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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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Prospective CDT Trials | Pulmonary Emoblism Interactive Lecture
Prospective CDT Trials | Pulmonary Emoblism Interactive Lecture
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Ablative Radioembolization | Interventional Oncology
Ablative Radioembolization | Interventional Oncology
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Why is Staging Important | Interventional Oncology
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Q&A Uterine Fibroid Embolization | Uterine Artery Embolization The Good, The Bad, The Ugly
Q&A Uterine Fibroid Embolization | Uterine Artery Embolization The Good, The Bad, The Ugly
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Pre-procedure Assessment | Procedural Sedation: An Education Review
Pre-procedure Assessment | Procedural Sedation: An Education Review
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Practice Guidelines | Risk Mitigation: Periprocedural Screening and Anticoagulation Guidelines to Reduce Interventional Radiology Bleeding Risks
Practice Guidelines | Risk Mitigation: Periprocedural Screening and Anticoagulation Guidelines to Reduce Interventional Radiology Bleeding Risks
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Pulmonary Ablation | Interventional Oncology
Pulmonary Ablation | Interventional Oncology
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Massive PE | Pulmonary Emoblism Interactive Lecture
Massive PE | 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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Indirect Angiography | Interventional Oncology
Indirect Angiography | Interventional Oncology
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What's Next | AVIR CLI Panel
What's Next | AVIR CLI Panel
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Complications & Pitfalls | TIPS & DIPS: State of the Art
Complications & Pitfalls | TIPS & DIPS: State of the Art
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The Basics of the Cath Lab - Curriculum Week 1 | Cath Lab Academy: An Adjunct to an Orientation Program Using an Interprofessional Approach
The Basics of the Cath Lab - Curriculum Week 1 | Cath Lab Academy: An Adjunct to an Orientation Program Using an Interprofessional Approach
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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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What type of PE is this? | Pulmonary Emoblism Interactive Lecture
What type of PE is this? | 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
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PET/MRI Case Study #2 | PET/MRI: A New Technique to Obtain High Quality Diagnostic Images for Oncology Patients
PET/MRI Case Study #2 | PET/MRI: A New Technique to Obtain High Quality Diagnostic Images for Oncology Patients
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Cone Beam CT | Interventional Oncology
Cone Beam CT | Interventional Oncology
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Definitions in PE | Pulmonary Emoblism Interactive Lecture
Definitions in PE | Pulmonary Emoblism Interactive Lecture
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Why is the Capnography Reading Abnormal- Physiology | Respiratory Compromise: Use of Capnography During Procedural Sedation
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Bland Embolization | Interventional Oncology
Bland Embolization | 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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Submassive PE | Pulmonary Emoblism Interactive Lecture
Submassive PE | Pulmonary Emoblism Interactive Lecture
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Outcome data | Uterine Artery Embolization The Good, The Bad, The Ugly
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The Landscape of PE | Pulmonary Emoblism Interactive Lecture
The Landscape of PE | Pulmonary Emoblism Interactive Lecture
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Pathophysiology | Pulmonary Emoblism Interactive Lecture
Pathophysiology | Pulmonary Emoblism Interactive Lecture
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Background on Interventional Oncology | Interventional Oncology
Background on Interventional Oncology | Interventional Oncology
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Why Do We Need Different Directions For Occlusions? | AVIR CLI Panel
Why Do We Need Different Directions For Occlusions? | AVIR CLI Panel
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Airway Assessment | Procedural Sedation: An Education Review
Airway Assessment | Procedural Sedation: An Education Review
airwayanesthesiologistangiogramapneachaptercongestivecopddifficultyeffectivehabituslungsmaskmusculatureNonepatientpatientspharmacologyproceduralproviderssealsedatedsedationstiffventilationwaveform
Transcript

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

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

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

so why staging important well when you go to treat someone if I tell you I have a lollipop shaped tumor and you make a lollipop shape ablation zone over it you have to make sure that it's actually a lollipop shaped to begin with so here's

a patient I was asked to ablate at the bottom corner we had a CT scan that showed pretty nice to confined lesion looked a little regular so we got an MRI the MRI shows that white signal that's around there then hyperintensity that's

abnormal and so when we did an angiogram you can see that this is an infiltrate of hepatocellular carcinoma so had I done an ablation right over that center-of-mass consistent with what we saw on the CT it

wouldn't be an ablation failure the blasian was doing its job we just wouldn't have applied it to where the tumor actually was so let's talk about

questions comments and accusations please hello this topic is very personal to me I've had it actually had a UFE so this is like one of my big things I work in the outpatient center as well as a

hospital where we perform you Effy's and frequently the radiologist will have me go in and talk to the patient it's from a personal perspective one of the issues which it may just have been from my situation was pain control post UFE

whether you normally tell your patients about pain control after the UFE someone say we are all struggling with this yeah oh it's not what's your question is going to be okay good I'm gonna get doctor Dora to answer Shawn the question

is what do you what do we do with this pain issue you know what are you doing for the home there at Emory there you know and a lot of practices we we don't rely on one magic bullet for pain control recently we've been doing

alternate procedures for two adjunctive procedures to help with pain control for example there are nerve blocks that you can do like a superior hypogastric nerve block there's there's Tylenol that can be given intravenously which is seems to

be a little more effective than by mouth there's there's a you know it and a lot of times it's it's a delicate balance right between pain post procedural pain because you can often get the pain well controlled with with narcotics opioid

with a pain pump but the problem is 12 hours later the patients is extremely nauseous and that's what keeps her in the hospital so it's a it's a balance between pain control and nausea you can you can hit the nausea

beforehand using a pain and scopolamine patch that that'll get built up in the system during the procedure and that kind of obviates the nausea issues like I said that the the nerve blocks the the tile and also there are some other

medicines that can can be used adjunctive leaf or for pain control in addition to to the to the opioids so the answer the question is there are multiple there multiple answers to the question there's not one magic bullet so

that helped it did one of the things that I tell the patients is that you know everyone is different and yet some people I've seen patients come out and they have no pain they're like perfect and then some come out and they are

writhing in the bed and they're hurting and they're rolling all around what and I always ask the acid docs are you telling them they could possibly have you know pain after the procedure because some have the expectation that

