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Massive PE | Pulmonary Emoblism Interactive Lecture
Massive PE | Pulmonary Emoblism Interactive Lecture
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MRI Safety & Screening | PET/MRI: A New Technique to Obtain High Quality Diagnostic Images for Oncology Patients
MRI Safety & Screening | PET/MRI: A New Technique to Obtain High Quality Diagnostic Images for Oncology Patients
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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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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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What's Next | AVIR CLI Panel
What's Next | AVIR CLI Panel
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Bland Embolization | Interventional Oncology
Bland Embolization | Interventional Oncology
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Definitions in PE | Pulmonary Emoblism Interactive Lecture
Definitions in PE | Pulmonary Emoblism Interactive Lecture
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Project Interventions & Improvements- Floor Co-ordination | IR Lean Sigma Team Improves Patient Experience and Throughput
Project Interventions & Improvements- Floor Co-ordination | IR Lean Sigma Team Improves Patient Experience and Throughput
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Submassive PE | Pulmonary Emoblism Interactive Lecture
Submassive PE | Pulmonary Emoblism Interactive Lecture
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The Last 5 Years in PE | Pulmonary Emoblism Interactive Lecture
The Last 5 Years in PE | Pulmonary Emoblism Interactive Lecture
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Case 1 - Non-healing heel wound, Rutherford Cat. 5, previous stroke | Recanalization, Atherectomy | Complex Above Knee Cases with Re-entry Devices and Techniques
Case 1 - Non-healing heel wound, Rutherford Cat. 5, previous stroke | Recanalization, Atherectomy | Complex Above Knee Cases with Re-entry Devices and Techniques
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The Disease Process | TIPS & DIPS: State of the Art
The Disease Process | TIPS & DIPS: State of the Art
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Pathophysiology | Pulmonary Emoblism Interactive Lecture
Pathophysiology | Pulmonary Emoblism Interactive Lecture
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How Do I Approach Submassive PE Today? | Pulmonary Emoblism Interactive Lecture
Where do we go from here for submassive PE | Pulmonary Emoblism Interactive Lecture
Where do we go from here for submassive PE | Pulmonary Emoblism Interactive Lecture
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What's ahead for PE | Pulmonary Emoblism Interactive Lecture
What's ahead for PE | Pulmonary Emoblism Interactive Lecture
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The Ways to Recanalize the Below the Knee Vessels | AVIR CLI Panel
The Ways to Recanalize the Below the Knee Vessels | AVIR CLI Panel
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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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Indirect Angiography | Interventional Oncology
Indirect Angiography | Interventional Oncology
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Treatment Options- CAS- Embolic Protection Device (EPD)- Proximal Protection | Carotid Interventions: CAE, CAS, & TCAR
Treatment Options- CAS- Embolic Protection Device (EPD)- Proximal Protection | Carotid Interventions: CAE, CAS, & TCAR
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Why is Staging Important | Interventional Oncology
Why is Staging Important | Interventional Oncology
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Prospective CDT Trials | Pulmonary Emoblism Interactive Lecture
Prospective CDT Trials | Pulmonary Emoblism Interactive Lecture
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Ideal Stent Placement | TIPS & DIPS: State of the Art
Ideal Stent Placement | TIPS & DIPS: State of the Art
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The Landscape of PE | Pulmonary Emoblism Interactive Lecture
The Landscape of PE | Pulmonary Emoblism Interactive Lecture
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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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Introduction to Establishing Periprocedural Screening Guidelines to reduce bleeding risk associated with Image-Guided Theraputic and Diagnostic Procedures | Risk Mitigation: Periprocedural Screening and Anticoagulation Guidelines to Reduce Interventional Radiology Bleeding Risks
Introduction to Establishing Periprocedural Screening Guidelines to reduce bleeding risk associated with Image-Guided Theraputic and Diagnostic Procedures | Risk Mitigation: Periprocedural Screening and Anticoagulation Guidelines to Reduce Interventional Radiology Bleeding Risks
anticoagulantscampuschapterclinicclinicalcoagulationgraduatedguidedguidelineshospitalinpatientinpatientsinterventionallabsmayomedicationsneuroNonenonvascularnursenursingpatientspracticeproceduresradiologistsradiologyrochesterspecialistultrasoundvascular
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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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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Summary of Carotid Interventions | Carotid Interventions: CAE, CAS, & TCAR
Summary of Carotid Interventions | Carotid Interventions: CAE, CAS, & TCAR
applycarotidchapterendovascularmedicalpatientsstentingtherapy
Cone Beam CT | Interventional Oncology
Cone Beam CT | Interventional Oncology
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Transcript

