just

catheter some other things that we can do is mechanical intervention so if you have a patient usually with massive PE

or the inner or the high-risk B you got to do something to help them out so what we do is put a pigtail catheter and inject a little bit of TPA on the table and then twirl the pigtail or put a wire through the side part of the pigtail and

make it sort of a mechanical fragment fragmentation the problem with that is that fragmented clot goes downstream so when it's in a main pulmonary artery it actually has less surface area than it is when it is in a distal pulmonary

capillary so when you break that clot up you have to be careful because it can actually make the patient worse the benefit there there's no thrombolytic so if we're doing this we we generally are doing it in patients who can't either

receive TPA at all frequently we get patients with who have have had recent spine surgery who get a massive PE had brain surgery get a massive PE and you have to try to treat them without any TPA or even heparin the drawbacks are

that again it increases pulmonary vascular resistance by sending all those little pieces of clot into the small pulmonary arteries and capillaries and it makes it actually much worse in some patients again there's no control trials

and sometimes you need to have a bigger

these are our prospective CDT trials it's a lot to go through them so I'm not going to suffice it to say that the only one of these that is randomized is the

one in the top left the ultimate trial with 59 patients the rest of these are single set are single arm studies the optimized trial was randomized but the key arm it did not have was a control arm so all it did was vary the amount of

drug but there was no control arm to tell us how are people doing if they just get heparin well and I'll show you one result from these trials that is the most important result and that is up from the ultimate trial at 24 hours CDT

catheter to thrombolysis reduces the RV to lv ratio to a greater extent than heparin alone what does that mean so you saw all those pictures with the big dilated right ventricles our surrogate measure for right ventricular

dysfunction is the ratio of the diameter the inner diameter of the right ventricle to the left ventricle what we found in this study was that that ratio got reduced to a greater extent at 24 hours in the CDT arm compared to heparin

alone that means that CDT seems to reduce our V dysfunction faster than heparin now importantly 30 days later the echos looked identical so really it's a question of time which is not surprising what we've noticed in

our practice is that patients feel better faster okay I'm gonna go through the rest of this because I'm out of time but I want to give you a little bit of a sense of where we're going because there's bleeding associated with CDT and

maybe I'll show you this that in the Seattle to trial there was an 11% major bleeding rate now this was a pretty conservative definition but there were some serious bleeds and there were no intracranial

hemorrhages in this study but we have realized that CDT is not risk-free it's not like we've all of a sudden gained all of the advantages of systemic thrombolytics and none of the disadvantages now the rate of

intracranial hemorrhage seems to be about tenfold less but it does happen about 0.2 to 0.4% of the time the rate of major bleeding seems to be about 5% which is about half the rate of major bleeding that we see with system or

thrombosis so bleeding is still there it just doesn't seem to be as frequent so that's where some of these other devices are coming in then our a float Reaver the the the extra penumbra indigo cat 8 device and so the the float Reaver is

has actually gone through the full trial and the results are about to be published what is this thing well it's this pretty big hose which is about 20 French and it goes through the right heart and goes up there and it takes

this clot and literally aspirates it out and these are some of the things that will come out and that's sort of your post picture right there the data showed something similar to what we saw with the catheter directed thrombolysis

trials they had looked at 106 patients are vlv ratio was reduced again there's no comparator arm here so this is just the device on its own with a 3.8 percent adverse event rate and so now we're talking about mechanical devices that

don't use a clot-busting medication therefore you're gonna you can expect less bleeding but you're trading some of that off for a mechanical device that can cause injury to either myocardial structures or to the pulmonary artery so

that's something we have to be highly cognizant of as they're introduced into the market this is the penumbra cat 8 this is from Jim Benenati publication basically showing a couple things that's the separator that is the actual

catheter and that's the sheath back there so you've got poor profusion because of a clot in the inter lobar pulmonary artery and then at the end of it you have better perfusion for lung down there so we actually just completed

enrollment into the extract PE trial 120 sub massive PE patients the same efficacy endpoint you have to remember that has been established by the FDA as a way to get approval this is not the final

study nor should it be the final study when we evaluate these devices so to summarize sub massive PE what does the data not tell us CDT probably reduces the RV to LV ratio at 24 hours that is the main outcome that I want you

guys to remember from the ultimate trial it's associated you didn't see this data so don't worry about that we do see major bleeding and sometimes rarely but sometimes we see intracranial bleeding with CDT as well so what we're missing

from catheter directed thrombosis for sub massive PE is what are the clinical outcomes the RV to LV ratio is a surrogate outcome what about death what about clinical deterioration what about recurrent hospitalization what

about recurrent VTE how are people doing in the long term are they walking as well as they were before we don't know any of this none of the data right so far can tell us any of this information so where do we go from here for sub

kind of the embolic protection because I think with carotid artery stenting the stents there's a lot of different types they're all self expanding for the most

part and there's not a lot to talk about there but there is with regards to embolic protection and there so there's distal and violent protection where you have this where that blue little sheath in the common carotid artery you got a

wire through the ica stenosis and a little basket or filter distally before you put the stent in early on they used to think oh maybe we'll do distal balloon occlusion put a balloon up distally do your intervention aspirate

whatever collects behind the balloon and then take the balloon down not so ideal because you never really asked for it a hundred percent of the debris and then whatever whenever you deflate the balloon it goes back it goes up to the

brain you still have some embolic phenomenon in the cerebral vascular churn and then there's this newer concept of proximal protection where you use either flow reversal reverse the blood flow in the cerebral circulation

or you actually cause a stagnant column of blood in the ica so you can't get you don't get anything that embolize is up distally but you have this stagnant column the debris collects there you aspirate that actively before you take

down the balloons that are in position in the X carotids and common carotid artery and then you take everything out so let's walk through each of these if you really wanted to pick out the perfect embolic

protection device it's got to be relatively easy to use it's got to be stable in position so it's not moving up and down and causing injury to the vessel but even while it's in place cerebral perfusion is maintained so that

balloon the distal balloon not a great idea because you're cutting off all the blood flow to the brain you might stop something from embolizing up distally but in the process of doing that you may patient may not tolerate that you want

complete protection during all aspects of the procedure so when we place a filter as you'll see just crossing the lesion with the initial filter can cause a distal embolus so that's a problem you want to be able to use your guide wire

choice as many of you know when we go through peripheral vasculature there's your go-to wires but it doesn't always work every time with that one go-to wire so you want to be able to pick the wire that you want to use or

change it up if needed for different lesions so if you get to use your wire of choice then then that's gonna be a better system than something that's man deter and then if you have a hard time using that wire to get across the lesion

you have a problem overall and then ultimately where do you land that protection device and a few diagrams here to help illustrate this generally speaking these distal embolic protection these filters that go beyond

the lesion have been used for quite a while and are relatively safe you can see them pretty easily and geographically they have little markers on them that signify if they're open or closed and we look for that overall and

blood flows through them it's just a little sieve a little basket that collects really tiny particles micrometers in size but allows blood flow to pass through it so you're not actually causing any cessation of blood

flow to the brain but you are protecting yourself from that embolic debris and it's generally well tolerated overall we had really good results in fact when not using this device there's a lot of strokes that were occurring in use of