I'm going to be pain-free and that's not always the case so they have an unrealistic expectation that I'm gonna have the UFE but not have pain what I also tell them is that the pain it's kind of like an investment right and

this is easy for a guy to say that right but but it's it's an investment the worst part the worst pain you should be feeling is the first 12 12 hours or so every day I tell my patient you're gonna be getting better and better and better

with far as the pain as long as you is you follow our little cookbook of medicines that we give you on the way home and I want you to make sure that you fill these prescriptions on the way home or you have someone fill those

prescriptions for you before he or she picked you up in the hospital and lately we have been and I see that you're there as well lots of other little tricks that are out there right and again there are all

little tricks so ensure arterial lidocaine doctor there is near alluded to and if you're on si R Connect you may it may spill over on some of your chat rooms here people have been using like muscle relaxant like flexural or

robertson with some success but just know that we don't have any studies that tell us how that's supposed to do so when i have someone that is like writhing in pain i just use everything so i do it superior hypogastric nerve

vlog and i actually will do some intra-arterial lidocaine although not so much lately i have been using the muscle relaxant but i will warn you that i've had two patients with extreme anticholinergic effects where they are

now not able to pee from that so you know where we're doing that balance act I see that you're there can I take that question here first just so we're we're doing the same thing we're using the multimodal just throwing all these

things at people and we're trying the superior hypogastric blocks but we're collaborating with anesthesia to do that right now do you all do your own blocks or do you collaborate with anesthesia we do our own blocks okay it isn't it is

not that difficult I would tell you that but again it's kind of like you know you got to do if you start feeling better and then you're like we don't really need them we'll just do it on our own okay thank you again yes what's the

acceptable interval between UFE and for IBF oh that's a your question what is the interval between UFE and IVF so if you wanted to get pregnant yeah and can you have a you Fe and then have an IVF like how long would you have to wait

wait and tell you before you can have that the IBF it I guess it really depends on the age of the patient because we know that that the threshold for which patient tend to have that inability to conceive

is around 45 years old so you know it did below the you know below the age of 45 the risk of causing ovarian failure or or the inability to conceive is significantly less it's zero zero to three percent so I would say that you

know you probably want the effects of the fibroid embolization to two to take effect it takes around 12 months for these fibroids to shrink down to their most weight that they're gonna they're going to shrink down the most I wouldn't

say you need to wait 12 months to put our nine vitro fertilization there's no good there's no good literature out there I don't believe that's your next and so I would say just remember that if you came to my practice and you said you

wanted to get pregnant I will be sending you to talk to fertility specialists beforehand we do not perform embolization procedures as a way to become pregnant there's no data to support that but if you saw your

gynecologist and they said let's do this then I'm sure they'll be doing lots of adjunct things to figure out what would be an ideal time then to for you to have IVF and if I dove not having any data to inform me I would ask you to wait a year

and what will be the effect of those hormones that they gave you if for example a patient has existing fibroids what would be the effect of those hormones that IVF doctors prescribed their patients yeah so fibroids actually

can grow during pregnancy so I would say that most of those hormones are pro fertility hormones so I would expect that maybe you can see some of that effect as well yeah alright if you have any other questions you can grab me oh

you're I'm sorry go with it okay yes we we have time I don't want to keep anybody here for that so I have a two-fold question the first one is post-procedure can you use a diclofenac patch or a 12-hour pain

patch that is a an NSAID have you have any experience with that and your next question my second part of the question is there a patient profile or a psychological profile that tips you that the patient is not going to be able to

candidate because of their issues around pain so they're two separate but we have in success sending people home that first day so I'm looking to just make it better I haven't had experience with the Clos

phonetic patch it's in theory it seems ok you know these are all the these are they're all these are non-steroidal anti-inflammatory drugs so there are different potency levels for all of them they you know they range from very low

with with naproxen to to a little bit higher with toradol like that clover neck I think is somewhere in between so we found that at least I found that that q6 our our tour at all it tends to help a lot so with that said I I don't have

much experience with it with the patch in answer to your second question the only thing I can say is there there is a strong correlation between size of fibroids and the the amount of a post procedural pain and post embolization

syndrome so there really you know we often say we don't really care too much about the number of fibroids but the size of the fibroid is is is should be you know you should you should look at that on pre procedural imaging because

if it gets too big it may not be worth it for the patient because they may be in severe pain the more embolic you put into the blood supply's applying the the fibroid the the greater the pain post procedural pain

are there multiple other factors that would contribute to pain but that's that's one aspect you can you can look at post procedurally on imaging okay thank you very much yes ma'am hi what what kind of catheter do you use

to catheterize the fibroid artery when you pass by radio access yeah so over the last three years the companies have been really very good about that so there are a few things that I without endorsing one company or the other that

you need to make sure that the sheath that you're using is one of those radial sheets a company that makes a radio sheath you should not use a femoral sheath for radial access so no cheating where that's concern you may get away

with it once or twice but it will catch up to you and you need a catheter that is long enough to go from the radio to the to the groin so I'm looking for like a 120 or 125 centimeter kind of angled catheter whether it's hydrophilic the

whole way or just a hydrophilic tip or not at all you can you can choose which one in our practice most of us still tend to use a micro catheter through that catheter although if I'm using a for French and good glide calf and it

just flips into like a nice big juicy uterine artery then I may just go ahead and take that and do the embolization if the fellow is not scrubbed in as well so thanks a lot but they make they make many different kinds like that and more

of those are to come all right I'm you can please please please send us any other questions that you have thanks for your time and attention and enjoy the rest of the living

includes an interview of the patient abnormalities of major organ systems like cardiac status do they have a reduced ejection fraction do they have coronary artery disease I want to know

if they have an EF of 10% because if they become hemodynamically unstable and I want to give them fluids I'm not going to bolus a patient with a very low ejection fraction with two liters of fluid you're gonna cause

pulmonary edema and you're going to worsen the situation renal status is huge a lot of our patients are renal e impaired and that can affect the way that they clear the sedation medications that we're giving pulmonary status do

they have COPD asthma or sleep apnea sleep apnea is major in procedural sedation neurologic status do they have a history of seizures endocrine status hyper or hypo metabolism of medications can occur if they have a thyroid

disorder we want to know about adverse experiences with sedation in the past do they have a history of a difficult airway for us at NYU if they have been already been identified as a difficult airway that automatically means we're

doing the procedure with anesthesia current medications potential drug interactions is very important we'll go over that a few slides drug allergies and herbal supplements that they're taking tobacco alcohol or

substance use and frequent or repeated exposure to sedation agents is just going to increase their tolerance of the medications physical exam vital signs auscultation of heart and lungs and then their airway assessment sorry excuse me