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

MRA safety is one of our top priorities in our unit we have set up MRI zones zone one being the patient waiting area

zone two is where they change and they get screened zone three is where our control room is and anyone who passes by zone three has to get screened our pet MRI injection room is actually inside zone three and zone four is an MRI

scanner itself we assess risk in our patients for their implants we were iterate to them the importance of bringing their implant card with them just so it's easier for us to assess the compatibility of their their implants

with MRI right now we have the capability of scanning cardiac pacemakers and defibrillators it just needs more coordination with our in-house cardiology service and the implant representative rest assure

expanders and aneurysm clips are so contraindicated inside the skin we tell our patients to remove some items that they are able to remove such as dentures hearing aids piercings and prosthetics if they have it as for radiation safety

we observed the concept of Alera or as low as reasonably achievable you know before we inject the patient with the isotope we keep them comfortable we give them blankets we give them the pillows and we tell them

after they get injected that they are radioactive so we try to limit our exposure to them after they get the injection now we try to keep our distance from them and we have shielding lead shielding within the pet MRI area

now we have lead shield syringes available for the nurses use and we have dedicated a hot hot bath room a hot room and radio pharmacy we Ritter we give these puppies this injection card to the patient after they get the scan and we

were either a to them the importance of this card we have the stories from our patients where after the after they scan gone home and they passed through the tunnels or the bridges that they actually have been pulled over by the

police because the police have very sensitive radioactive detectors there was one patient who may have forgotten his card may have lost his card and he got pulled over and the police had to call our institution to confirm that he

really did have an isotope injected we

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

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

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

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

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

right good morning my name is Jeff Andrus I'm one of the rad texts in the department and I function about once a week in the floor coordinator role

sometimes called the FC other places have different names such as an expediter or other names for it one of the things I do in the morning is to go up to the morning conference with all the physicians that includes all the

attendings the fellows the residents myself and whoever is the charge nurse for the day and we'll go through both the inpatients and outpatients to discuss what what the exam is and any sort of special equipment that might be

needed so we can kind of gauge how long these exams are gonna take after that we'll come downstairs and we'll lead the morning huddle and this is with all the texts and the nurses to kind of relay that information so we can kind of get a

idea of what our day is gonna be like and then throughout the day I act as the central hub I hold the phone I do a lot of coordinating between the different floors the icy use the emergency department anesthesia making sure

everyone is getting the support they need any sort of breaks or lunch coverage that's needed and also making sure that when the patients do come down they they're ready you know making sure they've got IVs that they've been NPO

trying to head off any sort of problems like that so everyone has different size departments ours is a a larger one there's 11 rooms altogether there's two neuro angio suites there's an

interventional CT room and interventional MRI and then seven body angio rooms every day one room is designated as an inpatient room between outpatients there might be gaps so if I know what those gaps are I can bring an

inpatient down to help get that get that going we do have piays that'll run one two two line rooms every day usually those are where we focus all of our outpatient line placements and then there is also a bedside service that is

managed by the chief techs and we'll talk about that later one of the things that we did start was we were using two Clint X we started using them as transporters because the hospital has one large pool of

transporters for the entire institution and sometimes that would cause delays you'd you know you're gonna have a room open in half an hour you put in for transport it might be an hour more before the patient makes it down so we

were using these two as transporters just to help expedite the process we found that we could also use them for room turnovers to help get the outpatients move through the department and overtime that role has evolved if

patients do get down to the department they can sit and watch the patients while we're getting the rooms ready like I said before they'll help with turning over so cleaning the area making sure that we're ready to accept the patient

when they come into the room if we need to send someone to the blood bank or the pharmacy to pick up chemo they are capable of doing that and also if we need supplies throughout the day if we need more linens or anything like that

they will communicate that with central storage so we can make sure we've got what we need for our patients you know I'm gonna introduce dr. Hong and you will talk about bedside and team empowerment thank you very much my name

