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PE (Submassive)|Thrombolysis (Catheter-directed)|23|Female
PE (Submassive)|Thrombolysis (Catheter-directed)|23|Female
2016anesthesiaAngiodynamicsarteriesarteriogramarteryAtriumbedsidecathetercathetersconsciousnessdefectsdilatedfemoralinfusioninjectinjectionslobelowerlungmainmodifiedpatientspeakperfusionpigtailpressurepressurespulmonarySIRsystolicthrombustrackingupwardveinvolume
CT Imaging- Acute PE | Management of Patients with Acute & Chronic PE
CT Imaging- Acute PE | Management of Patients with Acute & Chronic PE
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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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Q&A- Procedural Sedation | Procedural Sedation: An Education Review
Q&A- Procedural Sedation | Procedural Sedation: An Education Review
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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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Why is the Capnography Reading Abnormal- Physiology | Respiratory Compromise: Use of Capnography During Procedural Sedation
Why is the Capnography Reading Abnormal- Physiology | Respiratory Compromise: Use of Capnography During Procedural Sedation
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UFE and Adenomyosis | Uterine Artery Embolization The Good, The Bad, The Ugly
UFE and Adenomyosis | Uterine Artery Embolization The Good, The Bad, The Ugly
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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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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 Example | Management of Patients with Acute & Chronic PE
Case Example | Management of Patients with Acute & Chronic PE
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Where do we go from here for submassive PE | Pulmonary Emoblism Interactive Lecture
Where do we go from here for submassive PE | Pulmonary Emoblism Interactive Lecture
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Therapies for Acute PE | Management of Patients with Acute & Chronic PE
Therapies for Acute PE | Management of Patients with Acute & Chronic PE
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Massive PE | Pulmonary Emoblism Interactive Lecture
Massive PE | Pulmonary Emoblism Interactive Lecture
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Definitions in PE | Pulmonary Emoblism Interactive Lecture
Definitions in PE | Pulmonary Emoblism Interactive Lecture
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Diagnostic Criteria for CTEPH | Management of Patients with Acute & Chronic PE
Diagnostic Criteria for CTEPH | Management of Patients with Acute & Chronic PE
angiogramangiographyarterialarteriesarterycapillarycatheterchapterclassificationcurativediseasedistalflushlobesmanagementmedicationNonepatientpatientspressureproximalpulmonarysegmentalsheathstenosissurgeonsurgicalthrombustreatedtypevesselswebswedge
Q&A Uterine Fibroid Embolization | Uterine Artery Embolization The Good, The Bad, The Ugly
Q&A Uterine Fibroid Embolization | Uterine Artery Embolization The Good, The Bad, The Ugly
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Pulmonary Ablation | Interventional Oncology
Pulmonary Ablation | Interventional Oncology
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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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Balloon Pulmonary Angioplasty | Management of Patients with Acute & Chronic PE
Balloon Pulmonary Angioplasty | Management of Patients with Acute & Chronic PE
angiogramangioplastyarteryballoonballooningbandschaptercomplicationscontrastflowHorizonimageimagesluminalNoneocclusionocclusionspatientsproximallypulmonaryradiationrecanstenosisthrombustreatedultrasoundwebs
PE Case Summary | Management of Patients with Acute & Chronic PE
PE Case Summary | Management of Patients with Acute & Chronic PE
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Q&A Pulmonary Embolism | Management of Patients with Acute & Chronic PE
Q&A Pulmonary Embolism | Management of Patients with Acute & Chronic PE
acuteangiogramassistedcatheterchapterchroniccontrastdiagnosticechocardiogramembolismisisNonepressurepulmonarythrombolysistreatmentultrasound
Registry and Data | Management of Patients with Acute & Chronic PE
Registry and Data | Management of Patients with Acute & Chronic PE
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Submassive PE | Pulmonary Emoblism Interactive Lecture
Submassive PE | Pulmonary Emoblism Interactive Lecture
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Percutaneous Mechanical Intervention | Management of Patients with Acute & Chronic PE
Percutaneous Mechanical Intervention | Management of Patients with Acute & Chronic PE
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Case- May Thurner Syndrome | Pelvic Congestion Syndrome
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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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Cone Beam CT | Interventional Oncology
Cone Beam CT | Interventional Oncology
ablationanatomicangioarteriesarteryartifactbeamchaptercombconecontrastdoseembolicenhancementenhancesesophagealesophagusgastricgastric arteryglucagonhcchepatectomyinfusinglesionliverlysisoncologypatientsegmentstomach
CTEPH Studies | Management of Patients with Acute & Chronic PE
CTEPH Studies | Management of Patients with Acute & Chronic PE
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Prospective CDT Trials | Pulmonary Emoblism Interactive Lecture
Prospective CDT Trials | Pulmonary Emoblism Interactive Lecture
arterybleedingcatheterchapterclinicalclotdatadevicedevicesdiameterdysfunctionheparinintracranialmajormassivemechanicalpatientsPenumbrapulmonaryrandomizedrateratiorecurrentreducesstudysurrogatethrombolysisthrombosistrialtrialsultimateventricle
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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Pathophysiology | Pulmonary Emoblism Interactive Lecture
Pathophysiology | Pulmonary Emoblism Interactive Lecture
arteriesballoonbloodblowchaptercircuitcoronaryfibershypokinetichypotensionintramuralischemicleftmassivePathophysiologypressurepulmonaryresistancesystemicvasculatureventricleventricular
Transcript