do they have any Strider snoring or sleep apnea advanced RA they're gonna have a hard time tilting their neck back if they have cervical spine disease or they have rheumatoid arthritis chromosomal abnormalities like

trisomy 21 patients with Down syndrome can have an enlarged tongue that can impair your ability to manually ventilate them if respiratory depression wants to occur body habitus if they have significant obesity especially of the

head and neck areas and head and neck limited neck extension short neck decreased ornamental distance which is basically just looking at how far back they can tilt their head any neck mass and then again cervical spine disease or

trauma do they have a c-spine collar are they on c-spine precautions that's not a patient we're going to be able to manipulate their airway and then mouth opening we do use Mallampati and I'll review

that in a couple of slides so the AFC classification is a categorization of the patient's physiologic status that can be helpful in predicting operative risk it is recommended by the AFA that if a patient is an Asaf or that that

should prompt an evaluation by an anesthesiologist I will tell you at NYU we will still get procedural sedation to some patients who are in Asaf or but we like to identify it ahead of time because if they have significant

comorbidities that will potentially increase their likely hurt likelihood of having an adverse outcome we then have a lower threshold for activating a rapid response or a code if something was to happen if we got concerned about

something so the airway assessment is

now that you all have an overview and a refresher of nursing school and how these medications work in our body I want to now go over our practice

guidelines and the considerations that we take into place so as you know I'm not going to go over into detail the patient populations that are prescribed these meds but kind of knowing that these are the

patients that we see in our practice that for example are on your direct direct vector 10a inhibitors patients with afib or artificial valves or patients with a clock er sorry a factor v clotting disorder these oral direct

thrombin inhibitors patients with coronary artery thrombosis or patients who are at risk for hit in even patients with percutaneous coronary intervention or even for prophylaxis purposes your p2 y12 inhibitors or your platelet

inhibitors are your cabbage patients or your patients with coronary artery disease or if your patients have had a TI AR and mi continued your Cox inhibitors rheumatoid arthritis patients osteoarthritis vitamin K antagonists a

fib heart failure patients who have had heart failure mechanical valves placed pulmonary embolism or DVT patients and then your angiogenesis inhibitors kind of like Kerry said these are newer to our practice these are things that we

had just recently really kind of get caught up with these cancer agents because there really aren't any monitoring factors for these and there is not a lot of established literature out there knowing that granted caring I

did our literature review almost two years ago now so 18 months ago there is a lot more literature and obviously we learned things this morning so our guidelines are reviewed on a by yearly basis so we will be reviewing these too

so there is more literature out there for these thank goodness so now we want to kind of go into two hold or not to hold these medications so knowing that we have these guidelines and we'll be sharing you with you the tables that

tell us hold for five days for example hold for seven days some of these medications depending on why the patient is taking them are not safe to hold so some of the articles that we reviewed showed that for sure there's absolutely

an identified risk with holding aspirin for example a case study found that a patient was taking aspirin for coronary artery disease and had an MI that was associated with holding aspirin for a

radiology procedure they found that this happened in 2% of patients so 11 of 475 patients that sounds small number but in our practice we do about 400 procedures in a week so that would be 11 patients in one week that would have had possibly

an adverse reaction to holding their aspirin and then your Cox inhibitors or your NSAIDs as Carrie already mentioned it's just really important to know that some of those the Cox inhibitors have no platelet effects and then your NSAIDs

can be helped because their platelet function is normalized within 24 to 48 hours Worf Roman coumadin so depending on the procedure type and we'll go into that to here where we have low risk versus moderate to high risk

we do recommend occasionally holding warfarin however we need to verify why the patient is absolutely on their warfarin and if bridging is an option because as you learn bridging is not always on the most appropriate thing for

your patient so when patients on warfarin and they do not have any lab values available that's when you really need to step outside of guidelines and talk with your radiologists your procedure list and potentially have a

physician to physician discussion to determine what's best for a particular patient this just kind of goes into your adp inhibitors and plavix a few of the studies that we showed 50 are sorry 63 patients who took Plex within five days

of their putt biopsy they found that there was of those one bleeding complication during a lung biopsy so minimal so that's kind of why we have created our guidelines the way we did and here's just more information

regarding your direct thrombin inhibitors as cari alluded to products is something that we see very commonly in our practice and then your direct vector 10a inhibitors this is what we found in the literature

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

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

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

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]

after having these two cases one in our institution and one at University of North Carolina Chapel Hill that we would then basically upsize our particles to

100 micron and we have not seen that and we're doing a second clinical study and I'm not seeing that as either we had about a 70% reduction in pain so if you look at our visual analog score out to six months and if you look at our

disability it actually paralleled this exactly which is pretty impressive considering mostly patients had bilateral knee pain so out to six months very good results 90% of patients were responders so two

out of our twenty patients did not really respond one patient didn't respond at his one-month follow-up but did respond at his three and six so I still consider him a clinical failure because we expect

these patients to respond by one month here's just an example of a baseline MRI before and after and you can see all that joint effusion there the white that decreases just even after a month how much it decreases and we looked at this

in terms of synovial thickness and distension and even on MRI you can object objectively count calculate synovitis scores and we calculated that they actually statistically decreased this is another patient on the left the

image shows diffuse white enhancement if you will of the synovium of the lining on the right it shows the fluid this is an image just of embolization and I show this image because it's really shocking and this is actually one of our nurses

who's enrolled in a clinical study is this is before this is all we did we embolized the medial aspect of the knee this is one month later 30 days in fact somebody just asked me this when I was in the booth over at the meeting across

the street and basically I said listen I don't know why this happened so quickly I have no idea we didn't tap renu-it into anything else if you look at this premium post it's pretty dramatic so clearly there's an inflammatory process

that we are arresting or stopping in such a short period of time so is there a future for this I don't know it may just we may just fall down and find out that there really is in a great future but so far we know it's at least

technically successful it's the results are positive in the short term long term we're not so sure yet we do need to better understand these risks and I think in my opinion in the long term it'll probably be really really good for

this 40 to 65 year old patient population who's not yet ready for knee replacement surgery this is the algorithm for our clinical study which were almost done enrolling right now it's a randomized control study against

placebo so it's two to one randomization which means one third of the patients actually get a sham procedure so we do an angiogram on their leg they're asleep they have no idea for embolizing they're genetical it arteries or not we wake