this device dramatic reduction so a significant improvement in this procedural area by utilization of embolic protection however distal embolic protection or filter devices are not a perfect APD as you as you may know

those of you have been involved in carotid stenting there is no cerebral protection when you cross the lesion if you have a curlicue internal carotid artery this filter doesn't sit right and and ultimately may not cause

good protection or actually capture everything that breaks off the plaque and it can be difficult to deliver in those really tortuous internal carotid arteries so ultimately you can cross the lesion but you may not get this filter

up if you don't get the filter up you can't put the stent then ultimately you're out of luck so you gotta have a different option filters may not provide complete cerebral protection if they're not fully opposed and again it does

allow passage of really tiny particles right so your blood cells have to be able to pass but even though it's less than about a hundred microns may be significant enough to cause a significant stroke if it goes to the

right basket of territory so it's not perfect protection and then if you have so much debris you can actually overload the filter fill it up in tile and entirely and then you have a point where when you capture the filter there's some

residual debris that's never fully captured either so these are concerns and then ultimately with that filter in place you can cause a vessel dissection when you try to remove it or if it's bouncing up and down without good

stability you can cause spasm to the vessel as well and so these are the things that we look for frequently because we want to make sure that ultimately if we just sent the lesion but we don't believe the vessel distal

to it intact and we're going to have a problem so here's some kind of illustrated diagrams for this here's a sheath in the common carotid artery you see your plaque lesion in the internal carotid artery and you're trying to

cross this with that filter device that's what's the picture on the right but as you're crossing that lesion you're you're liberating a little plaque or debris which you see here and during that period of time until the filters in

place you're not protected so all that debris is going up to the brain so there's that first part of the procedure where you're not protected that's one of the pitfalls or concerns particularly with very stenotic lesions or friable

lesions like this where you're not protected until that filters in place that first step you never are protected in placement of a filter here's an example where you have a torturous internal carotid artery so you see this

real kink these are kinds of carotid internal carotid arteries that we can see and if you place that filter in that bend that you can see right at the bend there the bottom part the undersurface of the carotid doesn't have good wall

my position of the filter so debris can can slip past the filter on the under under surface of this which is a real phenomenon and you can see that you can say well what if we oversize the filter if you oversize the filter then it then

it just oval eyes Azure or it crimps and in folds on itself so you really have to size this to the specific vessel that you plan to target it in but just the the physics of this it's it's a tube think about a balloon a balloon doesn't

conform to this it tries to straighten everything out this isn't going to straighten the vessel out so it doesn't fully conform on the full end of the filter and you have incomplete a position and therefore

incomplete filtration so this is another failure mode I mentioned before what if it gets overloaded so here's a diagram where you have all this debris coming up it's filling up the really tiny tiny particles go past it because this little

micro sieve allows really small particles to go distal but approximately it's overloaded so now you get all this debris in there you place your stent you take your retrieval filter or catheter to take this filter out and all that

stuff that's sitting between the overloaded filter and your stent then gets liberated and goes up to the brain so you got to worry about that as well I mentioned this scenario that it builds up so much so that you can't get all the

debris out and ultimately you lose some and then when the filter is full and debris particles that are suspended near the stent or if you put that filter too close to the edge of the stent you run into problems where it may catch the

stent overall and you have all of this debris and it looks small and you don't really see it and geographically obviously but ultimately is when you do a stroke assessment and it's not always devastating strokes but mild symptoms

where he had a stroke neurologist and the crest trial or most of the more recent clinical trials we actually evaluate a patient and notice that they had small maybe sub sub clinical or mild strokes that were noted they weren't

perhaps devastating strokes but they had things that caused some degree of disability so not insignificant here's a case example of a carotid stent that was done this is a case out of Arizona proximal carotid

stenosis stent placed but then distal thrombus that developed in this case and had post rhombus removal after the epd was removed so there's thrombus overloaded the the filter you can see the filter at the very top of the center

image you can see the sort of the shadow of the embolic protection device there distally aspirated that took the filter out and then ultimately removed but you can imagine that amount of thrombus up in the brain would have been a

devastating stroke and this is what the filter looks like in real life so this is what the debris may look like so it's not this is not overloaded but that's significant debris and you can see the little film or sieve that's on the

distal part of this basket and that's what captures the debris any of that in the brain is gonna leave this patient with a residual stroke despite a successful stenting procedure so this is what we're trying to avoid so in spite

about massive PE so let's remember this slide 25 to 65 percent mortality what do we do with this what's our goal what's

our role as interventionalists here well we need to rescue these patients from death you know this it's a coin flip that they're going to die we need to really that there's only one job we have is to save this person's life get them

out of that vicious cycle get more blood into the left ventricle and get their systemic blood pressure up what are our tools systemic thrombolysis at the top catherine directed therapy at the right and surgical level that what

unblocked me at the left as I said before the easiest thing to do is put an IV in and give systemic thrombolysis but what's interesting is it's very much underused so this is a study from Paul Stein he looked at the National

inpatient sample database and he found that patients that got thrombolytic therapy with hypotension and this is all based on icd-10 coding actually had a better outcome than those who didn't we have several other studies that support

this but you look at this and it seems like our use of thrombolytics and massive PE is going down and I think into the for whatever reason that that the specter of bleeding is really on people's minds and and for and we're not

using systemic thrombolysis as often as we should that being said there are cases in which thrombolytics are contraindicated or in which they fail and that opens the door for these other therapies surgical unblocked demand

catheter active therapy surgical unblocked mean really does have a role here I'm not going to speak about it because I'm an interventionist but we can't forget that so catheter directed therapy all sorts

of potential options you got the angio vac device over here you've got the penumbra cat 8 device here you've got an infusion catheter both here and here you've got the cleaner device I haven't pictured the inari float

Reaver which is a great new device that's entered the market as well my message to you is that you can throw the kitchen sink at these patients whatever it takes to open up a channel and get blood to the left ventricle you can do

now that being said there is the angio jet which has a blackbox warning in the pulmonary artery I will never use it because I'm not used to using it but you talk to Alan Matsumoto Zieve Haskell these guys have a lot of experience with

the androgen and PE they know how to use it but I would say though they're the only two people that I know that should use that device because it is associated with increased death within the setting of PE we don't really know you know with

great precision why that happens but theoretically what that causes is a release of adenosine can cause bradycardia bradycardia and massive p/e they just don't mix well so

them so my particular area of interest is a blade of radium ization and what we'd like to do is to break the liver

down into a bunch of little tiny perfused volumes off of a single vascular pedicle or what we call angio zones and those are those allow us to segment out if you only have small volume disease for example like here in

segment three why do I have to treat the entire left to paddock low I can actually treat just that small portion just like it what it tastes only now I'm administering y9t but since it's expendable liver I

can administer doses that are way higher orders of magnitudes higher than what I could if our infusing into the liver just on its own so here's an example of that if you look at this lesion in the right of panic lobe you'll see these

little lines over them what we want to achieve is around a 205 GRA threshold for these lesions that's the red line everything that's south of red in terms of color orange Holly to blue is not cold enough to kill tumor so if we

administer a dose of a tea grade to the lobe we get this coverage which is to be a partial response if I administer 150 grey suddenly that red line gets larger what happens when you administer 400 grey now you've officially covered the