So first case is a 23 year old female on oral contraceptive pills. She presented, she works in finance, works at a desk all day, had

a recent travel to Europe about four weeks prior which we thought was probably not related to this particular incident. She was walking going to lunch near her work down in the Financial District and was going up an escalator, climbing some stairs and sink a pause/g found down, taken to our New York Lower Manhattan

Hospital. Relevant history, she had this one week insidious onset of progressive dyspnea and four days prior she remembers she can only do one minute on the treadmill, she's very active 23 year old. She runs, she does cycling classes, all these fitness type classes

which was pretty unusual for her. When she arrived at the Lower Manhattan Hospital this is some selected images of her CT so you can again appreciate the RV dilatation, no calipers necessary there. On the axial images you see some large volume thrombus within the main pulmonary arteries on either side in the coronal

view, you can see these are kind of extending from the main pulmonary arteries down into the lower branches on both sides. A little more history, so no relevant past medical history, she's not a smoker, no recent travel besides this four weeks ago which is probably not related,

no family history of thrombosis, her Troponin I was 0.2, BNP was 175 which is elevated in our institution. You can see her vitals here on the right. So her blood pressure 111 over 53, her heart rate is only 87, she's breathing at 20 a minute like everybody in the hospital, and her

SP02 is 99% on room air, her TT is very abnormal. So dilated RV, reduced function, severe TR, severe pulmonary hypertension measured by that tricuspid regurgitation jet and so the question now becomes, what do you do with

this patient? And a couple of issues that we have and probably most of you have when you're a big medical center and you're not just one hospital, what do you do with this patient? They're now at one of our affiliated institutions where maybe we don't have the expertise or the availability to bring them for

catheter directed lysis at that institution. Do we transfer this patient now from Lower Manhattan up to our main campus, do we give them systemic TPA at this Lower Manhattan Hospital because maybe there is an expertise or she's probably more of a stable submersive, so time is really on our side. So, go back a sec, I forgot to ask my important question here so,

she had a history of syncopy and lost her consciousness so, one important point you wanna make sure you re-stratify these patients and don't have a catastrophic event and so in everybody who loses consciousness at our institution we get a head CT just to make sure there isn't a bleed. So we got her head CT, we saw no bleeding and you'll trust me based on that

one image. All right, so I think this is the kind of best question that I get asked when we start to do these cases, how do you get into the PA and you've had I think four different ways to get into the pulmonary artery. Some people go in from the IJ approach, some people from the femoral approach, people use different catheters, pigtail catheters, copper catheter, some people float a swan,

we happen to use a modified grollman catheter and just for your entertainment pleasure, we have a clip of how we do that and there is some technique to do this when you are treating these patients and while this is playing I'll just kind of elaborate. I think at our institution we don't try to put this patients

under general anesthesia because the anesthesia comes with its own risk and all these patients are pre-load dependent. So once you induce these patients with anesthesia they are gonna loose their pre-load and we've had situations where these patients have become hypertensive and crash on table during induction of anesthesia because we've removed that pre-load on

them. And so we do this completely under local anesthesia and with our patients awake. And so for that reason I prefer to go into the groin where our patients are just more comfortable on the procedure and with that particular arrangement. We do two punctures into the right [INAUDIBLE] femoral vein if its open, if not we'll do the left [INAUDIBLE] femoral

vein both under ultrasound. As far as how you get this grollman catheter to go in where you needed to go. So the nice thing about the grollman is that it is a pigtail, so it's something that you can do your power injections, you don't have to do an extra exchange. When you come in you come in through the IVC and you get into the right atrium here and you

are gonna cross the valve, and then you take your modified grollman you start to rotate it posteriorly slowly as it kind of flicks across there over the valve. And then as you're seeing this kind of upward motion of that pigtail then you can advance it forward. And so if I just go back and just play this one more time,

you can see how this is right now sitting in the right atrium kind of slowly twisting it and you can see how it's having this kind of upward movement, enduring that upward movement just giving some gentle forward pressure as it kind of pops through the pulmonic valve, into the pulmonary artery.