them up I think about the table and we follow them up if they're no better they're allowed to cross over and get the treatment the other 2/3 of the

people were thinking about the covered

portion actually actually would be occlusive in that paddock veins a lot of people are concerned about that this could be kind of like a but carry you're gonna actually occlude flow in the paddy vein caused thromboses that didn't pan

out at least clinically okay it didn't pan out and that's another advantage of actually accessing very close to the paddock vein IVC junction that's where the biggest vein is so you don't get a lot of occlusive problems okay but

usually clinically it does not pan out so the bigger the hepatic vein the more likely you have a lot of room around your your graft you won't be occlusive to the paddock vein that's more important for for transplants than other

than others I told you it's rare this is actually a very rare case of such that where you actually have a segmental segmental kind of but carry after a tips okay and you know this is actually from a form of venous outflow from the ematic

vein this is a perfusion defect typical it's a wedge right typical perfusion defect in the liver that's how you death so you know this is vascular this is a perfusion problem but you've got hepatic artery readout artery the red arrows

running into the segments and you have portal vein running into the segments so what's the problem it's actually a paddock vein occlusion okay by the stents subclinical no no clinical complaints you let it be

in the patients usually recover okay treat the patients and not the images okay on the other side if you put their tips too deep sometimes you actually get thromboses of the portal vein branch

again you get a call from hepatology you've got portal vein thrombosis is the patient doing okay yes treat the patient and not the images they usually resolve this it's not not a big problem another technical problem

I'm gonna focus mostly on technical for you guys this is a but key area okay and the but carry especially in the acute stage the liver is not like a cirrhotic liver is big liver is actually engorged okay so it's very large usually

your needle is too short to even reach the portal vein okay that's a big problem okay because your access needle is too short for a very large engorged the portal vein so this is as deep as it

goes do I have a see that that do you see that needle tip that's as deep as the needle tip goes okay the portal vein is a good distance away okay luckily this is a co2 porta gram luckily I'm actually in a small branch right

there I just hit it on you know and on this is not the there's not a needle tract this is just luckily hitting it a little branch and on so I'm actually accessing the portal vein and I can do a co2 porta gram here okay

typical inexperienced person would say you know this looks good I'm lucky I'm in a branch but it's a nice smooth curve I'll just pass a wire down and I'll balloon it and I'll put a stent in it's a nice curve and you know so it's my

lucky day I don't need to extend my needle or get a bigger longer needle to reach the portal vein here's the problem with this and this is exactly what this is exactly what this is they pass a wire and it looks beautiful just put a stent

and go home okay here's the problem this is actually the small branch access sites this is actually where you really need to access world vane but your needle is not long enough okay

what we found out is that if you are in a small in a small portal vein no matter how much you balloon it it will come down again and it will be narrow so believe it or not if you go sideways in a portal vein and rip it open with a

balloon it will stay open but if you go down of small portal vein and balloon it open it will always contract down okay so you cannot do a tips simply by ballooning and putting a stent in in this case okay what we do is we actually

denude the vein itself we actually rip it off okay and make it a raw parenchyma and we do that with a Tortola device we literally rip off the paddock the paddock portal sorry the portal vein endothelium and media and adventitia rip

it off make it completely raw as if it's an access as if it's a liver brain coma which is which it is now and then we then we balloon dilates okay rip it off denude it angioplasty it's okay and then put the stent and see that aggression

despite all that aggression of ripping it off it still has an hour kind of an hourglass shape to the to the tips okay that little constraint there that's the hepatic venous access sites this is the parenchymal tract to see nice and open

with a balloon but the but the actual vein that we've been through despite our aggression in actually ripping it off it's still narrowed down but this is as good as it gets okay

want you to follow follow okay so our again we went from a six-week program now down to a three-week program and

incorporating simulation and so we took a lot of what we wanted to and like what we would recover in our first second and third week and here we're going to go into more detail so really week one as we talked about the basics so really

just doing some introductions you know what we did was a baseline assessment so we gave them a quiz and then we also talked about aseptic technique the cath lab environment essentially and then we also really talked about the team and

the environment and scopes of practice we really wanted to focus on that because this is kind of the Foundation's the fundamentals of working with a team because I know coming from critical care into the cath lab I was usually like the

one that owned the patient and now I have this team and so it was really kind of a difficult transition for me because they didn't understand the RT role and I think vice-versa so what we do is we have the nurses and

the text and so the nurses look up the RT scope of practice and vice versa and it's really an aha moment for some of those nurses and techs to see really what is our scope of practice and how similar they are yeah it's very

different too and so this is a lot of times we get a lot of good feedback of like oh I didn't know that they could do this or oh wow you know so like I said some really great aha moments and then our second day we go into a great detail

about radiation safety a lot again as a nurse I didn't know a lot about radiation safety the RT but we really wanted to blend the best of both worlds and really help learn from each other so that's the hence the

interprofessional approach and then really just basic cases so left heart calf so what wire is what catheters what do we need for this case and we would bring these wires and catheters to class so that they could look at them they

could play with them so especially if they've never been exposed to something like this before they have that hands-on you know the kinesthetic learning essentially so that they get to look at at some of these

pieces of equipment same with right heart cast some of our interventional procedures and structural heart peripheral etc so we wanted to cover a lot of different cases and then day three we really went into more of that

equipment some of the interventional equipment and then looking at radiographic views so we kind of wanted to like put it all in some sort of sequence and then the third day we went into doing some sort of simulation so we

wanted to introduce them to our simulation software the mentis and then our day four and five this is where they would work back at their home facility and do their clinical practice essentially or their orientation so so

segwaying into some of the examples that we've wanted to show everyone just on the first week of our academy and some examples of the activities that we do with our learners in class is trying to identify different areas of the cardiac

cath lab so essentially is your rhythm right your EKGs I think that's pretty number one important part of working in the cath lab is identifying your EKGs and your rhythms right so again our technologists may not have had this

prior experience so we really do need it we needed to start from the ground up identifying what a rhythm is and we asked them to take a class prior to attending the Academy if possible depending on their hire date and

depending on when they start the Academy I think it benefits them to understand a basic you know EKG rhythm what's a p-wave what's a QRS right so down to the very basics once they do that they can come into

class and we can show them examples of abnormal and normal cardiac rhythms and and have them identify them and and ensure that they understand that you know this is something that you see in the cardiac cath lab you need to raise

your hand and call it out rhythm rhythm hello or making sure that you identify that it is a normal rhythm another example that event an activity that we do is identifying our coronary Anatomy that's pretty important as well

injecting contrast and doing angiograms through the coronary arteries to identify any abnormalities or stenosis and so with that comes a little bit of complicated it's complicated for them to identify those arteries and different

views you know we have the left anterior descending we have a right coronary artery well how does it look in different views and as an RT we understand that every time we move that SI arm the image changes not only for

the artis to identify the coronaries but also the RNs we need them to identify what we're looking at some of these are ents have never seen an geographic views in five different ways so where's your Li D if my image intensifier is REO

caudal where is your right coronary artery if my image intensifiers le oh so we really wanted to incorporate that collaborative effort with both parties our T's and our NS learning this activity all right and no pun intended

