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Thrombosis causing Thoracic Outlet Syndrome|Thrombolysis, Angioplasty|48|Female
Thrombosis causing Thoracic Outlet Syndrome|Thrombolysis, Angioplasty|48|Female
2016angiojetangioplastyanticoagulationaxillarychoiceclotcollateralsdefectsextremityextrinsicfillinghematologicmechanicaloccludepatientreconstitutionrelieveresectionSIRstentthrombolysisvenogramvenous
Balloon Pulmonary Angioplasty | Management of Patients with Acute & Chronic PE
Balloon Pulmonary Angioplasty | Management of Patients with Acute & Chronic PE
angiogramangioplastyarteryballoonballooningbandschaptercomplicationscontrastflowHorizonimageimagesluminalNoneocclusionocclusionspatientsproximallypulmonaryradiationrecanstenosisthrombustreatedultrasoundwebs
Where do we go from here for submassive PE | Pulmonary Emoblism Interactive Lecture
Where do we go from here for submassive PE | Pulmonary Emoblism Interactive Lecture
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Ideal Stent Placement | TIPS & DIPS: State of the Art
Ideal Stent Placement | TIPS & DIPS: State of the Art
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Therapies for Acute PE | Management of Patients with Acute & Chronic PE
Therapies for Acute PE | Management of Patients with Acute & Chronic PE
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Complications & Pitfalls | TIPS & DIPS: State of the Art
Complications & Pitfalls | TIPS & DIPS: State of the Art
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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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Submassive PE | Pulmonary Emoblism Interactive Lecture
Submassive PE | Pulmonary Emoblism Interactive Lecture
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Systemic vs Catheter-based Thrombolysis | Management of Patients with Acute & Chronic PE
Systemic vs Catheter-based Thrombolysis | Management of Patients with Acute & Chronic PE
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General Screening Criteria (specific to bleeding risk) | Risk Mitigation: Periprocedural Screening and Anticoagulation Guidelines to Reduce Interventional Radiology Bleeding Risks
General Screening Criteria (specific to bleeding risk) | Risk Mitigation: Periprocedural Screening and Anticoagulation Guidelines to Reduce Interventional Radiology Bleeding Risks
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Registry and Data | Management of Patients with Acute & Chronic PE
Registry and Data | Management of Patients with Acute & Chronic PE
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Education Strategies to Reduce Human Errors | Looking for risk in all the Right Places: The Anatomy of Errors in Healthcare
Education Strategies to Reduce Human Errors | Looking for risk in all the Right Places: The Anatomy of Errors in Healthcare
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Ultrasound-assisted Catheter-directed Thrombolysis | Management of Patients with Acute & Chronic PE
Ultrasound-assisted Catheter-directed Thrombolysis | Management of Patients with Acute & Chronic PE
catheterchapterekosfibrinNonerequiresstudiesthrombolysisthrombustpaultrasound
MRI Safety & Screening | PET/MRI: A New Technique to Obtain High Quality Diagnostic Images for Oncology Patients
MRI Safety & Screening | PET/MRI: A New Technique to Obtain High Quality Diagnostic Images for Oncology Patients
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Pulmonary Ablation | Interventional Oncology
Pulmonary Ablation | Interventional Oncology
ablationactivitycancercandidatechaptercolorectalcryodiseaselesionslobelungmetastaticnodulepatientpulmonaryrecurrecurredresectionresidualscansurgical
Treatment Options- TransCarotid Artery Revascularization- TCAR | Carotid Interventions: CAE, CAS, & TCAR
Treatment Options- TransCarotid Artery Revascularization- TCAR | Carotid Interventions: CAE, CAS, & TCAR
angiographyangioplastyarterybleedbloodcalcifiedcarotidchapterclaviclecommondebrisdevicedistalembolicembolizationexposurefemoralflowimageincisioninstitutionlabeledpatientprocedureprofileproximalreversalreversesheathstenosisstentstentingstepwisesurgicalsuturedsystemultimatelyveinvenousvessel
Renal Ablation | Interventional Oncology
Renal Ablation | Interventional Oncology
ablationcardiomyopathycentimeterchaptereffusionembolizedfamiliallesionmetastaticparenchymalpatientpleuralrenalspleensurgerytolerated
Case 1 - Non-healing heel wound, Rutherford Cat. 5, previous stroke | Recanalization, Atherectomy | Complex Above Knee Cases with Re-entry Devices and Techniques
Case 1 - Non-healing heel wound, Rutherford Cat. 5, previous stroke | Recanalization, Atherectomy | Complex Above Knee Cases with Re-entry Devices and Techniques