entire lesion and so you're going to lose the adjacent liver at those kind of doses and as well - what what the real question then is not sort of how much dose you give it's you give what you need to to ablate the tumor in its

entirety and you see what the patient's left with if someone's left with anatomically a lot of remnant liver because of how you've segmented out that lesion then go ahead and dose extremely high and that's essentially what we've

seen in pathologic results it's one of the highest things of high school pathological crosa rates you can achieve with a trans arterial therapy it's highly competitive with thermal ablation in the correctly selected bleezin

so this is an example of what it looks like when you segment out a little lesion like this and this patient ultimately went to resection and this was a complete pathologic necrosis but as you can see even it was a cirrhotic

patient we chose a very small volume of liver that we felt the patient would tolerate so that's a blade of vernalization let's take a look at what looks like in real time so we have a little capsular lesion we felt that

ablating this patient who was a potential transplant candidate we felt we can probably with a blade of radium realization so you go in and this is the comb beam CT that looks at a complete enhancement of the lesion within the NGO

zone this is what the MAA looks like when we administer it you can see how it tends to cluster within the tumor but you can see what the adverse territory is the liver adjacent to it this is what the engine room looks like how highly

selective it is the day of and this is what the wine ID actually looks like is the wine 90 doing its job and you can see how conformal it is there's no risk whatsoever to the liver that's adjacent outside of that field of

a maximum of around 11 millimeters and this is a patient at one month with a complete imaging response and this patient never developed a recurrent to the site and what's actually sole mode of treatment for this person's liver

cancer this is how you get complete pathologic response if you look at those little tiny grey dots in there those are actually the spheres within tiny little vessels within the tumor sometimes they go even to the portal branch but you can

see how they're not clustered uniformly but when you make them super hot that allows them to give range where otherwise they would be fine a little bit short so this also applies to the whole lobe this was a patient that had a

very unusual presentation of colon cancer that was invading the portal II we weren't sure what to do with this patient no one was because a very rare occurrence so we said well we would like

to resect him but there's not enough liver and we're not sure if this person's gonna survive because we've never seen portal cancer invading the portal vein so we said let's treat it with the radiation lobectomy and what's

cool here is if you look at the the arteries even though the tumor is invading the portal vein it's bringing arterial supply along with it like a vagabond and that's the conduit that allows us to treat these patients so

when we saw that we felt this patient we good candidate for irradiation lobectomy which is applying an ablative dose of y9t to the entire low not just a small segment in patients where otherwise cannot because of the anatomy the tumor

or if you're trying to shrink that lobe to get that person ready for surgery why because if you look at the size of the lobe on the left from this first image and compare it here you can see how much larger it got what happens is that part

that the surgeon ultimately tens on resecting in volutes over time and becomes completely vitalized and turns into scar tissue so we know that if a surgeon goes in afterwards to cut it out it's going to not result in liver

failure and that level of security allows people to have sir who otherwise wouldn't this patient is not going to have metastatic disease because we followed their blood level markers let me see how low they are and

is going to have enough liver remnant so the patient went to resection and this is the pathologic specimen and this was also a complete pathologic necrosis so I

treatment is the ultrasound assisted catheter director thrombolysis or the echos divisor eCos this technique involves a slow infusion again over 12 to 24 hours

but the catheter has ultrasound built into it and that's thought to help disassociate fibrin strands and to help embed the thrombus bed the TPA into the thrombus I think most people have heard of or seeing eCos in the past

again lower doses much like the catheter directed so it's really the same type of procedure except at the end you're hooking up eCos rather than a uniform Craig Mac there is a lot of differences though in the sort of overall patient

experience because eCos as many of you know requires a lot more devices and for the patient's room so they're gonna have more pumps because it requires more fluid it requires more observation it beeps more frequently overnight but what

I will say is that there are studies that are used that have useful information with eCos and those are actually the main studies that have been done although they're all industry-sponsored but they're very

important studies nonetheless so the only device really that exists for this right now that approved is the eCos

stamp placement we talked a little bit about it I'm gonna talk to you a little

bit more about it and ideal stance is a straight stance that has a nice smooth curve with a portal vein and a nice smooth curve with a bad igneous end well you don't want is it is a tips that T's the sealing of the hepatic vein okay

that closes it okay and if there's a problem in the future it's very difficult to select okay or impossible to select okay you want it nice and smooth with a patek vein and IVC so you can actually get into it and it actually

has a nice hemodynamic outflow the same thing with the portal thing what you don't want is slamming at the floor of the portal vein and teeing that that floor where where it actually portly occludes your shunts okay or gives you a

hard time selecting the portal vein once you're in the tips in any future tips revisions okay other things you need it nice and straight so you do not want long curves new or torqued or kinks in your tips you

a nice aggressive decompressive tips that is nice and straight and opens up the tips shunt okay we talked a little bit you don't want it you don't want to tee the kind of the ceiling of the of the hepatic vein another problem that we

found out you want that tips stance to extend to the hepatic vein IVC Junction you do not want it to fall short of the paddock vein IVC Junction much okay much is usually a centimeter or centimeter and a half is it is acceptable

the problem with hepatic veins and this is the same pathology as the good old graft dialysis grafts what is the common sites of dialysis graft narrowing at the venous anastomosis why for this reason it's the same pathogenesis veins whether

it's in your arm for analysis whether it's in your liver or anywhere are designed for low flow low turbidity flow of the blood okay if you subject a vein of any type to high turbot high velocity flow it reacts by thickening its walls

it reacts by new intimal hyperplasia so if you put a big shunt which increases volume and increased flow turbidity in that area in that appear again the hepatic vein reacts by causing new into our plays you actually get a narrowing

of the Phatak vein right distal to the to the to the Patek venous end of the shunt so you need to take it all the way to the Big C to the IVC okay how much time do I have half an hour huh 17 minutes okay

Viator stents is one way let's say you don't have a variety or stent many countries you don't have a virus then what's an alternative do a barre covered stem combination you put a wall stent and then put a covered stance on the

inside okay so put a wall stent a good old-fashioned you know oldie but a goodie is is a 1094 okay you just put a ten nine four Wahl cent which is the go to walls down so I go to stand for tips before Viator

and then put a cover sentence inside whatever it is it's a could be a fluency it could be a could be a vibe on and and do that so that's another alternative for tips we talked about an ace tips as a central straight tips and it's not out

and fishing out in the periphery okay this is an occlusion with a wall stance this is why we use think this is why now we use stent grafts this is complete occlusion of the tips we're injecting contrast this is not the coral vein this

is actually the Billy retreat visit ptc okay that's a big Billy leaked into the into the tips okay and that's why we use covered stance I'm gonna move forward on this in early and early and experienced

technically step by step of how tips are done okay and and the ideal tips with

every step of this procedure I'm gonna show you two ways of doing it okay and the advantages and disadvantages of the two ways in every step okay so first of all the primary thing is to get into the portal vein and how do you visualize the

portal vein okay so one way is to do co2 Vinogradova nog Rafi to hit the portal vein me with experience no I don't need co2 venography to hit the portal vein but I still do it in an in a teaching institution because I have texture that

are learning nurses they're learning and physicians are learning so I actually do the imaging for them so they actually can get the general idea of what we're doing this is our target this is where we're coming off and that's it but in an