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

pressure of 60 over 40 minimally responsive I'll give you that

there are probably two right answers if you were going to figure to go by the book on this this PE qualifies as a good I agree with a now what about e somebody pointed this out the other day and I was like oh yeah it's a reasonable point

exactly it has to be greater than 15 minutes so theoretically e is correct as well but that's not what I meant when I put question together all these pitfalls okay

multiple choice question number two seventy year old woman blood pressure of 128 over eighty heart rate of 115 RV strain on echo elevated troponin what type of PE is this I hear a lot of C's that's correct

so let's go through this so yes this person has RV strain on both echo and an elevated troponin so meets that criterion but how do we know the especi is or the passier the especi is positive here the heart rate exactly so the heart

rate on that scale had to be greater than 110 it's 115 so positive especi RV strain and echo elevated troponin high risk intermediate PE 24 year old woman blood pressure of 150 over 80 heart rate of 95 no RV strain large central embolus

what type of PE is this sorry can someone be a little louder dee dee is correct so just the the the thing I was trying to trip you up on is the large central embolus at this point we still do not use where the embolus is as

a criterion for stratification okay now I will say that large central embolus tends to correlate with our V strain so you will see a lot more patients with central embolus have our V dysfunction at the same time and so they'll often

meet the criteria for the sub massive are massive but if you have just a totally normal right ventricle no elevation and the in their troponin and their BNP that is still technically a low risk PE and we'll see this sometimes

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

year old patient diagnosed with

glioblastoma lesion is located on the left frontal lobe this is done after radiation and surgery the image to your left is just a regular MRI with contrast gadolinium is the one used this time we always be the drum in the context of

choice is gadolinium in our institution you could notice the big size of the glioblastoma lesion onto the left frontal lobe of the patient as indicated in the round ring patient went for treat radiation and surgery look at the two

images to your right the one in the middle is done Pet MRI without the contrast take a note on the area where the lesion was before there is normal uptake but you don't notice any abnormal uptake and on to your right is post

treatment MRI is that those two are done the same day and with gadolinium the deletion the area where the the ring it is enhanced by the contrast but look at it there is no hypermetabolic uptake that means that the lesion is not viable

so the malignancy is not viable this time this scan is done to evaluate the effectiveness of the treatment it's a good sign before I go to the third case

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

that's background let's talk about what I mean when I say massive sub massive low risk high risk intermediate risk low risk all these definitions they're

actually pretty precise and so I think we need to be on the same page for that so when you see this what do you call it saddle saddle is a reasonable one large because there's I'm not sure automatically did that but would you

call it a massive PE how many would say yes this should be called a massive PE okay how many no okay it's not a big deal I'm not remembering faces but this is not necessarily a massive P I'd be surprised

if it wasn't but it's not necessarily because I haven't given you a key piece of information the hemodynamics massive PE is all about hypotension so what does that mean so this is from the American Heart Association in 2011 a massive PE

is an acute PE with sustained hypotension meaning a systolic blood pressure of less than 90 millimeters of mercury for greater than 15 minutes or requiring inotropic support okay so doesn't matter where the clot is

doesn't matter how much clot there is if you're hypotensive for greater than 15 minutes then you fit in the massive category okay sub massive PE okay you have a normal blood pressure but your right ventricle is dysfunctional so

either by echo CT biomarkers such as BNP or troponin your EKG shows right heart strain basically your right ventricle shows some measure of duress but it has not totally decompensated to the point you're starting to get hypotensive and

I'll give you a pathophysiologic explanation in a couple slides low risk basically means that you have no hypotension no RV dysfunction no myocardial necrosis so you have clot in your pulmonary arteries absolutely but

your right ventricle is acting normal and you have no issues with hypotension that's 60% of pease that present to the hospital fortunately sub massive about 25% and massive five to ten percent okay why do we care about this categorization

is there any functionality this yes massive PE carries about a 25 to 65 percent mortality so it's a coin flip whether these patients are gonna live or die that's how severe this disease is sub massive PE you know these are the

patients that are compensated from a blood pressure standpoint but have RV dysfunction these patients have a three percent mortality or so in the most recent randomized now back in the late 90s and early 2000s

the mortality seemed to be higher on the order of 10% but I think we're settling around a 2 to 4 percent mortality for this group now these patients do have a higher rate of clinical deterioration than the low-risk group meaning they can

progress from the sub massive category to the massive category that's that 5% number there so this this group is a little bit that's why I said in yellow and the top group is in red low-risk patients anticoagulate them they'll be

fine so that was the eh-eh-eh in 2011 well the Europeans have to had to have their own version in 2014 and they said you guys you Americans are not doing this quite right so that's where they I'm sorry I can't put two pointers at

the same time that would be pretty cool but I'll start on this side if I can everybody over there see that all right so this intermediate group here is the same as the sub massive category I'm gonna walk you through this just because

it's you know we're more and more going towards the European Society guidelines so they break down this sub massive category into intermediate high and intermediate low and the reason they did that is they're saying that not all sub

massive pease are the same and that's probably true there's some some sub massives that are really not looking good and going towards massive and sub some some sub masters that are just rock solid stable and beside a little bit of