abnormalangioangioplastyarteryAsahiaspectBARDBoston Scientificcatheterchaptercommoncommon femoralcontralateralcritical limb ischemiacrossCROSSER CTO recanalization catheterCSICTO wiresdevicediseasedoppleressentiallyfemoralflowglidewiregramhawk oneHawkoneheeliliacimagingkneelateralleftluminalMedtronicmicromonophasicmultimultiphasicocclusionocclusionsoriginpatientsplaqueposteriorproximalpulserecanalizationrestoredtandemtibialtypicallyViance crossing catheterVictory™ Guidewirewaveformswirewireswoundwounds
CTEPH Studies | Management of Patients with Acute & Chronic PE
CTEPH Studies | Management of Patients with Acute & Chronic PE
acutearterieschapterchroniccpapedemainterdisciplinaryjapanmultidisciplinarymultipleNoneoperatorspatientpatientsperformedpulmonaryreperfusionrequiringthrombolysistreatedtreatmentvascular
Cone Beam CT | Interventional Oncology
Cone Beam CT | Interventional Oncology
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Treatment Options- CAS- Embolic Protection Device (EPD)- Proximal Protection | Carotid Interventions: CAE, CAS, & TCAR
Treatment Options- CAS- Embolic Protection Device (EPD)- Proximal Protection | Carotid Interventions: CAE, CAS, & TCAR
angioplastyantegradearteryaspirateballoonballoonsbloodcarotidcarotid arterychaptercirclecirculationclampclampingcolumncommoncontralateralcrossdebrisdeflatedevicedevicesdilateddistaldistallyexternalexternal carotidfilterflowincompleteinflateinflatedinternalinternal carotidlesionmarkerspatientpressureproximalretrogradesheathstentstepwisesyringesyringestoleratevesselwilliswire
Treatment Options- Carotid Endarterectomy (CEA) | Carotid Interventions: CAE, CAS, & TCAR
Treatment Options- Carotid Endarterectomy (CEA) | Carotid Interventions: CAE, CAS, & TCAR
anesthesiaanestheticarterycarotidcarotid arterychapterclotcomparingdistallyexternalexternal carotidflowincisioninternalinternal carotidissuelongitudinalloopsmedicalpatientpatientsplaqueproximalstenosisstenoticstentstentingstrokesurgerytherapyultimatelyvascularvesselwound
The Landscape of PE | Pulmonary Emoblism Interactive Lecture
The Landscape of PE | Pulmonary Emoblism Interactive Lecture
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Indirect Angiography | Interventional Oncology
Indirect Angiography | Interventional Oncology
ablateablationablativeaneurysmangioangiographybeamBrachytherapycandidateschapterdefinitivelyembolizationentirehccindirectintentinterdisciplinaryischemiclesionographypatientportalresectionsbrtsurgicaltherapyvein
Massive PE | Pulmonary Emoblism Interactive Lecture
Massive PE | Pulmonary Emoblism Interactive Lecture
adenosineangiobloodbradycardiacatheterchaptercontraindicateddevicedirectedhypotensioninpatientinterventionalistsmassivematsumotopatientsPenumbrasurgicalsystemictherapythrombolysisthrombolyticthrombolyticsventricle
Case- May Thurner Syndrome | Pelvic Congestion Syndrome
Case- May Thurner Syndrome | Pelvic Congestion Syndrome
arterycatheterizecausingchapterclassiccliniccommoncommon iliaccompressioncongestionendovascularevidenceextremitygonadalhugeiliaciliac veinimagingincompetenceincompetentMay Thurner Syndromeobstructionoccludedpelvicpressuresecondarystentsymptomstreatmentsvalvularvaricositiesvaricosityveinveinsvenavenous
Percutaneous Mechanical Intervention | Management of Patients with Acute & Chronic PE
Percutaneous Mechanical Intervention | Management of Patients with Acute & Chronic PE
catheterchapterclotmassivemechanicalNonepatientpatientsPig Tail Catheterpigtailpulmonarysurgerythrombolytictpa
Carotid Artery Stenting- Case | Carotid Interventions: CAE, CAS, & TCAR
Carotid Artery Stenting- Case | Carotid Interventions: CAE, CAS, & TCAR
angioplastyarteryballoonballoonsbut want left carotid artery lesion stented firstcarotidcarotid arterychaptercommonCoronary bypass graftdistalECA balloonendarterectomyexternalexternal carotidimageinflatelesionosisproximalproximallystentstentingsurgicallyultimately
Aspiration Thrombectomy | Management of Patients with Acute & Chronic PE
Aspiration Thrombectomy | Management of Patients with Acute & Chronic PE
angioAngiodynamicsAngiovac CannulaAspirex CathetercatheterschapterclotdevicedevicesfrenchIndigo ThrombectomyNonepatientPenumbraPenumbra Inc.sheathStraub Medicalthrombectomythrombustpa
Q&A Pulmonary Embolism | Management of Patients with Acute & Chronic PE
Q&A Pulmonary Embolism | Management of Patients with Acute & Chronic PE
acuteangiogramassistedcatheterchapterchroniccontrastdiagnosticechocardiogramembolismisisNonepressurepulmonarythrombolysistreatmentultrasound
Prospective CDT Trials | Pulmonary Emoblism Interactive Lecture
Prospective CDT Trials | Pulmonary Emoblism Interactive Lecture
arterybleedingcatheterchapterclinicalclotdatadevicedevicesdiameterdysfunctionheparinintracranialmajormassivemechanicalpatientsPenumbrapulmonaryrandomizedrateratiorecurrentreducesstudysurrogatethrombolysisthrombosistrialtrialsultimateventricle
Transcript