So we get into the pulmonary artery and here's her initial pulmonary arteriogram we take. In all of our patients we take pulmonary artery pressures before we do our injections and basically my rule of thumb is anybody who has a peak systolic pulmonary artery pressure below 40, I'll inject at a rate of about 20 cc per second for a total volume of 25.

Once you get kind of in the 40 to 60 range, I drop that down, do 15 for 20 and then if they are above 60, then I drop it down even more and do ten for 15. And so just some practical aspects of how to get this pictures, and the reason for that is you don't really wanna overload the pulmonary arteriole system with more volume

and somebody who already has a high pressure in there. So her pulmonary pressures are obviously very elevated, peak systolic 59, on the right, peak systolic 68 on the left. This is a very surprising for a very young, healthy, active, woman. You can see the amount of clot burden on the screen.

She has this large thrombus here as well, some occlusive thrombus here in this lower lobe branch and you can see the tram tracking all around the thrombus here on the left side. What I tell everyone who does this with me at Cornell, not only

is it important to look at that initial pulmonary arteriogram and see if you can see tram tracking and sometimes it's better to look at it in DSA, sometimes it's easier to look at it unsubtracted, but more importantly it's probably the perfusion of the lung itself. So we always carry out our injections until

you see the aorta and at that time you can start to see perfusion of the lung parenchyma and you see these large perfusion defects on the right, the entire lower lobe is not perfused, same kinda thing is on the left. Big perfusion gaps, big perfusion defects.

So at this point, where do you place your catheters and how do you get there? What catheter combinations do you use? These are kind of the practical details and questions that we have so I'll just kinda answer each one of those individually. So I

like to have my sheaths all the way out in the main pulmonary artery crossing the pulmonic valve and the reason for that is there's a lot of pressure, the RV's dilated and this catheters if they are soft they are gonna tend to buckle in your RV, and you're gonna get a lot of arrhythmias over time. And you're gonna leave this catheters

in 12, 24 hours overnight and they are in the ICU, so you wanna be able to have a stable system that's not gonna back out by this buckling into the RV. So I use 7 French, 70 centimeter radio sheath that are nice and stiff and get them all the way out across pulmonic valve.

What was my other question? I forgot already. I always take my pictures at End inspiration, I think it spreads out the lung parenchyma, spreads out the vessels, allows you to

get the best appearance of the vessels as opposed to what we do basically everywhere else, if you're doing a liver embolization, you're gonna do it at End expiration rather than End inspiration. Again triangles, I'm sure we can probably argue on what gives you the best picture. I usually do ipsilateral obliques at 30 degrees,

I think that opens it up well for me and I'm able to do one injection to either side. And Access sites we talked about. So in this particular patient we put in Uni*Fuse catheters. Here we have them in both lower lobes.

Our protocol where we inject our patients 0.5 milligrams an hour through each side and we usually run it for 20 to 24 hours and a lot of that duration is based on our room availability. So if we can get them back sooner or later usually after about 24 hours, we can turn off the infusion at the bedside and just start running saline.

In the beginning of our experience we were bringing everybody back and doing follow-up pulmonary arteriograms, measuring repeat pressures, again like was said earlier, we've changed that policy to now basically at the bedside transdusing pressures from our infusion catheters

and pulling at the bedside. So here's her follow-up, pulmonary arteriogram, and you can see it's not perfect, there's still residual thrombus here in the right main pulmonary artery. However, pretty dramatic reduction in pulmonary artery pressures. Her peak systolic pressure

dropped by nearly 30. And again, to correspond that perfusion argument that really the perfusion of lung is so important. You can see how a lot of these perfusion defects that we saw previously

plan as well so I wanted to talk a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

are there any questions yeah yes that's a really good sure so the question was do you have any rules or guidelines in my institution about how long the procedure can be before you start

talking about anesthesia versus sedation is that right and positioning prone supine we did come up with a guideline with within our department we looked at a little bit of research but honestly was more expert opinion just best

practice and experience I in in general I would say if the procedure is 3 plus hours the patient should know they're going to be on the table not asleep for three plus hours and talk to them about what that means and if they're ok with

that I just think again that comes into setting realistic expectations that's one of the reasons actually that we're very interested in using Dex med otama Dean because that's going to be a better