RV dysfunction they're probably gonna do just fine and just you know go towards the low-risk with a little bit of anticoagulation so what how do they break this down well both of them have this positive especi or pecci I'll show

you on the next slide what that is basically it's a pulmonary embolism severity index okay so you have to have that being abnormal or positive for you to fit in the intermediate category but then this is where it differentiates so

if you have an imaging test such as a CT or an echocardiogram and you have your laboratory biomarkers such as a troponin or BMP being elevated or abnormal then you fit into this intermediate high-risk category but if you have only one of

them or neither of them being positive in the intermediate low-risk category so what's the big deal why does that matter well but we don't really know frankly but what the European guidelines recommend

is if you're in this intermediate high category you should be watched because you have a risk of clinical deterioration and if you're going towards that they say consider reperfusion reperfusion could be

anything it could be systemic thrombolytics it could be catheter directed lytx or it could it could be surgery that's that's the way they put it if you're in the intermediate low-risk category you can be discharged

pretty early this is that pesi score and you can see why they tried to simplify it the s pesky because you have all of these factors and they're all assigned these points the more points you have the worse you are but let's focus on the

simplified pesky scale if you have a score of one or more of these then you're considered to have a 10% mortality in the next 30 days so that's these are what they thought were the highest impact issues in a patient

presenting with PE it doesn't tell you that just because you have a positive s peso you should intervene it just says that this is what may happen with these circumstance and we'll go through the first set just for a second here so age

greater than 80 years that's a that's an issue if you have cancer if you have heart failure or pulmonary disease a heart rate greater than 110 the systolic blood pressure less than 100 or an arterial oxygen saturation off of nasal

canula or supplemental oxygen less than 90% you get a point okay all right are we ready for the first question 65 year old man blood

is my cap nog Rafi reading actually I want to back up a little bit here do I want to back up no I don't I don't want to back up so um let's look at the first

question why is my cap nog Rafi reading abnormal so let's first talk about physiology so a question I get a lot of times is sue the patient comes down for a procedure to the floor I put a sample line set on

them I plug them into the monitor and I'm getting a value of 28 29 30 why are my values abnormal anyone ever see this is anyone still awake okay so there's a few reasons the patients that we are dealing with generally aren't

healthy right I mean sometimes I go to work and I get chest pain I'm like can I just be in an ambulatory gallbladder room today because the patients that are coming from down to IR are sick what their physiology is sick too so we have

Krebs cycle we take oxygen in right it circulates to ourselves it participates in aerobic metabolism we get the byproducts of heat and energy and we get carbon dioxide as a by-product carbon dioxide really diffuse about diffuses

into our blood travels to the lungs and gets exhaled where we measure it so let's talk metabolism really quickly so if someone has a fever if their metabolism is ramped up you think they're gonna be producing more carbon

dioxide yes let's say they're a little hypothermic maybe they're gonna be producing a little bit less you see it for sure in the car patients who are cardiac arrest that are cool to status post cardiac

arrest right those values go way down normal physiology normal physiologic response somebody comes down and they're mildly hypoxic they've got pneumonia or some sort of VQ mismatch and they're hyperventilating to UM debeso

compensate for their hypoxia do you think there's co2 values gonna be a little lower at baseline yeah so these are the patients that you're seeing right so we have reasons that patients could be hyper cap neck like metabolism

right somebody who's in pain someone who's developing a fever early stages of sepsis they may actually have a little bit of a higher value somebody who's sedated or hypoventilating may have a higher value and when we talk about

perfusion is the blood moving round and round is that circulating co2 coming back to the core do we have increased cardiac output with continuous constant ventilation and certainly we can we're gonna look at equipment issues next and

the same goes true more probably in your cases of the hypocapnia patient so someone who is not fully exhaling someone who's in bronchospasm or a COPD or you're not getting that nice square waveform you're only getting some of the

mixed gas ventilation that they're exhaling rights and the conducting airway is mixing with the alveolar gases someone's a little hypothermic someone who's been NPO for 24 hours right it's the opposite of carb-loading right so

you kind of throw them into a little bit of like acidosis you know they're kind of not burning carbs for fuel are they gonna be producing as much carbon dioxide not so much right so when you're coming so when

patients come down to you and you put them on the monitor consider these things so ventilation perfusion gradients so we have what we call our VQ matches and our body is designed beautifully right so when everything is

working great it works great so the way we ventilate all of our lungs owns is very closely matched to the perfusion of all of our lungs ohms so by me standing up here I'd like to think I'm pretty healthy if you did a blood gas and you

put me on one of those filter line sets right now you would hopefully see a gradient that's very small the normal gradient between a PA co2 on a blood gas so the level of carbon dioxide on a blood gas in the arterial blood and what

you see when I fully exhale into the monitor should be between two and five millimeters so these are your patients come down healthy physiology you put them on and you get a value of like 32 then you

could assume that if they were healthy two to five millimeters okay their blood gas would probably like 35 for POC to everyone follow now does any of our patients read the physiology tech books textbooks no they typically don't so

when you have patients come down they may have shunt right so they may have we have our little airway here a and B you're out like picture them as lungs and lung a is blocked so we have no ventilation going to lung a but blood is

still chugging through right so blood is still going through the pulmonary circuit so we're gonna have Patapsco a dia depending on the size of the shunt is this the end of the world are we gonna cancel the case no but just being

aware of the patient's physiology would explain to you why I put this patient on this and I'm getting a value of 30 you follow and it's not the end of the world you document 30 and you monitor for trends as you're going along with your

sedation same thing goes through with dead space dead spaces were ventilating but we have an area of the lung that is not being perfused pulmonary emboli other circulations some medications hypovolemia shocky patients same thing

the VQ mismatch not the end of the world it's part of the patient's physiology maybe part of the reason why they're down there just being aware of these things though so the technology works right our equipment works if just amazed

it's picking up something that we don't connect all the dots on physiologically that sometimes confuses us a little bit so I hope that clears up part of it so when we're monitoring capnography certainly ventilation is what we think

of first and it's important co2 being expired by the lungs that's what we're looking for but if we back up and look at the physiology of carbon dioxide production in the body we are also inferring that

it's being metabolized and being created from Krebs cycle and aerobic metabolism and that we have perfusion occurring okay I'm sure if some of us have seen in our you know nursing careers patients who are kind of peri-arrest and

the capnography kind of drops off it's like a poor man's swan you're watching cardiac output drop in real time because carbon carbon dioxide is not being delivered to the lungs so when we're looking at our patients when

they first come down we first want to establish a baseline value we want to put on a monitor have a patient take some nice deep breaths full ventilations not just one but a few you want to you know have them take a few and look at

their other vital signs their mental baseline status and we're gonna look for trends in their carbon dioxide value so if someone starts off at twenty nine I don't care that they're not 35 to 45 which is textbook normal this person may

not have the stimulus to breathe if I let too much co2 accumulate so we're really looking for the trends okay now somebody will say well how much of you know how much should we look for 10 to 20 percent change from your baseline is

somewhere where you want to start paying attention to what's going on okay maybe like titrating your sedation or just being a little bit more cautious with how much more sedation but again it's more important to look at the trend

value behavior of your carbon dioxide than it is the absolute numbers themselves so first you having a problem let's consider the patient's physiology