So we'll talk about Paget-Schroetter Syndrome, which is effort venous thrombosis. Our patient is a 48 year old female,

who presented with a one week history of acute right arm swelling. She had no previous history of venous thromboembolism, or indwelling venous catheter or hematologic disorders. So we performed a venogram. And you can see the images from one

of our stations here, with filling defects seen within the axillary vein, and multiple enlarged collaterals with reconstitution eventually of the SCC/g centrally. And so this is the abnormality that we see on the venogram

and [BLANK_AUDIO] At this point you are faced with a decision on what's the next step, what you do now? And so this is our sam/g question here.

Based on the clinical and imaging findings, which of the following would be the most appropriate next step in management? Choice A, therapeutic anticoagulation alone. Choice B, catheter-directed thrombolysis and angioplasty.

Choice C, venous stent placement. And choice D, surgery. [BLANK_AUDIO] All right, excellent. So most of us got that right. What you really need to figure out is,

well what is the purpose of our therapy here? What are we trying to achieve? And in these cases we have to realize well what is the cause? And the cause most of the time is really a mechanical obstruction. And so the mechanical obstruction can only be relieved with removal of

that obstructing agent, whatever that may be. In these cases, it's either a scalene muscle or a burst rib, or a cervical ribbon in some instances. And those can only be remedied with surgery.

So what's our role in this? Our role is to decrease the clot burden to try and re-establish fault, or relieve symptoms until such time that they actually get to surgery. And it's not to actually get a permanent fix of this, because it will need to be fixed surgically.

So we get our wire across and did some AngioJet lysis, with powerful/g spray initially and then some thrombectomy. We were able to clear most of the clot out of the axillary vein, you no longer see a lot of filling defects anymore. There is still some, but not as much as there was. And you still see the collaterals, a

little bit of filling centrally of the SCC/g. [BLANK_AUDIO] So the next step was, because of that long segment that was still non-visualized, was to place a balloon across that and angioplasty it to establish a lumen again. And re-establish flow to allow for better drainage,

venous drainage of the upper extremity and relieve the patient's symptoms. And once we achieve that, then our job is almost complete in this case, where we actually leave the access across that area and make sure that we've got adequate flow.