drug for those longer procedures first was giving functional and versed for four hours it's just not it's not appropriate but you know and some people would say we'll just get an anesthesiologist them but a lot of these

patients are really thick so in our institution anesthesia is just really super regulated and they require all of these clearances for their involvement no matter what they're giving sometimes they'll require all these clearances and

they give exactly what we were going to give so you know it's it's really a juggling act I would say in our department we really just make sure the patient knows what the expectation is and then we'll usually say to the

provider to if if something goes like if anything looks a little concerning during the case we're stopping and they have to be ok with that and they are they really are but that took a lot of work to get everybody on board with that

type of communication yeah we don't know so they I know I think Sloane is anyone here from Sloane no I think Sloane has with dedicated anesthesiologists they work really closely with them and it's easier for

them to get cases scheduled they will give us they will assign us an anesthesiologist for the day but if we don't have any anesthesia cases they get reassigned somewhere in the o.r and it's a different analysis every time it tends

to be the same group some are stricter than others some will have a patient say I really want anesthesia and we can call up the provider and there they say no problem let me do a quick chart review whereas the next day the provider goes

no absolutely not send them for clearances that's a little tricky yeah right so what I showed you is from the american society of anesthesiology i am not affiliated with them at all i just think they bide non anesthesiologist

sedation so i rely heavily on what they say and they recommend waiting till peak effects so i would look at the pharmacokinetics so for versed it's 3 to 5 minutes so i would wait at least 3 minutes before your readmit a stirring I

think a good example with that is when diazepam with the sedative of choice the on the peak effect for diazepam is 1 minute so when midazolam came onto the market there were a lot of adverse outcomes

with patients because providers administering it weren't familiar with the pharmacokinetics and assumed that the peak effect for versed was the same for diazepam so in theory you could give a patient in 5 minutes 5 milligrams of

versed so by the time that fully hits them they could be in a negative 5 on your raft scale so you know just look at those pharmacokinetics look at that peak effect and I would use that to drive your dosing scheme Atlee that's what I

do and I think since we've done that we've seen better meet info cities and better safety outcomes yes okay yeah we don't do that we do one thing with uterine fibroid embolization swear they'll do a superior mesenteric block

but otherwise we don't do any other type of regional blocks but I have read about that I think that's really are the IR providers giving the block okay right I've seen two with uterine fibroid embolization we'll do an epidural in

advance some I think some institutions or some literature exists about that it's interesting it would be interesting if the IR providers could actually give it though I'm not sure if that's kosher in the anesthesia world but they're

certainly qualified to do it they they do already kind of do it really but so I mean that's certainly something interesting and if you have a provider that is comfortable taking that on and their institution I think it's worth

looking at because anything that's sort of I think mixes things up and and provides a different Avenue especially for high-risk patients is worth looking into definitely yes I believe it yeah

mm-hm right so I'll just repeat what she said so just jumping on the talk about blocks so in her institution they the providers to administer blocks and I think you said

coleus estas Tamizh and PTC's and biliary dream placements they'll use that and it will decrease the amount of sedation that's required sedation being versed and fentanyl that's required during the case which like yes like you

said is really great for patients who are already on opioids previously and habit aller ins yes [Music] something right so we again he left same provider though had a patient on Groupon

or Fein and it was our first experience within about a year ago and it was terrible and she did not have realistic expectations going in of how sedated she would be and she was very very unhappy

afterwards so we talked a lot about that and in that guideline I had mentioned that we made about when we involve anesthesia and when we don't there's a caveat about that that says that if a patient is on

methadone or buprenorphine that a discussion needs to take place making them aware that they will probably not feel very sedated but we will try our best and if they're not comfortable with that we reschedule the procedure with

anesthesia but they have to know going into it that they they may not feel completely sedated and we just keep that open and honest communication but we haven't really come up with a scheme of what's best we did actually try with her

we had her come in one day having taken her buprenorphine the day of the procedure and she seemed okay with that and then we tried having her go off of it so that the receptors wouldn't be blocked she was not happy with that

experience so that's really when a person like that probably would do great with propofol but we can't give propofol so you know if the and if the patient tells us no then we just reschedule with the anesthesia

right - hmm right right right you could at least if they're if they're on an opioid uh if they're on people nor Fein then in theory they should respond to the verse said you could go heavier hand it on the

versed just to get them sedated but they will probably still feel pain but it they hopefully won't remember it that's true I you know with the Richmond agitation sedation scale that's not going to fit every patient that's a

really good point I gave a patient seven of versed during an adrenal vein sampling and she was just talking my ear off I got I fed are you okay you know do you need me to give you anything else no no I'm good I'm good and then I wheeled