experience hands is it necessary absolutely not okay so co2 photography very helpful for in teaching and teaching institutions so everybody and the whole team can actually know exactly what our target is so not essential like

like we discuss and there are two methods of doing this and in a funny way I'm gonna show you that's actually the same method but one is a micro of the other one okay so two ways one way is then wedge a catheter that's the old way

kind of more traditional way than let's not call it always more traditional way of doing a co2 port and the other one is using a balloon of balloon occlusion castra and this is wedging it with a four French five French catheter you

take it all the way to where the catheter is larger than the hepatic vein and now you've wedged it okay and this is kind of a mag up you see that that's a little that's a little wedge okay you wedge you inject contrast the contrast

just sits there it's wedged it's trapped okay and then this is with a balloon to your left is a balloon full of air to the right full of contrast and you basically trapped it again you fill contrast and consciousness it's there

what's the difference between this image and this image no difference the only difference is size that's all it's the same idea you're just trapping a segment of the liver the difference is this is a very

small segment and this is a larger segment okay so essentially it's actually the same technique one is just well technically when it comes to your side all one needs a four or five French calf the other one needs a balloon

occlusion caster okay same image so then you inject co2 the key thing here if you're the type of physician where you put contrasts you have a balloon sitting or a wedge and you have to count contrast there okay

rookie mistake is that they leave the contrast and then they hit the co2 okay what is that you've lost the advantage of the co2 in the beginning of your bolus is actually contrast okay so you need to bleed out the contrast and

replace it completely co2 so your entire bolus okay is co2 and not and not and not the and not the contrast okay that defeats the purpose why is co2 advantageous over contrast contrast is a thick fluid co2 is gas is viscous it's

volatile it actually can squeeze through tight spaces as it's a gas and that's what we want we want to squeeze that co2 which is a contrast through the sinusoids reflux it back into the portal circulation so we're trapping it and

we're trying to push co2 squeezing it through the sinusoids refluxing it back into the portal circulation so you can actually visualize the portal circulation okay and all and the disadvantage of a wedge is what you see

here if you're a wedge and you're immediately sub capsular and you slam you slam that co2 aggressively what you will get is an explosion you get a rip of those of the hepatic capsule scroll the glisten capsule and then you've got

a leak and if the patient is quite low is a quite low path they can actually die from this believe it or not they will die from this and not die from the needle passes okay so that's kind of co2 and that's kind of

a little a little passive air into the perineum nice imaging not a good outcome so one way to avoid this is to still wedge but wedge away from the hepatic capsule so you're out in the periphery in the paddock veins but you're deep

inside the liver you're not you're not right underneath the capsule so that's one way of doing it the other another way is to actually use a balloon okay so this is this is just another wedge here okay and you actually use a balloon I'm

just showing you a correlation with a balloon it's a little safer because you're a little distance away from from the hepatic capsule I'm just showing you a more and more image of the same thing co2 with correlation after you access

since it's a beautiful correlation with with the portal vein venogram okay there are problems with wedges and with balloons is that sometimes you get a gas you know a co2 leak you're wedged but there's hepatic veins at vadik vein

connections and all you see is a fatty veins you can't force reflux the co2 into the portal circulation so that's one problem okay so what do you do with that you change the sights just change a different different branch okay try to

avoid that connection between the badeck veins and it back veins go somewhere else where there is no connection where you can actually make a true hip wedge and force that co2 into the portal circulation okay another way this is

just a draw a drawing out whether it alone or a catheter you get that you get the escape from the Patek vein to fatty vein is to go distal go beyond that connection so if you can go distal go distal if you can't go distal then

change your branch try to find a place where there is no hepatic vein tip a degree engine attraction preferably but not necessarily not the same branches connected to because that usually goes both ways but not always sometimes

you're lucky and if that connection is kind of like a one-way valve one way street and it's not a two-way street but that's just sheer luck okay this is an example hepatic vein to about a vein connection and what we did was basically

switch to another place another vein and we actually get the portal venogram here okay next up sting crafts Viator's thank

massive PE well let's remember this at this point including all the trials that preceded the pytho trial almost 1 700 patients have been randomized into systemic lytic trials for some massive p yep all we have on the CDT side is the

ultimate trial of 59 patients non-us single was a single trial that's where this initiative is coming from to improve the data this trial called P track and I have preliminary information that we just made our first breakthrough

in fronting from the NIH so very excited that we have a planning grant to potentially get this thing moving so P tract is basically designed to be a randomized control trial of catheter directed therapy versus no catheter

directed therapy for sub massive PE to really try to answer this question just like the pytho trial tried to do for systemic thrombolysis in the setting of catheter Ida thrombolysis and this time we're not just using surrogate endpoints

we're not you the rvw ratio is probably not even gonna be calculated but what we want to know are these are patients doing better in one arm or the other and we're going to use outcomes that are important to both patients and providers

400 to 500 patients most likely looking at sites all across the so but we are still in this time when

her I couldn't help but throw this in

just talking about back device here's a patient that had a iliac occlusion the right it was very difficult to get past the very proximal plaque cap so in this case I did a sub into a we can remember I talked about that out back device it

has like a little L and upside down L that you can use to point into the vessel lumen so what I did was on the healthy side I put in a sauce on me this allows me to know exactly where the arches and where the right coming he

like origin is certainly I don't want to be out backing into the aorta deeply right so this allows me to identify where that location is once I've out backed into the vessel here then I just pre dilated and then stent it up into

the vessels so just sort of interesting case one thing since I am Austin there's a couple of places just you may or may not be aware of this is a Barton Creek it's actually not just a cross town lake not far from here it's about a seven

mile a little Greenbelt inside the city where basically you don't feel like getting your traffic your gaze definitely away from everything this is called the land bridge oops so there's a couple of guys right here

that's about probably about a 20-foot jump there's this guy right here who just took off from that ledge it's about a 40 50 foot drop I did try to get up to that part one time it's about it one foot with ledge so I didn't get the ax

courage to do it now I'm sort of happy because during the summer months it does get just dry up so what I noticed with this is this is about a 10 12 foot depth here this guy's jumped in something's about

12 to 15 deep so it's sort of interesting the the balls enos of these guys some guys are doing backflips out there there is water there so you know if you guys have a chance check it out

if you do happen to find it I'm not encouraging it excited I wanna get sued but if you want to take a jump off have fun all right thank you [Applause]

you see again renal Dena Graham you can see a hint of the gonad of Ain selective

vena Graham again showing us the large gonadal vein and that's my post so charcoal with the occlusion balloon and then treat I showed the cartoon slide before that we look at all four of those territories so I always start with the

left but then I'm gonna look at the right gonadal vein as well as the internal iliac veins on both sides in this case the right go Natalie was normal as were the internal iliac veins so not seeing any varicosities

normal venous outflow so this patient it was only treated with a left gonadal vein embolization

that was one example so these are there have a lot of potential complications reperfusion pulmonary edema is a very very big potential complication so you could get through the case patient does

great you open up multiple pulmonary arteries and then they start coughing up blood and then they end up started drowning in their own blood and the ICU so we do not want to push that and the initial papers that you can see down

below on that table they had a very high almost 10% in some cases pulmonary edema requiring treatment requiring patients being put on CPAP or being intubated and that is because they treated too much at one time

and so now as this when this first started in the early 2000s the operators were treating multiple segments at multiple times at one time and they were using large balloons and we figured out that that was what was killing patients

and so we changed our treatment so this is the first study that was ever performed for this it was performed by dr. Feinstein I believe this was published in circulation it was done in Harvard at MGH they had 18 patients with