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

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

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

new data of the Emmy trial that came out last year our ten-year results saying

that after ten years after ten years women who wanted to retain their uterus they looked at them in ten years three-quarters of those women were still very very satisfied and also were still able to retain their uterus so ten-year

data came out randomizing people for uterine artery embolization versus hysterectomy of the women who chose you to an artery embolization ten years later they were still very happy so I tell my patients that this is what you

should expect that you will have symptomatic improvement in 12 months around 85 to 95 percent of the patients are pretty happy there is a entry intervention rate it is not zero and it can be higher than ten

depending on what kind of Imogen is seen ahead of time and that we know that dysfunctional uterine bleed tend to do a little bit better than bulk type symptoms and that's partly because of subjective nature of that so this is one

of the patients that I treated when I was in in Virginia and Riverside and she's a former miss Brazil and she came to see us with what she also called reversed cycles like she would bleed more than she would not and she was

wearing depends and it took everything to just coach her out of the car to come inside to do a consultation because she was so afraid that if she got out she would be sitting in a pool of blood and she had an MRI showing what looked like

a eleven point seven centimeter fibroid she had embolization and that was her six month follow-up MRI to the right which looks like a very impressive result they don't all look this way which is why I save this image something

that looks like a normal uterus now I for the persons that I told to hold your high horse here is the time okay so what happens if I want to have a baby because these are the things you remember we're being ambassadors for this procedure we

need to be having the answers for the things that are our friends and family members are going to be asking us so if you want to have a baby I would say that the data that informs us as to what to do with you is still very weak but the

only randomized prospective trial that we have out there says that you should actually have myomectomy and a Cochrane review was also done and it still says that there's very low level evidence suggesting that myomectomy may be

associated with better fertility outcomes as opposed to UAE but more research is needed and we still require more research so at the very least what I have to do and now you feel compelled to do is to send my patients to see

someone who is a fertility specialist in consultation so we can make this decision together so if your poor surgical candidate if you have the gazillion fibroids and if you've had surgery before a hostile

abdomen and the patient says you know what dr. Newsome there's nothing that you can tell me ever to say that I'm going to have surgery then we're going to be doing something else that is not surgery okay the other thing that your

I want this to be as instructive as possible I do have some multiple-choice questions that are peppered in there and hopefully you guys feel comfortable enough to shout out answers I really don't care if you get it right or wrong so but if I teach it right I hope it's

clear what the answers are okay so and and I know the title test says that I'm going to be talking about parts frankly I think there's a lot more to talk about about PE other than parts and I'm not going to be emphasizing that

but if there's time to ask questions or I'm happy to speak about that as well because I think the disease and the treatments are really the crux of PE at this point okay so I start with something called the landscape where are

we with pulmonary embolism well you know I don't know how many of you have seen PE in the IR suite or have dealt with these patients or even have friends or family that have had a PE but I don't think anybody who's interacted with this

disease would argue with the fact that PE is a big deal why do I say that statistically speaking well there are 900 000 VTE events per year that's DVT or PE that's a lot it's almost a million now the number of deaths from PE every

years quoted to be as high as 300 000 but is around 60 150 is what we think so quite a few this affects everybody you know you might have heard of Serena Williams getting a PE Chris Bosh and Serena Williams I think had a massive PE

which I'll tell you the definition of that later but it's a it's it's something that can affect a young person and kill that young person so that's what makes it a little bit tougher than some of the other diseases it's the

third most common cause of cardiovascular death stroke mi then PE ten percent are fatal within the first hour so a lot of these patients you're not even gonna see and when you do see them you've got a big task ahead of you

because they're you're trying to rescue them from death that's basically the same statistic now if you were to take every patient who comes into the hospital and you put an echocardiogram on them and you looked at the right

ventricle their right ventricle would show some evidence of dysfunction and so that's an interesting statistic because right ventricular dysfunction is you'll see on a subsequent slide is actually a pretty big deal and is actually at the

crux the pathophysiology of PE now if you were to do a VQ scan around six months after people got a PE you would find that 1/3 of those patients actually have residual thrombus so we think that you

know PE is a acute disease but what we're finding is that it's actually a cute disease that can become chronic and a lot of people and we're actually revealing unveiling the fact that maybe a year or two years after their PE these

patients aren't doing as well as we thought so that this is a burden it's a chronic it's a chronic disease that causes a burden on their lives so this is the disease and and you know as an IR you look at this and you say well that's

pretty exciting looks like we can intervene on something meaningfully but there are some caveats we should remember first most patients have low risk PE s I'll define that in a little bit but these patients don't need an

intervention they just need anticoagulation to the best of our knowledge that says all this this group needs sub massive PE I'll spend quite a bit of time on and it's a very controversial topic and there's a

lot of different attitudes between interventionalists and non interventionists about sub massive PE when you get a massive PE patient this is the patient that's crashing and burning most of them should receive

systemic thrombolysis which is an IV in the arm and a drug through their vein it's the fastest thing you can do and it doesn't involve corralling an IR suite the team for the IR suite or a surgical team and as I just said there's a wide

range of attitudes regarding treatment aggressiveness so I'm not going to go

okay pathophysiology right ventricular the right ventricle is everything when it comes to the pathophysiology of this disease I'm gonna lead you through this because I think it's interesting and important I'm gonna go to this side this

time be fair to both sides of the room so when you have a PE that increases your pulmonary vascular resistance normally the pulmonary vasculature is a very low resistance circuit but when you start putting clots in it it's restive