her out we got her in the recovery area and she goes sit over I said yeah she said wow I don't I don't remember anything the power of her said that that was like a true and music effect I hadn't seen that so strongly in a

patient before but if you if I had done you know I was documenting that she was a zero it looked like I wasn't doing much for her but then I was putting comments you know patient comfortable denying needing any more sedation so

won't fit every patient so it is good to look at that but yeah as far as the buprenorphine I mean it's it's it's tough yeah if they have an addiction specialist I would say talk to them and they might be

able to come up with a scheme that works for them and if there's a lot of pain expected afterwards those patients are gonna have to be on parenteral opioid therapy they'll probably have to stay you know if you're in a hospital they

would have to stay overnight so those are all things you have to consider yeah yes hmm yeah I'm like it so Adam and Alexa are nurse practitioners that we work with and I'm looking at Adam because

this is actually was a very hot topic for us in the last six months so we actually cheat we met with our sedation committee that's run by that in a physiologist who's blocking us from using pres of X and discuss with him

that in the protocol that guides our practice it's said that you did the timeout and then gave sedation but Ari anesthesiologists don't do that right so they intubate the patient and everything and then and they and then the provider

comes in and does the timeout right before the puncture or incision so we talked about to him about how well if we're gonna do the latency to peak effect it's not enough time right so we do now bring the patient in and start

sedation right away our orders are put in in advance I know some by the attending or the Li P so we have a PRN dose and with an a certain number of occurrences and a titrate to a certain Ross scale

yes yeah so and that our anesthesiologist mentions that our providers are present but it's it's a certain use of the language I think it might be like direct observation or immediately available and our providers

are immediately available it's up to your hospital so our profit our providers aren't like down the street on their way in to work with coffee and street clothes and we're sedating they're they're just down the hall maybe

or the way our department looks is we have a control area and it's like the you know the Central Station and you can see all of the rooms so they might be in the Central Station but just haven't gone in to do the time out yet that

being said I always talk to them before I bring the patient in and say what's the goal Rath and I address any concerns that I have and I think people think I'm a little kooky when I do that for every case but it I think it works really well

and I think the providers really like it so we just already start from the Gecko our line of communication I tell them the patient seems really anxious this is my plan what do you think agree disagree yes the procedural if does the procedure

list or the Lak but I've sedated the patient so the patient if you look at what Jayco describes in the universal protocol it's ideal if they can participate in the timeout however not required because then when they do the

timeout they're right there stabbing them with lidocaine so I like to you know I mean I would argue that by starting I would argue about that by starting at the sedation earlier and getting the patient into a comfortable

state you're more safe because you're doing the dosing appropriately according to the a sa yeah correct right right right

okay I think it's important to say though it's not about getting around Joint Commission this is what Joint Commission says you may feel uncomfortable with it and that's okay

but it is what our accrediting body says is okay we're also not intimating the patient and paralyzing them like an Asst the anesthesiologist is now having said that it's not like we walk the patient in and we go oh I think you're mr. Jones

we throw you on the table there is an initial timeout that's done with the nurse and the technologist and the other people in the room shaking his head yes as so the acceptable amount of time after reversal

yes so if it happens if it happens mid procedure you need to it's I believe the language the a sa uses that you have to have a discussion amongst the care team about whether or not you're going to proceed if it happens after the

procedure in the recovery area or it happens mid procedure and you abort then it has to be at least two hours before you discharge that patient or move them back to their unit where they came from because of that recitation effect and

because you can have really adverse effects from sedation like flumazenil can cause serious delirium I had a patient like that one time it was it was awful and it can cause serious cardiac arrhythmia so at least two hours if you

continue with the procedure I would just make sure everyone knows that you have to be really careful with recitation effects and and all of the adverse effects that you'd be looking at yes I think one more question I'm sorry

with hyperkalemia I have come across I want to say it was in perioperative guidelines when I was looking at the labs that we do cuz we do a lot of unnecessary labs in our department you guys might - I feel like we just really

overdo it I believe the perioperative recommendations are to check a serum potassium if the patient has a reason to have hyperkalemia however right if their hyperkalemic and

they develop a cardiac arrhythmia you know could hypoxia also precipitate that cardiac arrhythmia the results from the hyperkalemia maybe I just went in I wouldn't take an ounce

I would I would consider hyperkalemia severe hyperkalemia and unstable patient because that patient could go into a fatal arrhythmia so I would correct that before you bring them into an elective Percy what's often an elective procedure

so if you're doing a fistula gram you know right five point yeah why are we will go up to five point eight we personally will go up to five point eight because a lot of times they're hyperkalemic

because they're fish too less clothes now and we need to open it right so just again it I don't think there's ever going to be any hard and fast data that you see it's all about making sure everyone knows this patient has a serum

potassium of five point eight we're going to be really closely watching the ECG monitoring yeah thank you everyone thank you so much [Applause]