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

individually into each one of these trials but I want to just point out to you how busy the last 5 years have been because it has really caused a

resurgence in our interest in both treating PE better and what the gaps are in our knowledge so I will point out in 2014 this was an inflection point for 10 years we didn't have a major trial actually more like 12 or 15 years we

hadn't had a major trial in in PE and pytho was a 1000 patient study that informed us about how systemic thrombolytics interact with sub massive P and I'll go through the data that same year

catheterized thrombolysis is everybody familiar with catheter at the thrombolysis for submasters before Pease that's totally off the grid okay good well this was the first time we had a randomized trial for catheter directly

thrombolysis with some with some massive PE only problem was it was 59 patients in Europe so and that's all we have as far as randomized trials for CDT this is my soapbox issue I'm sorry if you've heard me say this but that's that's my

big goal is to try to change that 2015 had some follow-on CDT trials 2017 this is when we started thinking about the long term effects of PE on patients both of these studies started to examine the issue where a year after the PE patients

are not normal if you did a for example this elope long term study almost 50% of patients had an abnormal cardio pulmonary function test one year later 2018 we started to experiment with the dosage that we're

administering during CDT that's the optimized trial and we saw the first trial completed for a mechanical device called the NRA flow trailer which I'll show you later in the talk as well so that was an exciting inflection point as

well the extract PE trial which uses the indigo cat 8 device to aspirate thrombus in pulmonary embolism we just completed enrollment this year the future is hopefully bright for generating more data the PERT consortium registry is up

and running and is hopefully going to help us aggregate data and make better decisions and then you have a couple more devices coming in and I'll tell you our efforts to try to really improve the knowledge base on what CDT for sub

massive P that's the P track trial that's the last bullet point there okay

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

so these are a lot of slides most limited you know I'm talking I'm talking to you guys I'm talking showing you a lot of technical stuff you know and a lot of slides and I'm gonna talk mostly technical of you know how tips and dips are done kind of a step by step so even

the title it's kind of a workshop step by step of how basically you do you do tips and dips and what and and what are they so in general when you have when you have this is basically kind of out flow spleen spleen dumps blood into the

portal vein the mesentery dumps blood into the portal vein portal vein goes into liver liver does its thing and then dumps the blood into the eppadi veins to the right atrium okay for that because the liver is connected with the spleen

and the guts in series unlike any other organ basically the liver has to be a low-resistance organ because the portal circulation is low-pressure look the liver has to be a low-resistance organ with liver disease especially liver

cirrhosis you actually get increased resistance and in the liver with that disease and you get basically a backup of the blood flow in the portal circulation and increases the pressure in the portal circulation that's kind of

the genesis of or the pathogenesis of portal hypertension backing up circulation the spleen and in the guts then you get ascites and hydra thorax that's kind of think of it as weeping of fluid into the pleural space and into

the and into the perineum part of it is oncotic part of is osmotic basically think of it nutritional and pressure driven causes at the same time we all have potential portosystemic connections in other words they're there but they're

not connected or they're not opened up in plumbing they hold them bleed valves or pressure valves when the pressure is high and you know they start weeping or leaking you know in your in your basements we have the same thing

we have so many portosystemic connections there are about 55 named ones there are innumerable ones that are actually that are actually not named the common ones that we know are because of because of bleeding is esophageal

varices that's the connection usually between the left gastric vein and the azekah can be hazardous system you can also get gastric varices and that's usually connecting between a spleen and the left renal vein through a gas renal

shunts you can get also all sorts of connections even down in the internal hemorrhoids we get actually portal hypertension hemorrhoids and bleeding and so many numerous other shunts that we just don't have time to cut to cover

it to cover all these so the general to the general thought of treating all these complications of portal hypertension is to decompress the system to reduce the pressure and that's along the lines of years and decades of

surgery shunts that were placed and now tips ism largely replaced all these surgical shunts with the exception of Vancouver and Tampa okay that they still do some surgical actually a lot of surgical shunts most most other places

in North America converge to a tip to a tip shunt the the advantage of the tips of over surgical shunts is the usual what we hear is minimally invasive it you know it's a quick recovery less morbidity and mortality areason for

white tips has beaten the surgical shunts is the transplant era all these surgical shunts are actually extrahepatic so when you go for a transplants and liver hits the buckets they actually have to go and shut down

these shunts wherever they created them steena renal portal cable in the tips it goes out with a liver in the bucket so there's no complication of transplantation that's the real advantage of tips over surgical shunts

and that's why it's become very very prevalent in in in North America with a transplant error when approaching gastric varices just briefly another way is a BRT Oh which is to go basically into the left renal vein go up the shunt

and specifically screw rows the stomach and that's not the that's not this kind of subject of our of our discussion here I'm gonna talk to you