36 month follow-up they all improved in their ability to walk as well as their lifestyle but many of them 11 out of 18 patients had reperfusion injury so this was the first paper and at that time it became the last paper because so many

patients did poorly but here's what they're sort of what they did and the ones that did okay they you could see that they had an improvement in the New York Heart Association classification again that just means they can walk

further they're not less short of breath and that they could walk further in 6 minutes which is again our sort of first test outcomes over time whence this has become increased so you can see that study was in 2001 and then

it kind of went away for a long time and it came back in 2012 in Japan where the most operators are there they've treated up to 255 procedures now since this slide was made we're up to a thousand in Japan and those patients are doing very

well but you'll notice that they have multiple procedures so again you don't try to one-and-done these patients they come back four to six times we've treated a couple patients where I work and we've treated that was patients four

times already and so they do much better but it's a slow slow and steady treatment so I want to wrap up with saying that the IR team is very critical to patients who are getting treated for PE we're involved in the diagnosis as

the radiology team acute and chronic PE it's very important to know as I've shown you in some of the examples and some of the images which when it's acute and versus chronic doing thrombolysis on a patient with chronic PE is useless all

you're doing is putting them at a risk you're not going to be able to break up that clot it's very important to have inter and multidisciplinary approach to patient care so interdisciplinary meaning everybody in this room nurses

technologists and physicians working together to take care of that patient that's on your table right now and multi-disciplinary because you have to work with cardiology vascular medicine the ICU teams and the

referring providers whether it's neurosurgery vascular surgery whomever it is who's Evers patient gets a PE you have to work together and it's very important again to have collaborative care in these patients if we're doing a

procedure and somebody notices that the patient is desaturating that's very very important when you're working in the pulmonary arteries if somebody notices that the patient's groin is bleeding you have to speak up so it's very important

that everybody is working together which is really what we need to do for these patients so there's my references and there's my kid so thank you guys very much hopefully this was helpful I'd be

plan as well so I wanted to talk a

little bit about imaging I know with our residents and fellows and radiology that's all we do is talk about the imaging and then when go on to IR we talked to them about the intervention but I think it's important

for everyone in this room to see more imaging and see what we're looking at because it's very important for us all to be doing on the same page whether you're a nurse a technologist a physician or anybody else in the room

we're all taking care of that patient and the more information we all have the better it is for that patient so quick primer on a PE imaging so this is a coned in view of a CT pulmonary angiogram so yeah sometimes you'll see

CTS that are that are set for a pulmonary artery's and you'll see some that are timed for the aorta but if the pulmonary arteries are well pacified you're gonna see thrombus so I have two arrows there showing you thrombus that's

sort of blocking the main pulmonary arteries on the left and right side on the patient's left so the one with the arrow that is a sort of very classic appearance of an intro luminal thrombus you can see a little rim of contrast

surrounding it and it's usually at branch points and it's centered in the vessel the one on the right with the arrow head is really at a big branch point so that's where the right lower lobe segmental branches are coming off

and you can see there's just a big amount of thrombus there you can see distal infarct so if you're looking in the long windows you'll see that there's this kind of it's called a mosaic perfusion but it also what kind of looks

like a cobweb and that's actually pulmonary infarct and maybe some blood there which actually will change what we're gonna do because in those cases freaken we will not perform PE thrombolysis it's also important to note

that acute and chronic PE which we're here to talk about today may look very similar on a CT scan and they have completely different treatment methods so here's a sagittal view from that same patient you can see the CT scan so

between the arrow heads is with the tram track appearance so you'll see that there's thrombus the grey stuff in the middle and you'll see the white contrasts surrounding it and kind of like a tram track and that's very

classic for acute PE and then of course where the big arrow is is just the big thrombus sitting there here's another view of a coronal this is actually on a young woman which I think we show some images on but you can see cannonball

looking thrombus in the main pulmonary arteries very classic variants for acute PE and then this is that same patient in a sagittal view again showing you in the left pulmonary kind of those big cannon balls of

thrombus here's some examples from the literature showing you the same thing when you're looking at an acute PE it's right centered on all the image all the way in the left if the classic thrombus is centered right in the middle of the

vessel you can usually see a rim of normal contrast around it and you can see on a sagittal or coronal view kind of like a thin strip of floating thrombus so the main therapies for acute

PE the first one of course is

anticoagulation so heparin and bridging the patient to coumadin or now aid a direct oral anticoagulant is really the mainstay of treatment most patients again 55 percent of patients with PE have low risk PE all of those patients

should be on according to the chest guidelines three months of anticoagulation so they're gonna get heparin as an inpatient if they even need it and they're gonna get sent home on lovenox bridge to coumadin or they're

gonna get the one of the new drugs like Xarelto or Eliquis but here's all the other things that we do so these patients that are in the intermediate high risk so I'm gonna try to keep saying those terms to try to kind of put

that in everyone's brain because I think the massive and sub massive PE is what everyone used to talk about but we want to keep up with our colleagues in cardiology who are using the correct terminology we're gonna say high risk

and an intermediate but in those patients - intermediate high risk or Matt or the high risk PE patients we're gonna be treating them with systemic thrombolysis catheter directed thrombolysis ultrasound assisted

thrombolysis and maybe some real lytic and elected me or thrombectomy there's other techniques that we can use for one-time removal of clot like rotational and electa me suction thrombus fragmentation and then of course

surgical mblaq t'me so when anticoagulation is not enough so I like to show this slide because it shows the difference between anticoagulation and thrombolysis they are very different and sometimes I think everybody in this room

understands the difference but I think our referring providers don't and so when we when we get consulted and we recommend anticoagulation they're like yeah TPA well that's not the right thing so anticoagulation stops the clotting

process so when you start a patient on a heparin drip they should theoretically no longer before new thrombus on that thrombus so when you have thrombus in a vessel you get a cannon you get a snowball effect more

and more thrombus is gonna want to form heparin stops that TPA however for thrombolysis actually reverses the clouding process so that tissue plasminogen activator or streptokinase or uro kindness will actually dissolve

clot so there you're stopping new clot forming versus actually dissolving clot anticoagulation allows for natural thrombolysis so your body has its own TPA and so when you put a patient on heparin you're allowing your natural

body defenses to work you're giving it more time TPA accelerates that process so you give TPA either systemically or through a catheter you're really speeding up that process anticoagulation on its own has a

lower bleeding risk you're putting a patient on heparin or Combe it in it's it is less but it is still real thrombolysis however is a very very high bleeding risk patients when I when I consult a patient for thrombolysis I

tell them that we are about to do give them the absolute strongest blood clot thinning agent or an reversal agent which is the TPA and we're gonna just run it through your veins for hours and hours

um and that sort of gives them an idea of what we're doing anticoagulation in and of itself is really not invasive you just give it through an IV or even a pill thrombolysis however is given definitely through an IV through