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

patients may be asking you is like what about adenomyosis and I've been hearing something about that which is not exactly fibroids right it's a different entity though the symptoms could be kind of the same and for the years and years

and years we wouldn't have any options for patients who had adenomyosis in fact the only option for patients with adenomyosis is surgery but adenomyosis can coexist with fibroids and sometimes patient presents with adenomyosis alone

so we've had some studies now that have looked at that and although the data is not as robust and not as awesome as for patients with fibroids we do provide a performing bolas Asian for those patients with particles that are little

smaller than what we would use for fibroids with results as you're seen there before now the only other new thing that's on the market and it's not so new to you guys that are probably doing radial in femorals anyway working

in cardiac labs and IR labs it's actually what we call the trophy if you go back one slide for me mr. a the person and press play then we will be able to see that radial access I do not work for Merritt they don't give me a

dime I just thought that this was a good video is there volume on that at all if not I can just talk about it and really what it says is that if you need to a radial UFE or have radial axis for a uterine embolization patients just love

it more they and especially like patients that are already just intimidated they don't want you going near their groins at all they actually could just lay on the table we don't have to put up we don't put a Foley in

they just get a radial access the same way that you would just be starting in a line except we have special types of radial catheters and and sheaves to do that and I don't offer a radial access to

patients who are too tall for our catheters or if they've had multiple prior radial access and don't have an intact ulnar artery to complete their hand but it's much like any of that femoral access that you would normally

see they make special hydrophilic sheaths now they're called from this particular company slender technology where the inner diameter of the sheath essentially the sheath is the same like five French on the outside but they have

cored out the inside so it's a bigger diameter so it's a five six so on the outside it's a five but it will take a six French in the inner inner lumen and you know my practice we do more than 80% of all our arterial punctures with a

radial access and everybody here comes dr. Sean Deroche Nia who is the leading author of that paper for SI R and one of my esteemed partners so most patients are able to get up and walk out if you are go from a radial access the access

is actually closed with just a radial band and the complications of having a hematoma or having the patient's bleed out those just all go away but radial axis have their own complications so I'm not here to say that it is not that but

in our practice we found it to be safe and effective our patients want it and it's become like a practice differentiator so if you're working in a practice that don't do radial you EFI's right now you should mention it because

if you're in a population where the other providers are only doing femoral then you will automatically get the patients that only want that so here's a patient that had a radial access you can see a catheter that is coming from the

aorta while you can't see that it's not up and over the bifurcation but maybe you do can see that and there's a catheter in the uterine artery with the characteristic

shape of the uterine artery and the characteristic curlicue vessels of of the fibroid and on the left you can see the Imogen for beforehand and the Imogen on the right of post embolization where there is stagnant flow in the main

uterine not main uterine artery in the horizontal portion of the uterine artery for greater than five cardiac beads and again there's there's no reason that you have to know that level of detail except that you're scrubbing in but if you're

in the audience you're looking at this you're like dr. Newsome I see an air bubble there as well then I'd say good because because I do see it too so you can see the preimage and you can see the post image for pre and post embolization

these these procedures can be quick these procedures are very very rewarding and and I love to do it

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

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 I'm gonna show an example this is a 57 year old male who presented with a dis neo

he had World Health Organization functional class 3 meaning it's significantly affected his life he can't walk up the flight of stairs really tired walking from the parking lot of his favorite restaurant back to this car

can't really walk around the grocery store he had a history of DVT and PE also had afib he actually went to the ER and was diagnosed with upper respiratory tract infection which many of these patients are they've put him on

antibiotics then for pneumonia he had a VQ after one of his doctors just felt like he just wasn't getting better and it found multiple mismatch defect I'm sorry I don't have those pictures he was actually started on home oxygen after

all of that work up it was found that he had CTF and this required I think three different hospital visits and every time got kicked up to sort of a higher acuity place and then he ended up at our place so these are his pulmonary angiogram

images here I don't know if I can play these but the still images kind of show you that the images on the right show that there's basically no vessels going out distally so I mentioned pruning of vessels there's no branches in the right

upper lobe if you look at the right lower lobe at the tip of the catheter there's areas of stenosis right where the segmental arteries start and on the left you can see that the left pulmonary artery is denuded essentially the entire

left upper low branch is excluded by a rim of thrombus and in the left lower lobe the image on the bottom my bottom right there's actually no branches going to the left lower lobe into the lingula so this is a patient that has had very