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

sub massive PE is an unknown entity so we still have these patients coming to us how do I approach it today

well those patients that are high-risk sub massive so high risk intermediate just like that ESC slide who look like they're about to Crump or look bad like they have an elevated lactate even if they don't meet the criteria for

hypotension those are patients that I'll almost always try to repr fuse and and that can be reproducing with any technique it could be surgical unbel ectomy it could be systemic thrombosis it could be Katherine directed therapy

but that's where the PERT concept where you bring together multiply multiple disciplines in a relatively short time and and make a consensus life decision that is thought to be the added value of the pert these other ones are getting

less and less common in terms of intervention so I used to intervene on a lot of these patients but as the data has come out and I've noticed that with the tincture of time 24 hours of heparin actually gets these people out of the

danger zone I've actually made my practice a little more conservative than it used to be and low risk sub massive Pease should pretty if if you're frequently doing this it's probably a time to re-examine your practice because

it may not be based on evidence or truth

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

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

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

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

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

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

quo in 2009 looked at the data for this and basically unfortunately we do not have high with so strong level 1 data to tell us how to treat this disease but

this showed that we had an 86 and a half percent success rate at treating massive PE if that's the case this should be the first-line treatment from a soapie problems you look at the data and 500 of the patients actually came from

retrospective case series which really does not capture the full gamut of massive PE you're only going to report the cases that you're successful with that's just something we do so we there's a lot there's a lot more cases

that are excluded from this that we don't know what happened to them either with or without so where are we with the data for ass massive p/e we have these techniques from a catheter standpoint it can be

used if systemic lytx are contraindicated we don't know which one of these devices works the best we definitely don't know we probably won't know that on a comparative basis because massive P happens relatively rarely

whether it should be used in combination with other therapies and which patients should get this therapy and we should get surgery and we should get lytic sore which should get some combination and so where do we go from here for massive PE

I won't belabor this point but I think what we need is a is a massive PE prospective registry and hopefully something like the perk insertion will help us gather all the data from all the Centers it's just that you know we're

probably gonna see five to ten ten to fifteen massive pease per year per institution that's just not enough information to rapidly get up to speed with what's working so if Li if we can get all our resources together put it in

one place then we can develop algorithms around how to better treat massive PE but there's a lot of promise out there I'll give you that okay sub massive PE

they travel together so that's what leads to the increased pain and sensitivity so in the knee there have been studies like 2015 we published that study on 13 patients with 24 month follow-up for knee embolization for

bleeding which you may have seen very commonly in your institution but dr. Okun Oh in 2015 published that article on the bottom left 14 patients where he did embolization in the knee for people with arthritis he actually used an

antibiotic not imposing EMBO sphere and any other particle he did use embolus for in a couple patients sorry EMBO zine in a couple of patients but mainly used in antibiotic so many of you know if antibiotics are like crystalline

substances they're like salt so you can't inject them in arteries that's why I have to go into IVs so they use this in Japan to inject and then dissolve so they go into the artery they dissolve and they're resorbable so they cause a

like a light and Baalak effect and then they go away he found that these patients had a decrease in pain after doing knee embolization subsequently he published a paper on 72 patients 95 needs in which he had an

excellent clinical success clinical success was defined as a greater than 50% reduction in knee pain so they had more than 50% reduction in knee pain in 86 percent of the patients at two years 79 percent of these patients still had

knee pain relief that's very impressive results for a procedure which basically takes in about 45 minutes to an hour so we designed a u.s. clinical study we got an investigational device exemption actually Julie's our clinical research

coordinator for this study and these are the inclusion exclusion criteria we basically excluded patients who have rheumatoid arthritis previous surgery and you had to have moderate or severe pain so greater than 50 means basically

greater than five out of ten on a pain scale we use a pain scale of 0 to 100 because it allows you to delineate pain a little bit better and you had to be refractory to something so you had to fail medications injections

radiofrequency ablation you had to fail some other treatment we followed these patients for six months and we got x-rays and MRIs before and then we got MRIs at one month to assess for if there was any non-target embolization likes a

bone infarct after this procedure these are the clinical scales we use to assess they're not really so important as much as it is we're trying to track pain and we're trying to check disability so one is the VA s or visual analog score and

on right is the Womack scale so patients fill this out and you can assess how disabled they are from their knee pain it assesses their function their stiffness and their pain it's a little

bit limiting because of course most patients have bilateral knee pain so we try and assess someone's function and you've improved one knee sometimes them walking up a flight of stairs may not improve significantly but their pain may

improve significantly in that knee when we did our patients these were the baseline demographics and our patients the average age was 65 and you see here the average BMI in our patients is 35 so this is on board or class 1 class 2

obesity if you look at the Japanese study the BMI in that patient that doctor okano had published the average BMI and their patient population was 25 so it gives you a big difference in the patient population we're treating and

