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Saddle PE (Submassive)|Thrombolysis (Catheter-directed)|38|Female
Saddle PE (Submassive)|Thrombolysis (Catheter-directed)|38|Female
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Registry and Data | Management of Patients with Acute & Chronic PE
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Catheter-directed Thrombolysis | Management of Patients with Acute & Chronic PE
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Case 1 - Non-healing heel wound, Rutherford Cat. 5, previous stroke | Recanalization, Atherectomy | Complex Above Knee Cases with Re-entry Devices and Techniques
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Diagnostic Criteria for CTEPH | Management of Patients with Acute & Chronic PE
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Mechanical Thrombectomy | Management of Patients with Acute & Chronic PE
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Pulmonary Ablation | Interventional Oncology
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Case- May Thurner Syndrome | Pelvic Congestion Syndrome
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Prospective CDT Trials | Pulmonary Emoblism Interactive Lecture
Prospective CDT Trials | Pulmonary Emoblism Interactive Lecture
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CT Imaging- Acute PE | Management of Patients with Acute & Chronic PE
CT Imaging- Acute PE | Management of Patients with Acute & Chronic PE
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Introduction to Establishing Periprocedural Screening Guidelines to reduce bleeding risk associated with Image-Guided Theraputic and Diagnostic Procedures | Risk Mitigation: Periprocedural Screening and Anticoagulation Guidelines to Reduce Interventional Radiology Bleeding Risks
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The Case that Launched the Cornell PERT (PE Response Team) | Pulmonary Emoblism Interactive Lecture
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Ultrasound-assisted Catheter-directed Thrombolysis | Management of Patients with Acute & Chronic PE
Ultrasound-assisted Catheter-directed Thrombolysis | Management of Patients with Acute & Chronic PE
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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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Transcript

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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]

thrombectomy is another popular way of treating patients there's a lot of different aspiration catheters the SPX catheter is actually not available currently in the US but what it basically is I can have the rectum a

device that spins in such backlot the Indigo thrombectomy system from penumbra is a yet another device that sucks out clot I think many of us have used that it's kind of like a vacuum cleaner but usually more like a dust

hand vac where it's going to suck up thrombus the angio vac is much more like a Hoover where you're going to use and put a patient on veno-venous bypass that requires a 22 French sheath and a 17 French sheath but that will take out

thrombus I personally prefer using NGO vac in the IVC in big large thrombus for that and not in the pulmonary arteries because it's very inflexible but it's very very useful in a few patient populations in

all of these devices there is no TPA that needs to be given you're just sucking out the clot and you're actually removing it from the patient's body rather than dissolving it and sending it downstream the drawbacks on all of these

devices is their larger access points the SP or X is around six French although that's not that much bigger penumbra device is 8 French and the as we mentioned the angio vac is 22 French

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

so what what venous insufficiency is is really leaky valves so if you want to hit the play on that so that's all venous insufficiency that's what we

talked about it's it's leaky valves and so you can see this the valve leaflets there which are paper-thin is allowing blood to go the wrong way if you want to hit play on that one when we looked for valve

insufficiency for sure in the legs we use ultrasound and there's a bunch of different things that we look at an ultrasound you first look if you can augment blood flow so that was that first part we see if it's compressible

to make sure there's not a clot in it that's this part you can see the vein winking at you and then finally we look at valsalva or some type of way to determine if the valves are competent or incompetent and what this figure is

showing is that when a patient valsalva Zoar tenses up their abdominal muscles you see the gray line for the ultrasound crossing the access and going the opposite way all that means is it's got opposite directional flow which you

should not be able to do if your valves work so if your valves work you would not see that ultrasound picture crossing the line here it would just continue right there or would just stop and then flow would start again once you stop fel

salving so that's how we check in a leg but for pelvic venous insufficiency that's kind of hard to ultrasound the deep pelvic veins I could certainly look for varicosities with a an ultrasound of the pelvis but you can't really find the

source of an usually the source veins are the internal iliac veins or the gun at Elaine's and those are tough to ultrasound so secondary evidence of incompetence or leaky valves in those systems is varicosities

and so in the case of pelvic venous insufficiency those varicosities are in the pelvis and you see on the slide here you got varicose veins deep in the pelvis here and here and see some larger ones in that same

area on that CT scan so that'll tell us varicose veins that doesn't necessarily tell you whether the issue is with a gonadal vein or an internal iliac vein it just tells you that there are sequelae of varicosities much like in

the leg you might have varicose veins in the ankle but the problem is really higher up in the leg at this afterno femoral Junction so that gives us secondary evidence but it hasn't really told us the cause of the varicose veins

this is just a CT image that it also may show a large gonadal vein right here so you normally should not see it that big it's right there also secondary evidence that the valve is incompetent but it doesn't really test the valve itself

it's it just gives you the idea that veins enlarge and the valves gonna be leaky this is a cartoon schematic of the