Gong its its resistance goes up it's kind of analogous to the left an electrical circuit what does that do to the right ventricle well it increases the after load on that right ventricle so what that does is it causes the right

ventricle to blow up like a balloon now by Laplace's law if you take a balloon and you blow it up the intramural pressure is higher in the balloon so if you can imagine that thin walled balloon if you took the pressure at each point

inside of the balloon because it still got a finite thickness the pressure is higher than if it's decompressed now the problem with that is that how does the right ventricle get blood it gets blood from the coronary arteries but if the

pressure inside the ventricle is higher than the pressure differential is less and what what what is Flo rely upon it relies upon a difference in pressure from point A to point B so if that starts to equalize your blood flow to

the right ventricle decreases okay that's why the right ventricle gets ischemic now when the right ventricle becomes ischemic it can't squeeze as hard so it gets hypokinetic when it dilates it also does

not seem to squeeze out as well because the muscle fibers aren't overlapping as well okay so both of those things lead to both so that the right ventricle is now not squeezing is hard and it's not getting blood forward to the left

ventricle so that results in LV preload reduction though LV is not seeing as much blood on top of that when the right ventricle dilates it starts impinging on the left ventricle so now the left ventricular cavity is smaller and it can

accept less blood your output is only as good as your input okay so that's where you start developing systemic hypotension because your left ventricle can't pump out as much blood what happens when your left ventricle can't

pump out as much blood you don't get as much blood into your coronary arteries you don't get as much blood into your coronary arteries you're not getting as much blood into your right ventricle this is the vicious cycle that leads to

right ventricular failure and the progressive death that you see with massive PE now if you were to draw a line like that everything above the line is sub massive PE everything below the line is massive PE okay this is a big

experiment I did we were trying to create sub massive PE we created a massive PE this used to be mostly the L the left-sided chambers and all of a sudden became the right-sided chambers to me this drove home how much the right

side can blow out and dilate that's the only point of this picture I hope I didn't cross you out okay so let's talk

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

and you can see on this t1-weighted image that increased area of enhancement which is the area of synovial thickening you actually see this on MRI beforehand and there it is located over the lateral aspect of the knee on the axial image

and so what we're doing sorry in the medial aspect of the knee so what we're doing here on the angiogram is and you solve these leg angiograms where everyone doesn't really care about these Janicki lit arteries they're really

important when you have sfa or popliteal occlusive disease because they serve as a collateral source but otherwise and people have arthritis they can be a real pain and pain in the knee if you will so this is a this is the superior medial

genicular artery it always drapes over the femoral condyle and you'll see here on this image you don't really see very much once we get into the vessel look at this it almost looks like a small about a cellular carcinoma like when you're in

the liver you get this tumor type blush vascularity that's what we're looking for that corresponds to the patient's area of pain and then after embolization this is what it looks like takes a very small amount

of embolic we're using maybe 0.4 2.6 sometimes 1 CC at most of dilute embolic that we're injecting this is another case again before and after if you look here on the right and then on the left you don't really see much until you

select the vessel out once you get into that super medial vessel you can see how much enhancement there is so in our clinical study of 20 patients this is what we did you'll see on the bottom here we used embassy and 75 micron in 9

patients and 1111 patients got a 100 micron and I'll explain why we upsized our particles so initially we wanted to go very small because that's what dr. o Cano had done in Japan but then we wanted to actually up size our particles

and I'll explain this here in our complications so like all clinical studies the purpose of doing really good clinical research is because this is early and we don't know if they're going to be complications and it's always fun

when you're the first one to figure it out and you tell patients I don't really know what's gonna happen and this is what happens so 13 patients had this kind of skin discoloration over their knee now we knew this because we've been

doing knee embolization for about 10 years in bleeding patients not necessarily arthritic patients so we had seen this before but none of these patients in this clinical study went on to have any alteration of the skin and

it resolved in all patients there was some minor side effects from basically medications and one small groin hematoma but there were two patients who developed plantar numbness over their great toe so under their great toe

basically in the medial distribution of their tibial nerve they ended up getting plantar numbness and this is believed at least in our experience to probably be related to non-target embolization to the tibial nerve the tibial nerve

probably gets its blood supply from many of these generic arteries so we decided

all about effective bag-valve-mask it's the mainstay of airway management and procedural sedation but also in the o.r so you're gonna see if you're ever working with an anesthesiologist that

the first thing they want to see is how easily they can ventilate the patient with a mask and if they have trouble they know that's potentially going to be a patient that may give them difficulty later on when they're attempting to

intubate because when they go to intubate the patient if they're not successful they immediately stop and go back to bagging the patient they want to know that that's gonna be there their failsafe and that they have an

effective way of delivering breaths the difficult airway is going to be defined in terms of whether effective gas exchange can take place with an Ambu bag so at NYU we use the sorry we use the Mallampati so this classification system

attempts to grade the degree of airway difficulty the foundation of the assessment is that the tongue is the largest anatomical structure that can inhibit mask ventilation now again if you look at the research surrounding

this Mallampati used in isolation it's not useful you really want to look at all of the other airway assessment criteria that I just previously discussed because it's on our required documentation you know it can be

something that maybe providers get focused on just open your mouth cool and move on but it really is important to look at all the other components not to call out my attending sitting over there so this is a great mnemonic that I like

moans it's just a quick easy way to identify a patient that may give you a little bit of trouble when it comes to manual ventilation so M is for mask o for OB 3a for age and for no teeth and s for stiff lungs so you can see with this

patient here with the beard he has a lot of facial hair so that's a patient that you're gonna have a difficulty getting a good seal with and if you can see they actually covered his beard with Tegaderm in order to get an effective seal right

painful later but great for his airway um last thing yes at this point oh great this points you guys can still hear me okay so for this patient for for obese patients in general my biggest pain point I guess you could say is when I

see patients inappropriately position during procedural sedation and a nurse will call and say the patient's not really well sedated but his his capnography waveform looks all off he's occasionally having periods of apnea can

you come and help and the patient looks like this so a patient who's sedated is not going to be able to comfortably spontaneously mentally win their position like that you can see his airway is a little bit compressed here

he has to overcome extra body habitus in order to effectively take a breath so what you want to do is just ramp your patient and this is obviously extreme like if you're doing an angiogram you're not the providers gonna say what on

earth are you doing but what you can do is take that pillow out and put a little roll underneath the shoulders and you're gonna see the airway open up and if I get patients who come in and they can't be flat maybe they have congestive heart

failure so they have that pillow orthopnea you can position them like this give them the sedation and then take everything out that's what I always do you you want to make sure that you have

good positioning and that's going to set you up for success patients who are elderly or have no teeth are going to be what we call a dentist and they essentially just have loss of musculature in the face which is going

to correlate with surface area which means you're not gonna be able to get a good seal so what they did in this particular patient is they actually put gauze in to just increase that surface area and then patients with stiff lungs

are going to be patients who have a history of COPD or any other restrictive lung disease and they just may be difficult to ventilate Pharmacology and

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