bad CTF their main the pulmonary artery pressures are listed there of 77 where the normal high is 25 so three times the normal pulmonary artery pressure so this patient went on to an operation so the image on the right the photograph is

actually the clot that they removed from the operation and that patients pressures improved from 77 to 22 immediately after the operation so they go to the ICU they have a swan-ganz catheter left in place and you can

measure their pressure right afterwards and you can see that that clot they grabbed it it looks like a bunch of fingers well what they do is they crack the chest open like with a mini sternotomy they make an incision in the

pulmonary artery after they put them on bypass and then they basically grab they use they're a little deBakey's the DeBakey forceps and they grab this little elevator and they just start scooping

out the clot and they try to grab it as one big piece take it out and then you get that nice photograph on the side if they break off pieces it's actually worse because that's an area that a pulmonary artery dissection can occur so

it's a very complex operation but you get very nice results and afterwards these patients are sent home usually on lifelong anticoagulation thereafter so

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

PE the first one of course is

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

criteria for CTF means that the patient has a mean pulmonary arterial pressure which we measure intraoperatively exceeding 25 millimeters mercury at rest with the mean pulmonary capillary wedge pressure less than 15 so I'm not a

cardiologist but what that means to me is a mean capillary pulmonary wedge pressure less than 15 means that their left heart is not failing so if you have a capillary wedge pressure higher than 15 that means your left heart is not

working correctly and you can't blame it on the CTF so you can't blame it on the right side if the left side isn't working other things that matter are the abnormal pulmonary vascular resistance and having a systolic pulmonary artery

pressure greater than 40 so what I want to show you and highlight is the law the lost art of pulmonary angiography which i think is now sort of again a lost art some places do a lot of it and some places don't do very much but diagnostic

pulmonary angiography is actually the gold standard in the planning of either surgery or medical management for patients with CTF we do we do these on almost all of our patients with CTF to make that decision with the surgeons and

the cardiologists so the utility is very it's very useful you're able to measure our pressure you're able to decide whether we're the where the thrombus exists in this image here in patients with disease in the

blue and yellow outlined areas those are the patients who can have the operation the operation is curative it's not just medication that you have to take for the rest of your life you can actually remove that chronic clot it's much like

a femoral endarterectomy that are done for patients with peripheral arterial disease although it's a lot more complicated because they have to crack your chest open what's important is getting very very

good high-quality pulmonary angiogram xand so we do we used to do about we do about a hundred of these a year where I trained or actually where I work now and you get very magda up views and you're gonna show all of the vessels and so

these are the views that we use at our institution they happen to be the pipette criteria so it's the same thing you used to do for acute PE you put a flush catheter in the main pulmonary arteries when you're looking at the

upper lobes and when you're looking at the lower lobes you want to push the catheter further into the pulmonary arteries and inject usually what I do is a two to three second injection so that you can stack the images very well and

show all of them in one view this allows your surgeon to make a decision easily as to whether they can operate or they can't operate on this and then I use a higher frame rate usually because these patients are wide awake we when we do

this case we give our patients twenty five mics of fentanyl one time and that's it just to help get the sheath in I usually do this with a seven French sheath and then use a flush cap pulmonary artery catheter many of which

are currently off the market but when we do this we just give them that twenty five Mike's because they have to hold their breath and I usually go up to a high frame rate in the first run and then adjust based off of how well that

patient is holding their breath this really takes a team effort from our nursing technologists and the and the physicians in the room to make sure that this patient does a good job because it's gonna change their management so

there are a lot of different types of angiographic findings on one of these pulmonary angiogram they're really really interesting pulmonary angiogram zin these patients and they're sometimes not at all subtle so you're looking for

a pruning of distal vessels if we start in the top left where you're just not seeing the Brent normal branch pattern you look for stenosis so we're not usually used to looking at stenosis and the pulmonary arteries but this is

actually what you're looking for in CTF you're looking for webs or bands so you'll usually see little areas where you just doesn't look like there's great opacification there's little areas that there's not good at pacification those

are little webs inside the vessel believe it or not looks like a cobweb that grew inside there from that thrombus and then you're looking for areas of complete occlusion that there's just no vessels there those are all

vessels that can be treated in patients with CTF so this is the Jameson classification before we talk about the sort of the interventional management the surgical management is again the curative and dr. Jameson is the head

surgeon at University of California in San Diego which is the largest Palm CTF program in the in the world and he's done I think over 3 500 of these operations I think he's retired at this point but they named the classification

after him and so type 1 is proximal disease so it involves the main pulmonary arteries these are the ideal patients who can get the best benefit from this in their life type 2 is the next best

it's segmental proximal just type 3 is distal segmental and then type 4 is just a mess of sort of all of it but you can't really get a good surgical plane so type 1 and 2 are treated with pulmonary thromboembolism

towards balloon pulmonary angioplasty or BPA and type 4 are generally treated with medication so PT II or pulmonary