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

few different devices and techniques to do this so that everyone sort of again understands what are the different options available to us so you can of course do catheter directed thrombolysis

this can be any of a few different types of catheters so this is an example of a unifier when I talk to the residents and fellows and I just tell them it looks kind of like a garden hose that you poke a bunch of holes in right and you turn

it on and so that's what that looks like you're gonna give delivery of thrombolytic right into the pulmonary arteries ideally you're bathing the pulmonary arteries and you have a catheter on both sides usually on with

two N's one on normal throught normal vessel and the other on the normal vessel in the holes basically embedded in the clot the benefit of this is that you get the drug to the clot very quickly very directly

and you can do it in lower doses than systemic therapy alone the drawbacks are that there are actually no control studies for this there's no randomized control trials that have started everything is a case control series

maybe one institution versus another or within your own institution looking at several things or a registry which I'll show you a few of examples of different types of catheters our unify our Craig McNamara being the two most commonly

used another main mainstay and PE

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

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

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

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

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

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

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

systemic TPA so I wanted to go through a

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

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

thank you so much for inviting me and to speak at this session so I'm gonna share with you a save a disaster and a save hopefully my disclosures which aren't related so this is a 59 year old female she's lovely with a history of locally advanced pancreatic cancer back in 2016

and and she presented with biliary and gastric outlet obstructions so she underwent scenting so there was a free communication of the biliary system with the GI system she underwent chemo and radiation and actually did really well

and she presents to her local doctor in 2018 with ascites they tap the ascites that's benign and they'll do a workup and she just also happens to have n stage liver disease and cirrhosis due to alcohol abuse in her life so just very

unlucky very unfortunate and the request comes and it's for a paracentesis which you know pretty you know standard she has refractory ascites and because she has refractory ascites tips and this is a problem because the pointer doesn't

work because a her biliary system is in communication with the GI system right so there's lots of bugs sitting in the bile ducts because of all these stents that have opened up the bile duct to list to the duodenum and so you know

like any good individual I usually ask my colleagues you know there's way more smart people in the world than me and and and so I say well what should I do and and you know there was a very loud voice that said do not do a tips you

know there there's no way you should do a tips in this person maybe just put in a tunnel at drainage catheter and then there was well maybe you should do a tips but if you do a tips don't use a Viator don't use a covered stand use a

wall stunt a non-covered stunt because you could have the bacteria that live in the GI tract get on the the PTFE and and you get tip situs which is a disaster and then there was someone who said well you should do a bowel prep you

like make her life miserable and you know give her lots of antibiotics and then you should do a tips and then it's like well what kind of tips and they're like I don't know maybe you should do a covered said no not a covered tonight

and then they're you know and then there was there was a other voice that said just do a tips you know just do the damn tips and go for it so I did it would you know very nice anatomy tips was placed she did well

the next day she has fevers and and her blood cultures come back positive right and you can see in the circle that there's a little bit of low density around the tips in the liver and so they put her on IV antibiotics and then they

got an ultrasound a week later and the tips that occluded and then they got a CT just to prove that the ultrasound actually worked so this really hurt my gosh to rub it in just to rub it in just just to confirm that your tips occlude

it and so you know I feel not so great about myself and particularly because I work in an institution that defined tip seclusion was one of the first people so gene Laberge is one of my colleagues back in the day demonstrated Y tips

occludes and one of the reasons is because it's in communication with the biliary system so bile is very toxic actually and when it gets into the the lining of the tips it causes a thrombosis and when they would go and

open these up they would see green mile or biome components in the in the thrombus so I felt particularly bad and so and then I went back and I looked and I was like you know what the tips is short but it's not short in the way that

it usually is usually it's short at the top and they people don't extend it to the to the outflow of the hepatic vein here I hadn't extended it fully in and it was probably in communication with a bile duct which was also you know living

with lots of bacteria which is why she got you know bacteremia so just because we want to do more imaging cuz you know god forbid you know you got the ultrasound of her they because she was back to remake and

you know that and potentially subject they got an echo just to make sure that she doesn't have endocarditis and they find out that she has a small p fo so what happens when you have a thrombosed tips you go back in there and you do a