systemic means and a large volume there thereafter or catheter directed so again

quick I did want to mention t-carr briefly and try to get you guys closer to back on time this is a hybrid procedure this is combining the surgical procedure we talked about first and carotid stenting it takes combined

carotid exposure at the base of the clavicle or just above the clavicle and reverses blood flow just like we talked about but tastes slightly different technique or approach to doing this and then you put the stent in from a drug

carotid access here's the components of the device right up by the neck there is where the incision is made just above the clavicle and you have this sheet that's about eight French in size that only goes in about us to 2 cm or 1 and a

half cm overall into the vessel and then that sheath is sutured to the the chest wall and then it's got a side arm that goes what's labeled number six here is this flow reversal urn enroute neuroprotection kit it reverses the

blood flow and then you get a femoral sheath in the vein right in the common femoral vein and you reverse the blood flow so this is a case a picture from our institution up on the right is the patient's neck and that's the carotid

exposure and the initial sheath is in place so the sidearm of that sheath is the enroute protection system which is going up up at the top of the image there we're gonna back bleed that let that sidearm of that sheath continue to

bleed up to the very top and then connect that to the common femoral venous sheet that we have in place there's a stepwise of that and then ultimately what we see at the end of the procedure is that filter inside that

little canister can be interrogated after and you can see the debris this is in the box D here on the bottom left the debris that we captured during the flow reversal and this is a what we call a passive and then active flow reversal

system so once the system is in place the direct exposure carotid sheath in place the flow controller and AV shunt in place you see the direction of blood flow so now all that blood flow in that common carotid artery is going reverse

direction and so when you place a sheath or wire and and ultimately through that sheath up by the carotid artery there's no risk for distal embolization because everything is flowing in Reverse here's a couple

case examples ferns from our institution this is a patient who had a symptomatic critical greater than 90% stenosis has tandems to nose he's so one proximal at the origin and one a little bit more distal we you can see the little

retractors down at the base of the image there in the sheath that's essentially the extent of the sheath from the bottom of that image into the vessel only about a cm or two post angioplasty instant patient tolerated that quite well here's

another 71 year-old asymptomatic patient greater than 90% stenosis pretty calcified lesion a little more extensive than maybe with the CT shows there's the angiography and then ultimately a post stent placement using the embolic

protection device and overall the trials have shown good good safety met profile overall compared to carotid surgery so it's a minimum minimal exposure not nearly as large the risk of stroke is less because you're not mucking around

up there you're using the best of a low profile system with flow reversal albeit with a mini surgical exposure overall we've actually have an abstract or post trip this year's meeting this is just a snapshot of that you can check it out

this is our one year experience we've had comparable low complication rates overall in our experience so in summary

let me show you a case of massive PE

this launched our pert pert PE response team 30 year-old man transcranial resection of a pituitary tumor post-op seizures intracranial frontal lobe hemorrhage okay so after his brain surgery developed a frontal lobe

hemorrhage and of course few days after that developed hypotension and hypoxia and was found to have a PE and this is what the PE look like so I'll go back to this one that's clot in the IVC right there and

that's clot in the right main pulmonary artery on this side clot in the IVC clot in the right main pulmonary artery systolic blood pressure was around 90 millimeters of mercury for about an hour he was getting more altered tachycardic

he was in the 120s at this point we realized he was not going the right direction for some reason the surgeon didn't want to touch him still to this day not sure why but that was the case he was brought to the ir suite and I had

a great Mickey attending who came with him and decided to start him on pressors and basically treat him like an ICU patient while I was trying to get rid of his thrombus so it came from the neck because I was conscious of this clot in

the IVC and I didn't want to dislodge it as I took my catheters past it and you see the Selective pulmonary and on selective pulmonary angiogram here and there's some profusion to the left lung and basically none to the right lung

take a sheath out to the right side and do an injection that you see all this cast of thrombus you really see no pulmonary perfusion here you can understand why at this point this man is not doing well what I did at this point

was give a little bit of TPA took a pigtail started trying to spin it through aspirated a little bit wasn't getting anywhere he was actually getting worse I was starting to feel very very nervous I had remembered for my AV

fistula work that there was this thing called the cleaner I don't have any stake in the company but I said you know I don't have a lot to lose here and I thought maybe this would be better than me trying to spin a pigtail through

the clock so the important thing about the cleaners it does not go over a wire so you have to take the sheet out then take out the wire then put the cleaner through that sheath and withdraw the sheath

you can't bareback it especially in the pulmonary circulation the case reports are poking through the pulmonary artery and causing massive hemorrhage and the pulmonary artery does not have an adventitia which is the outer layer just

a little bit thinner than your average artery okay so activated it deployed it and you started to get better and this is what it looked like at the end now this bonus question does somebody see anything on this this picture here that

made me very happy on this side this picture here that made me feel like hey we're getting somewhere I'm sorry the aorta the aorta you start to see the aorta exactly and that that was something I was not seen before the

point being that even though this doesn't look that good in terms of your final image the fact that you see filling in the aorta and mine it might have been some of the stuff I had done earlier I can't I can't pinpoint which

of the interventions actually worked but that's what I'm looking for I'm looking for aortic blood flow because now I've got a hole in that in that clot that's getting blood flow to the left ventricle which starts to reverse that RV

dysfunction that we were concerned about make sure I'm okay with time so we'll

so just a compliment what we everybody's talked about I think a great introduction for diagnosing PID the imaging techniques to evaluate it some of the Loney I want to talk about some of the above knee interventions no disclosures when it sort of jumped into

a little bit there's a 58 year old male who has a focal non-healing where the right heel now interestingly we when he was referred to me he was referred to for me for a woman that they kept emphasizing at the anterior end going

down the medial aspect of the heel so when I literally looked at that that was really a venous stasis wound so he has a mixed wound and everybody was jumping on that wound but his hour till wound was this this right heel rudra category-five

his risk factors again we talked about diabetes being a large one that in tandem with smoking I think are the biggest risk factors that I see most patient patients with wounds having just as we talked about earlier we I started

with a non-invasive you can see on the left side this is the abnormal side the I'm sorry the right leg is the abnormal the left leg is the normal side so you can see the triphasic waveforms the multiphasic waveforms on the left the

monophasic waveforms immediately at the right I don't typically do a lot of cross-sectional imaging I think a lot of information can be obtained just from the non-invasive just from this the first thing going through my head is he

has some sort of inflow disease with it that's iliac or common I'll typically follow within our child duplex to really localize the disease and carry out my treatment I think a quick comment on a little bit of clinicals so these

waveforms will correlate with your your Honourable pencil Doppler so one thing I always emphasize with our staff is when they do do those audible physical exams don't tell me whether there's simply a Doppler waveform or a Doppler pulse I

don't really care if there's not that means their leg would fall off what I care about is if monophasic was at least multiphasic that actually tells me a lot it tells me a lot afterwards if we gain back that multiphase the city but again

looking at this a couple of things I can tell he has disease high on the right says points we can either go PITA we can go antegrade with no contralateral in this case I'll be since he has hide he's used to the right go contralateral to

the left comment come on over so here's the angio I know NGOs are difficult Aaron when there's no background so just for reference I provided some of the anatomy so this is the right you know groin area