that may impact their results how do we actually do the procedure so we palpate the knee and we feel for where the pain is so that's why we have these blue circles on there so we basically palpate the knee and figure

out is the pain medial lateral superior inferior and then we target those two Nicollet arteries and as depicted on this image there are basically 6 to Nicollet arteries that we look for 3 on the medial side 3 on the lateral side

once we know where they have pain we only go there so we're not going to treat the whole knee so people come in and say my whole knee hurts they're not really going to be a good candidate for this procedure you want focal synovitis

or inflammation which is what we're looking for and most people have medial and Lee pain but there are a small subset of patients of lateral pain so this is an example patient from our study says patient had an MRI beforehand

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

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]

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

I'm Nikki Jensen Nicole is what my mother calls me but that's alright thank you all for joining us today I am the clinical resource nas I work in a clinical nurse specialist position I graduated in May so I'll finally be called the clinical nurse specialist

after I passed my boards in nonvascular radiology so at Mayo Clinic Rochester we are kind of split up between I are in our IR practice where we have non vascular procedural Center CT MRI ultrasound guided procedures we'll go

over a list of our standard perform procedures as well as our neuro interventional and vascular interventional practice so Kerri and I work in the non vascular so we do not do any neuro interventional or vascular

vascular interventional procedures so these guidelines are going to focus on your LR CT or ultrasound guided procedures how many of you went to the combined session this morning great this is going to be an overview because what

we saw presented there really reiterates what we are have brought into our practice but then we're also going to share how we created nursing guidelines and how we rolled that into our practice this is Carrie Carrie is a staff nurse

in our department I worked as a staff nurse for seven years prior to this position I've been in this position now for four years and really enjoy it I do want to give a little shout-out to Carrie and I presented or sorry we

published an article in the June 28th volume 37 issue - that really coincides with our presentation today so I would encourage you to read that publication and then you'll get additional information on how we did this yes all

right we have nothing to disclose unfortunately or fortunately right so the purpose of this presentation is to help you all understand the importance of creating reviewing the literature

understanding your for one your coagulation casket as well cascade as well as anticoagulants that are out there or new up-and-coming medications and understanding that yes it's very important to establish and create these

guidelines so that within your practice you don't have differing radiologists that have differing opinions if you're working with doctor so-and-so today you need to worry about these labs if you're working with you know dr. Johnson

tomorrow he doesn't care about the labs we did this to help standardize that to help reduce the amount of questions our nurses have how many times we're interrupting our radiologists but then also we need to take into consideration

the importance of the patients and their different disease processes and we'll be going over that too so it's nice to have established guidelines but then also we need to take into consideration why patients are on certain medications this

here is our list of objectives I'm not going to read them for you you can all read them and we've provided you all with handouts too but really we want to just help kind of explain mechanism of actions and different medications and

how we established our guidelines this here is where Kari and I come from full disclosure we do have snow on the ground so these pictures were not taken before we came we are really enjoying this nice warm weather but for those of you who

are not familiar with the history of Mayo Clinic in Rochester who we have a hundred and fifty plus year tradition of implementing evidence-based care to assure the needs of our patient come first we are divided up into one

downtown campus but we have three different main areas so we have our st. Mary's Hospital this is where Kerry is based out of this is this houses most all of our ICUs as well as most all of our inpatients so we do a lot of

inpatients but we also see outpatients in this hospital Rochester Methodist Hospital this is where our he mock patients typically are we do have one ICU within Hospital as well but then right here my

office is right there this is our Mayo downtown campus so this is where most of our patients come for outside procedures or outpatient diagnostic imaging exams this here is the group that I'm part of the clinical nursing specialist group

within our clinical nursing specialist group there are 77 of us there are five like myself clinical resources as we have not graduated as of yet I'm right there in the middle w

that work in over 70 ambulatory areas in 58 inpatient areas we also support some areas in our Arizona and Florida campuses and then we have Mayo Clinic Health System hospitals that are scattered throughout Iowa

Wisconsin in Minnesota as well I am the only one in radiology across all of our

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

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

I think it's important to understand what options we have in in treating patients with carotid disease or those

in our practice medical therapy is a mainstay so all these patients regardless that they get t'car carotid stenting or otherwise need to get the best medical therapy there is a role though for each of these surgical

endovascular or a hybrid such as t'car and hopefully you have a better understanding of that option and ultimately if you understand the different techniques then we can apply the best ones depending on the patient's

anatomy or current clinical scenario and and apply that to that patient thank you [Applause]

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

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