tips or vision you line it with a beautiful new stent that you put in appropriately but would you do that when the patient has a shunt going from one side of the heart to the other so going from the right to the left so sort of

similar to that case right and so what do we do so I you know certainly not the smartest person in the room we've demonstrated that so I go and I asked my colleagues and so the loud voice of saying you know I told you this is why

we don't practice this kind of medicine and then there was someone who said why don't we anticoagulate her and I was like are you kidding me like you know do you think a little lovenox is gonna cure this and then the same person who said

we should do a tunnel dialysis tile the tunnel drainage catheter or like a polar X was like how about a poor X in here like thanks man we're kind of late for that what about thrombolysis and then you

know the most important WWJ be deed you guys are you familiar with that no what would Jim Benenati do that's that's that's the most important thing right so so of course you know I called Miami he's you know in a but in a big case you

know comes and helps me out and and I'm like what do I do and you know he's like just just go for it you know I mean there are thirty percent of the people that we see in the world have a efo it's very small and it probably doesn't do

anything but you know I got to tell you I was really nervous I went and I talked to miner our colleagues I made sure that the best guy who was you know available for stroke would be around in case I were to shower emboli I don't even know

what he would do I mean maybe take her and you know thrombolysis you know her like MCA or something I don't know I just wanted him to be around it just made me feel good and then I talked to another one of my favorite advisors

buland Arslan who who also was at UVA and he said why don't you instead of just going in there and mucking around with this clot especially because you have this shunt why don't you just thrown belay sit and then you

know and then see what happens and so here I brought her down EKOS catheter and I dripped a TPA for 24 hours and you know I made her do this with local I didn't give her any sedation because I wanted and it's not so painful and I

just wanted her to be awake so I could make sure that she isn't you took an intervention location you turned it into internal medicine I I did work you know that's that's you know I care right you know we're clinicians and so she was

fine she was very appreciative I had a penumbra the the the Indigo system around the next day in case I needed to go and do some aspiration thrombectomy and what do you know you know the next day it all opened up and you can still

see that the tips is short the uncovered portion which is which is you know past the ring I'm sorry that which is below the ring into the portal vein is not seated well so that was my error and and there was a little bit of clot there so

what I ended up doing is I ended up balloon dilating it placing another Viator and extending it into the portal vein so it's covered so she did very

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

another device that's new in the market

is the inari device it is a combi combination of suction thrombectomy and mechanical thrombectomy and it you can see it looks like three Amplatz or plugs on a catheter but that blue catheter is actually a very nice suction system as

well so you can go beyond the clot pull it in and then suck it into the catheter this is very useful because you can pull clot out without giving any TPA and you have a lot less blood loss so if you can take the clot out with a lot less blood

loss I think you can out patients again the benefit is that there's no thrombolytic and the patients have less bleeding drawbacks like many of these devices is there's really no studies to prove that they work we can prove that

they can remove clot from the patient's body but that we don't know that that actually helps in the long run so what we really want to know in all the studies which we're actually going to show three of the main studies is

whether this actually helps patients life in the long term do they does it improve their mortality so the first

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

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

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

so we kind of had a bunch of portal vein cases I think we'll stick with that theme and this is a 53 year old woman who presented to the emergency room with severe abdominal pain about three hours after she ate lunch she had a ruin why two weeks prior the medications were

really non-contributory and she had a high lactic acid so she they won her a tan on consi t scan and this is you can see back on the date which is two years ago or a year and a half ago we're still seeing her now and follow-up and there

was a suggestion that the portal vein was thrombosed even on the non con scan so we went ahead and got a duplex and actually the ER got one and confirmed that portal vein was occluded so they consulted us and we had this kind of

debate about what the next step might be and so we decided well like all these patients we'll put her on some anticoagulation and see how she does her pain improved and her lactate normalized but two days later when she tried to eat

a little bit of food she became severely symptomatic although her lactate remain normal she actually became hypotensive had severe abdominal pain and realized that she couldn't eat anything so then the question comes what do you do for

this we did get an MRA and you can see if there's extensive portal vein thrombus coming through the entire portal vein extending into the smv so what do we do here in the decision this is something that we do a good bit of

but these cases can get a little complicated we decided that would make a would make an attempt to thrombolysis with low-dose lytx the problem is she's only two weeks out of a major abdominal surgery but she did have recurrent

anorexia and significant pain we talked about trying to do this mechanically and I'd be interested to hear from our panel later but primary mechanical portal vein thrombus to me is oftentimes hard to establish really good flow based on our