right femur so the right common from artery and SFA you have a downward down to the knee so here's the pop so if we look at this he has Multi multi multiple areas of disease I would say that patients that have above knee disease

that have wounds either have to level disease meaning you have iliac and fem-pop or they at least have to have to heal disease typically one level disease will really be clot against again another emphasis a lot of these patients

since they're not very mobile they're not very ambulatory this these patients often come with first a wound or rest pain so is this is a patient was that example anyway so what we see again is the multifocal occlusions asta knows

he's common femoral origin a common femoral artery sfa origin proximal segment we have a occlusion at the distal sfa so about right here past the air-duct iratus plus another occlusion at the mid pop to talk about just again

the tandem disease baloney he also has a posterior tibial occlusion we talked about the fact that angio some concept so even if I treat all of this above I have to go after that posterior tibial to get to that heel wound and complement

the perineal so ways to reach analyze you know the the biggest obstacle here is on to the the occlusions i want to mention some of the devices out there I'm not trying to get in detail but just to make it reader where you know there's

the baiance catheter from atronics essentially like a little metal drill it wobbles and tries to find the path of least resistance to get through the occlusion the cross or device from bard is a device that is essentially or what

I call is a frakking device they're examples they'll take a little peppermint they'll sort of tap away don't roll the hole peppermint so it's like a fracking device essentially it's a water jet

that's pulse hammering and then but but to be honest I think the most effective method is traditional wire work sorry about that there are multiple you know you're probably aware of just CTO wires multi weighted different gramm wires 12

gram 20 gram 30 gram wires I tend to start low and go high so I'll start with the 12 gram uses supporting micro catheter like a cxi micro catheter a trailblazer and a B cross so to look at here the sheath I've placed a sheet that

goes into the SFA I'm attacking the two occlusions first the what I used is the micro catheter about an 1/8 micro catheter when the supporting my catheters started with a trailblazer down into the crossing the first

occlusion here the first NGO just shows up confirmed that I'm still luminal right I want to state luminal once I've crossed that first I've now gone and attacked the second occlusion across that occlusion so once I've cross that

up confirm that I'm luminal and then the second question is what do you want to do with that there's gonna be a lot of discussions on whether you want Stan's direct me that can be hold hold on debate but I think a couple of things we

can agree we're crossing their courageous we're at the pop if we can minimize standing that region that be beneficial so for after ectomy couple of flavors there's the hawk device which

essentially has a little cutter asymmetrical cutter that allows you to actually shave that plaque and collect that plaque out there's also a horrible out there device that from CSI the dime back it's used to sort of really sort of

like a plaque modifier and softened down that plaque art so in this case I've used this the hawk device the hawk has a little bit of a of a bend in the proximal aspect of the catheter that lets you bias the the device to shape

the plaque so here what I've done you there you can see the the the the the teeth itself so you can tell we're lateral muta Liz or right or left is but it's very hard to see did some what's AP and posterior so usually

what I do is I hop left and right I turned the I about 45 degrees and now to hawk AP posterior I'm again just talking left to right so I can always see where the the the the AP ended so I can always tell without the the teeth

are angioplasty and then here once I'm done Joan nice caliber restored flow restored then we attacked the the common for most enosis and sfa stenosis again having that device be able to to an to direct

that device allows me to avoid sensing at the common femoral the the plaque is resolved from the common femoral I then turn it and then attack the the plaque on the lateral aspect again angioplasty restore flow into the common firm on the

proximal SFA so that was the there's the plaque that you can actually obtain from that Hawk so you're physically removing that that plaque so so that's you know that's the the restoration that flow just just you know I did attack the

posterior tibial I can cross that area I use the diamond back for that balloon did open it up second case is a woman

now other causes this is a little bit different different scenario here but it's not always just as simple as all

there's leaky valves in the gonadal vein that are causing these symptoms this is 38 year old Lafleur extremity swelling presented to our vein clinic has evolved our varicosities once you start to discuss other symptoms she does have

pelvic pain happiness so we're concerned about about pelvic congestion and I'll mention here that if I hear someone with exactly the classic symptoms I won't necessarily get a CT scan or an MRI because again that'll give me secondary

evidence and it won't tell me whether the veins are actually incompetent or not and so you know I have a discussion with the patient and if they are deathly afraid of having a procedure and don't want to have a catheter that goes

through the heart to evaluate veins then we get cross-sectional imaging and we'll look for secondary evidence if we have the secondary evidence then sometimes those patients feel more comfortable going through a procedure some patients

on the other hand will say well if it's not really gonna tell me whether the veins incompetent or not why don't we just do the vena Graham and we'll get the the definite answer whether there's incompetence or not and you'll be able

to treat it at the same time so in this case we did get imaging she wanted to take a look and it was you know shame on me because it's it's a good thing we did because this is not the typical case for pelvic venous congestion what we found

is evidence of mather nur and so mather nur is compression of the left common iliac vein by the right common iliac artery and what that can do is cause back up of pressure you'll see her huge verax here and here for you guys

huge verax in that same spot and so this lady has symptoms of pelvic venous congestion but it's not because of valvular incompetence it's because of venous outflow obstruction so Mather 'nor like I mentioned is compression of

that left common iliac vein from the right common iliac artery as shown here and if you remember on the cartoon slide for pelvic congestion I'm showing a dilated gonna delve a non the left here but in this case we have obstruction of

the common iliac vein that's causing back up of pressure the blood wants to sort of decompress itself or flow elsewhere and so it backed up into the internal iliac veins and are causing her symptoms along with her of all of our

varicosities and just a slide describing everything i just said so i don't think we have to reiterate that the treatments could you go back one on that I think I did skip over that treatments from a thern er really are also endovascular

it's really basically treating that that compression portion and decompressing the the pelvic system and so here's our vena Graham you can see that huge verax down at the bottom and an occluded iliac vein so classic Mather nur but causing

that pelvic varicosity and the pelvic congestion see huge pelvic laterals in pelvic varicosities once we were able to catheterize through and stent you see no more varicosity because it doesn't have to flow that way it flows through the

way that that it was intended through the iliac vein once it's open she came back to clinic a week later significant improvement in symptoms did not treat any of the gonadal veins this was just a venous obstruction causing the increased

pressure and symptoms of pelvic vein congestion how good how good are we at

no thanks to the avir we really wouldn't be able to do anything that we can without y'all so I take great great pride in sharing things from our perspective said you folks can start contributing your own thoughts your own opinions and your own vision during

these cases I think it's certainly something that I've appreciated since the first day of doing invention where do you all do so having said that we're just a smidge in the behind side so we'll try to focus today is mainly a

survey to stimulate everyone in terms of what's actually happening on the other end of the catheter with respect to the patient why are we doing these things where's our role and I think that's gonna add hopefully some value the next

time you folks step in on one of these cases alright so as you know dr. daughter first was able to visualize the inside of a blood vessel and find a stenosis and a lady who had limb ischemia and then was able to use a

dilator to fix that so obviously that gave birth to interventional radiology so we started taking pictures of tumors just to diagnose tumors back in the day before we had actual imaging and what we found

was well if tumors have a high demand for blood just like anything else what happens if we take away that blood and this is a 1975 image of renal cell carcinoma is to call them hyper and if Roma's back then but basically the