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

talk here with something that's new on the horizon believe it or not it was actually on the horizon 20 years ago and then it went away because there were a lot of patients that were treated with a

lot of complications and it's making a resurgence and this is balloon pulmonary angioplasty or BPA for short so this is an intervention which may be feasible in non-operative candidates so I mentioned to the Jamison classification earlier

type 1 and type 2 disease should be treated with surgery again it should be treated is curative but patients with type 2 and a half or 3 disease can be treated with balloon pulmonary angioplasty in the right in the right

frame which means that a surgeon has said I cannot operate on this a medical doctor has said boy they're not going to get better with their medicine let's try something else well this is that something else and that's what involves

everyone in this room so this is these are usually staged interventions with potentially high radiation and contrast dose if you think about it it's like Venis recan and a pulmonary AVM all-in-one so it's a potentially a long

complex procedure with a lot of contrast and a lot of radiation but it can provide a lot of benefit to these patients I'm going to talk about the comp potential complications at the end which is one reason why not

everyone should do these all the time so this is a pulmonary angiogram from the literature when you're injecting a selective pulmonary artery you can see that this patient has multiple stenosis there's no real good flow there the

vessels look shriveled up like I mentioned to you before you can get a balloon across it and balloon the areas and then you can see afterwards so the image a on the left is before an image D is afterwards believe it or not this are

in the most experienced hands because the most experienced hands are for palm the BP AR in Japan they do hundreds of cases of these a year at each hospital I've personally only done five so but this is a something that I'm very

interested in and you can see how how much benefit it has for that patient another way you can see these are the webs and the bands that I mentioned to you earlier so what's interesting is that if you look on the first set of

images on the top and the images on the bottom those are the same patients it's the same view before top rows before and the bottom rows after balloon pulmonary angioplasty so the first image is a pulmonary angiogram where if you kind of

see this there's there's some area areas of haziness those are the webs and bands the image on the the middle is the blown-up views and you can see those areas and then the image on the right is intravascular ultrasound which I use

every day in my practice it's a catheter with an ultrasound on it and when you look at it on the top image image see you can see a lot of thrombus you're actually not seeing flow and on image F on the bottom you're seeing red which is

the blood flow so these patients can actually improve the luminal diameter bye-bye ballooning them you can treat occlusions again image on the left shows you a pulmonary artery with a basically an occlusion proximally and then after

you reek analyze it and balloon it you can see that they can get much more

from our acute to chronic again just to recap this patient had what was

confirmed categorized as intermediate high risk PE for many of the reasons that you can see here so again here's their scan showing that there's thrombus in the left and right pulmonary arteries here's an echo that showed that the

patient had right ventricular strain and that had an enlarged right ventricle so this patient got a pulmonary artery Graham you can see here there's thrombus you basically don't see contrast going past the main pulmonary artery on the

right or the left sorry I didn't have the DSA images so we check we put a pulmonary artery catheter we do some initial runs and get pressures and then afterwards we put wires into the main pulmonary arteries ideally we try to go

down into the lower lobe so you get the most bang for your buck and have throw-up I have TPA infusing in the area that has the most rhombus and then we in this case placed eCos catheters and you can tell whether catheters Annie Coast

catheter not because of the little hash marks one thing that's important to notice is that the hash marks don't go all the way to the end the first time I need to Nicko's catheter I didn't know that and I was like I think the wire is

too short that's inside of it but it actually is short by a few centimeters the patient came back 24 hours later you can already see that there's an improved profusion in the left lung all the way distally and then in the right lung you

can also see improved perfusion so they're still thrombus they're in the right lower lobe again we're not going for a perfect picture what we're going for is the patient to be better and their pulmonary and the right

ventricular pressures to be improved if the pressure is reduced about 20% I think most interventional radiologists will say that that's a successful procedure but more importantly what I'd like to

see is that the patient is no longer on pressors they're no longer requiring a high amount of oxygen they can be extubated they say that they don't have any more chest pain they're able to talk better all of those clinical factors

that we sort of sometimes don't think about those are signs that the patient is doing well and that maybe that's not worth the risk of continuing giving him the TPA so this is a follow-up scan on this patient showing that pretty much

all the thrombus is gone so what happens

happy to take any questions or in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

and sometimes you need to have a bigger

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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