prior results we felt we need some thrombolysis so we started her decided to access the portal vein trance of Pataca lee and you can see this large amount of clot we see some meds and tera collaterals later i'll show you the SMB

and and so we have a wire we have a wide get a wire in put a catheter in and here we are coming down and essentially decide to try a little bit of TPA and a moderate dose and we went this was late in the afternoon so we figured it would

just go for about ten or twelve hours and see what happened she returned to the IRS suite the following day for a lysis check and at that what we normally do in these cases is is and she likes a good bit but you can see there's still

not much intrahepatic flow and there's a lot of clots still present it's a little hard to catheterize her portal vein here we are going down in the SMB there's a stenosis there I'm not sure if that's secondary to her surgery but there's a

relatively tight stenosis there so we balloon that and then given the persistent clot burden we decide to create a tips to help her along so here we are coming transit paddock we have a little bit of open portal vein still not

great flow in the portal vein but we're able to pass a needle we have a catheter there so we can O pacify and and pass a needle in and here we are creating the tips in this particular situation we decide to create a small tips not use a

covered stent decide to use a bare metal stent and make it small with the hope that maybe it'll thrombosed in time we wouldn't have to deal with the long-term problems with having a shunt but we could restore flow and let that vein

remodel so now we're into the second day and this is you know we do this intermittently but for us this is not something most of the patients we can manage with anticoagulation so we do this tips but again the problem here is

a still significant clot in the portal vein and even with the tips we're not seeing much intrahepatic flow so we use some smart stance and we think we could do it with one we kind of miss align it so we

end up with the second one the trick Zieve taught me which is never to do it right the first time joking xiv and these are post tips and yo still not a lot of great flow in the portal vein in the smv

and really no intrahepatic flow so the question is do we leave that where do we go from here so at this point through our transit pata catheter we can pass an aspiration catheter and we can do this mechanical

aspiration of the right and left lobes you see us here vacuuming using this is with the Indigo system and we can go down the smv and do that this is a clot that we pull out after lysis that we still have still a lot of clot and now

when we do this run you see that s MV is open we're filling the right and left portal vein and we're able to open things up and and keep the the tips you see is small but it's enough I think to promote flow and with that much clot now

gone with that excellent flow we're not too worried about whether this tips goes down we coil our tract on the way out continue our own happened and then trance it kind of transfer over to anti platelets advanced or diet she does

pretty well she comes back for follow-up and the tips are still there it's open her portal vein remains widely Peyton she does have one year follow-up actually a year and a half out but here's her CT the tip shuts down the

portal vein stays widely Peyton the splenic vein widely Peyton she has a big hematoma here from our procedure unfortunately our diagnostic colleagues don't look at any of her old films and call that a tumor tell her that she

probably has a new HCC she panics unbeknownst to us even though we're following her she's in our office she ends up seeing an oncologist he says wait that doesn't seem to make sense he comes back to us this is 11 3 so

remember we did the procedure in 7 so this is five months later at the one year fault that hematoma is completely resolved and she's doing great asymptomatic so yeah the scope will effect right that's exactly right so so

in summary this is it's an interesting case a bit extreme that we often don't do these interventions but when we do I think creating the tips helps us here I think just having the tips alone wasn't going to be enough to remodel so we went

ahead and did the aspiration with it and in this case despite having a hematoma and all shams up resolved and she's a little bit of normal life now and we're still following up so thank you he's

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

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

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

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

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

other things that we look at tools that we use include the ankle and toe brachial indices those are these at blood pressure comparisons between the

arm and the foot or the toe the great first toe we use segmental pressures your blood pressures and multiple levels down the leg pulse volume recordings which look very similar with cuffs down the leg but they're looking at the size

of the leg per heartbeat PPG's which is basically pulse ox for the four individual toes TCP o2 which is very important and not used enough which is looking at the oxygen tension within the tissue itself and skin perfusion

pressure so ABI as I mentioned as a comparison the arm and the leg pressures and people with CLI often have an ABI less than point for the pressures gonna be less than 50 millimeters in mercury so the ABI may be falsely elevated

people who have chronic kidney disease because the vessels get calcified and they don't compress very well when you blow up the cuff increasing it above 0.45 after if it's been below that is somewhat predictive of wound healing but

not that helpful at the time of an angiogram so as the higher the two pressures is often used to calculate this because you have two pressures and each leg right you have it dorsalis pedis pressure that

you can get and you have posterior tibial so the way that you do in ABI is you look at the higher of the two and compare that to your arm pressure so just remember if your ulcer is being supplied by the vessel that's got the