concept of interventional ecology was born the moment you could do something to make the environment for the tumor less hospitable and to try to palliate patients if they weren't subject to the the gold treatment standards like

resection in this case so fast forward to 2016 there was a huge study was International where they looked at over 3 000 patients who have primary liver cancer or her pata cellular carcinoma and what they found was that regardless

of where but if you sum all the treatment decisions that are related to those patients about 70% will see treatment by an interventional radiologist as you know that was a astounding amount

so si are listened to a lot of these types of messages even outside of obviously oncology basically we realize that there's a tremendous responsibility and the best thing to do is to dedicate ourselves fully to that and that's why I

think with IR now is a separate medical specialty we're going to start seeing more of the clinical involvement of this and certainly think the caseloads going to go up so why interventional oncology

we're gonna move on to embolization there a couple different categories of embolization bland embolization is when

you just administering something that is choking off the blood supply to the tumor and that's how it's going to exert its effect here's a patient with a very large metastatic renal cell lesion to the humerus this is it on MRI this is it

per angiogram and this patient was opposed to undergo resection so we bland embolized it to reduce bleeding and I chose this one here because we used sequentially sized particles ranging from 100 to 200 all

the way up to 700 and you can actually if you look closely can see sort of beads stacked up in the vessel but that's all that it's doing it's just reducing the blood supply basically creating a stroke within the tumor that

works a fair amount of time and actually an HCC some folks believe that it were very similar to keep embolization which is where at you're administering a chemo embolic agent that is either l'p hi doll with the chemo agent suspended within it

or drug eluting beads the the Chinese have done some randomized studies on whether or not you can also put alcohol in the pie at all and that's something we've adopted in our practice too so anything that essentially is a chemical

outside of a bland agent can be considered a key mobilization so here's a large segment eight HCC we've all been here before we'll be seeing common femoral angiogram a selective celiac run you can make sure

the portals open in that segment find the anterior division pedicle it's going to it select it and this is after drug living bead embolization so this is a nice immediate response at one month a little bit of gas that's expected to be

within there however this patient had a 70% necrosis so it wasn't actually complete cell death and the reason is it's very hard to get to the absolute periphery of the blood supply to the tumor it is able to rehab just like a

stroke can rehab from collateral blood supply so what happens when you have a lesion like this one it's kind of right next to the cod a little bit difficult to see I can't see with ultrasound or CT well you can go in and tag it with lip

Idol and it's much more conspicuous you can perform what we call dual therapy or combination therapy where you perform a microwave ablation you can see the gas leaving the tumor and this is what it looks like afterwards this patient went

to transplant and this was a complete pathologic necrosis so you do need the concept of something that's ablative very frequently to achieve that complete pathologic necrosis rates very hard to do that with ischemia or chemotherapy

alone so what do you do we have a

study that was done was the perfect registry so all these studies have some name perfect the PE stands for pulmonary

embolism I don't know what the rest means but it's a registry of a hundred and one consecutive patients so these are patients that had what they termed at that time massive PE as well as sub massive PE it was seven sites and they

took all their data over three years so basically they said if you treated a patient with PE let us know send us all their info we're gonna put it in this one paper the therapy was all over the place for so patients with sub massive

or intermediate high risk PE they got catheter directed thrombolysis usually over 12 to 24 hours but again it was not specific it was whatever they did we want to know about it put it in one and sort of reported patients with

massive PE which are very different from those patients with intermediate high risk PE got mechanical fragmentation with some low-dose TPA and this was left open to whatever you were doing at your institution and then they looked at how

patients did overall and they looked at only survival to hospital discharge so they just want to know if patients like made it through that hospitalization overall they found that most patients were treated successfully so they didn't

die on the on the table and that they were able to get through there were six deaths for four mostly from the massive PE group and two from the sub massive and eighty nine point one percent had reduction in RV strain so that's one of

the risk factors or that's one of the goals endpoints that we look in in every study is RV strain did we improve their RV strain pre and post intervention and that can be measured either under an echo or on a CT scan one thing that we

don't know is by reducing that RV strain did we actually improve their life their quality of life or their overall survival and that's one some of the other studies mentioned 84% of these patients are almost 85 had a reduction

in their pulmonary artery pressure so as interventional radiologists and I believe interventional cardiologists also when we start our case we measure the pulmonary artery pressure we're really measuring the strain on the heart

as a result of the high pulmonary artery pressure so at the end of the case we want to know if we didn't even better and I always talk with our trainees and our team about the fact that once you do one of these cases you're really only

looking at the pressure you're not necessarily looking at what the picture looks like because sometimes the picture doesn't look very very good at the end of a PE lysis but the patients are doing much better one thing that's important

to notice is that there was a thirteen point one percent who had complications had complications that's a large number of patients so when you give patients thrombolysis they can have complications and many of them require blood

transfusions or have large hematomas or pseudo aneurysms and things that require further intervention the ultima study is another study this is a study looking at patients receiving unfractionated heparin so patients got just heparin and

other patients got Kathryn directive thrombolysis so this is the standard of care which is heparin versus TP a from a catheter this was a small group of patients only 59 patients and they were all patients who had acute PE with

an r v lv ratio greater than one so that's sort of night now the new standard the RVL v ratio should be less than one and that's basically just looking on a CT scanner and echo how big the RV is the left ventricle pumps all

the blood to the main to your body so that is much stronger than the than the right and it has a much larger size in on average and this is one of the methods that we use in all studies so what they looked at over time here is

these patients and how there are VL v ratio changed after they either received TPA or whether they got just the standard of care which is heparin and you'll see that there is an improvement in the patients who had a catheter

directed thrombolysis and overall they had better a change in their RV LV ratio so that's sort of the marker that we we have been using but again it still doesn't tell us do these patients live longer do they have better quality life

afterwards this Seattle to study is another study that was performed and this is actually a sort of a changing game-changing study at least for a catheter directed thrombolysis in the beginning this was a

industry-sponsored study it's May it was sponsored by the the makers of eCos catheters but it was what was nice about this study is that it was very well defined everyone had to do the same thing so if you're trying to study if

something works or not it's got to be consistent in this group they had massive patients and sub massive but they all had an RV LV ratio greater than 0.9 on CT every patient got unfractionated heparin or or lovenox low

molecular weight heparin and then they all received 24 milligrams of TPA that's the study everybody got the same thing and what you see here on this on the right is that the patients who had T who had catheter directed thrombolysis all

had a reduction in their RV LV ratio they all had a reduction in their mean systolic mean or systolic pulmonary artery pressure and they all had a reduction improvement in their Mead modified Miller index which is actually

a score of how much clot there is in the pulmonary arteries so that suggests that there's an improvement at least in the short term and these patients had reduced bleeding 13% vs. 10% is reduced it's not still

not great but these patients all got TPA so this is a summary slide from chest to in the chest guidelines in 2015 looking at the three studies I just mentioned to you so perfect Seattle - and Altima and it's basically again

showing you that there has been improvement in patients right ventricular strain as well as the patients mean systolic PA pressures but I will tell you even with this data we still don't know what the right answer

is because we don't know how this affects patients in the long term and how they're gonna do in their overall life so back to our patient to move on

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