lower pressure than your ABI is could be normal you could still have CLI so again not always that helpful the toe brachial indices is a it is a little bit more helpful people with diabetes only because the toe arteries tend not to

calcify as quickly in these patients less than 0.75 is considered abnormal and increasing it up into the normal range of course is predictive of fluid wound healing so limitations these only really look at

the macro vascular so that you know the named ves blood vessel patency they don't really tell you what's going on at the level of the capillaries and a recent meta-analysis suggests that neither of them can be consistently

relied upon as okay it came to a normal range we're definitely not gonna get an amputation now so I think I really do have to press both buttons each time so the systolic pressure measurements for segmental pressures you basically look

at the pressures on multiple levels of down the leg a drop of greater than 20 is considered significant and then severity of a number of lesions can't be totally determined from that again this only really tells you what's going on in

the named vessels pulse volume recordings these are cuffs that are looking at the volume of the limb with each pulse it's helpful and patients would they have non compressible vessels because the leg actually has a it's a

microscopic but detectable increase in size with each pulse and so this is better in people who have non compressible vessels and changes in PVR's often will actually precede angiographic findings CTA findings and

recent publication from the s from the society vascular surgery however calls into question their usefulness compared to a bi alone the good pictures are coming soon so this is an example what you may see in

the chart for some of your patients with critical limb ischemia so this is actually segmental pressure and pulse while recording from where I trained in Miami and basically what we're looking at is a combination of things on one of

these sheets so the pressures are listed in the middle but each sheet is going to be different depending on your institution so you're looking for a big drop and pressure from one level to the next so if you look for example in the

middle at the right leg you know there's a 176 in the arm and then there's a 126 in the high thigh normally because of gravity you should have an increase in flow at that level so that's already I have normal on the right side and then

progressing down any grade any drop greater than 20 suggested that something may be abnormal at that level PPG's these are really good for detecting what may be going on at the foot or lower levels so you transmit an infrared

signal through the toe and then try to see how much of that light comes out the other side essentially and so the amount of it it's depending on how much bloods in the digit and the flow the flow of the blood vessels so if you had a

previously flatlined signal then restoring a pulsatile signal is considered a and it you know an approved marker of tissue perfusion so this is essential in patients who have distal ulcers particularly in the level of the

toe because restoring you see you've probably all seen those of you that work in labs that do a lot of peripheral disease seen an angio graphic result where you get flow down to like the mid foot but you see no perfusion down to

the digits and unfortunately that's often not going to be enough to heal a wound so the PPG's are something I try to get in all patients who have tote tote ones so there's an example of a patient who

has flatline and all five digits on the right foot and we recant alized their anterior tibial artery and had flow all the way down there and there was a wound blush in the toe and this is the restore pulsatilla T in all five digits the next

day so at our institution now and also I've modeled after what it was with my training which is the day after the procedure we keep all these patients overnight we get an ABI i segmental pressures and pulsefire

recordings and PPG's and anyone who has flat waveforms in them in their foot level or anybody with a toll sir and if possible we try to get a duplex which you get which I'll go over next it's not always reimbursable at all institutions

if you do them in the same day though so TCP o2 as I mentioned is something that's a little underutilized I think the the task two recommendations that we actually use to stratify the different types of disease and perf arterial

disease suggest that all patients with CLI should have this testing done but it's hard because patients have to not smoke and not drink coffee or tea the morning of the exam and that's hard to get patients to do you have to keep the

room temperature controlled and so it's office availability is limited so an improvement values greater than forty millimeters of mercury in the area surrounding an ulcer suggests that it's going to have successful healing so we

often will do this before we take the patient for an angiogram as a baseline and then bring them back afterwards and if we're if we have a very large increase that you know that's a good sign but of course we're our goal is

usually to be greater than forty and it's one of the few of these tests that's actually useful in patients who don't have Doppler signals so this is a totally not fake wound on this right foot this is example of what it looks

like you basically put multiple probes around the area of the foot and you're testing for the different oxygen tensions skin perfusion pressures is analogous but slightly different basically you're inflating a cop over

different areas of tissue and until the blood flow stops and then slowly deflating it until you can detect light being transmitted through that area again greater than thirty values or predictive of wound healing a lot of

numbers and there will be a test at the end of this so this is a chart kind of showing the ischemic wounds healing likelihood is correlated with an increase in the skin perfusion pressure so if you're less than 30 you're

unlikely to heal if you're greater than 40 it's most likely not an excuse mcquown and you should start looking at other ideologies like venous disease or neuropath neuropathic disease or infection duplex ultrasound is extremely

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

strategies so some things that we have

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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