The patient will usually go to the OR in a couple of days after we establish that flow, just to give time for inflammation to subside. And in this case this patient underwent a first rib resection and patching of the vein. Now one of the choices, was well should you stent that mechanical

obstruction. And that's not really something that is advised because the stent will actually occlude afterwards because of the stressors on the stent from the mechanical obstruction, the extrinsic compression on it.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

people were thinking about the covered

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

guys do so when we do our screening phone calls and our pre screens before

the actual procedure there's a few factors that we look at for the patients with blood pressure the patient needs to be vitally stable before we do a procedure there may be a slightly increased risk of bleeding for kidney

biopsy if patients are hypertensive although it hasn't been noted to be statistically significant in the literature so we are always aware of patients being hypertensive we do want them to be taking their medications the

day of the procedure we also do a full medication reconciliation with the patient making sure that we're checking on any anti platelets anticoagulant medications and we have a list of our hold times that we use for a reference

we already discussed for those of you who are at this session this morning the issue of liver disease is it stable liver disease they may have adequate he stasis even though their INR is not within the normal range and so we

recommend a stable INR of less than 2.5 for those patients and in our practice a lot of the providers are going away from correcting the INR s for our patients we also screen for hematological disorders do they have some known condition that

makes them more likely to bleed or conversely more likely to clot and that may factor into whether or not anticoagulation can be held do they have a current diagnosis of cancer are they going to be getting one of those

angiogenesis inhibitors might they have thrombocytopenia and we just do a brief review of the patient's chart before we call them to kind of look for those diagnoses do they have a history of bleeding especially if they have no one

platelet dysfunction you know a known history of bleeding can be a reliable predictor of bleeding risk for some patients and do they have a cardiac or a neurological history as we learned this morning patients that have recently had

a cardiac stent placed we can't just say yeah stop your plavix hold off 5 days it'll be fine that could be a very serious risk to the patient did they recently have a stroke have they had a PE why are they on their anticoagulation

if they're on it so we really need to be aware of the whole patient and having that pre-screening phone call with them can allow our nurses to figure out a lot of these problems and then alert the radiologists and try and troubleshoot

before the patient walks in the door and says yeah I took my warfarin this morning I'm all ready for my liver biopsy the radiologists don't like that much in it you know it's really a bad thing for our high volume area to have

that happen and this is just another chart of our oh did I get mixed up here you guys are gonna fire me from running this clicker there we go so the whole times are again based on the half-life and the mechanism of action and this is

pretty similar to what you saw in the the presentation earlier today and specifically that imbruvica that's something that we alert the radiologists who they have a discussion with the patient decide is this something that we

want to continue with and I will say that in our practice with the volume and the the level of acuity of our patients I think that a lot of our providers are fairly comfortable with a certain level of risk because that's just who our

patient population is you know we have a very large hospital two large hospitals and very sick patients so that's something that we you know some of them are more comfortable than others but it's a risk-benefit thing that they have

to decide on themselves with the patient obviously all right so here are our

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

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

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

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

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

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

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

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

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

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

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

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

really did have an isotope injected we

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

different applications renal ablation is very common when do we use it

high surgical risk patients primary metastatic lesions some folks are actually refused surgery nowadays and saying I'll have a one centimeter reno lesion actually want this in lieu of surgery people have

familial syndromes they're prone to getting a renal cancer again so we're trying to preserve renal tissue it is the most renal parenchymal sparing modality and obviously have a single kidney and a lot of these are found

incidentally when they're getting a CT scan for something else here's a very sizable one the patient that has a cardiomyopathy can see how big the heart is so it's you know seven centimeter lesion off of the left to superior pole

against the spleen this patient wouldn't have tolerated bleeding very much so we went ahead and embolized it beforehand using alcohol in the pide all in a coil and this is what it looks like when you have all those individual ice probes all

set up within the lesion and you can see the ice forming around I don't know how well it projects but in real time you can determine if you've developed your margin we do encompass little bit of spleen with that and you can see here

that you have a faint rim surrounding that lesion right next to the spleen and that's the necrotic fat that's how you know that you got it all and just this ablation alone caused a very reactive pleural

effusion that you can see up on the CT over there so imagine how this patient would have tolerated surgery pulmonary

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

it's obviously either done with general

anesthesia or perhaps a regional block at our institution is generally done with general anesthesia we have a really combined vascular well developed combined vascular practice we work closely with our surgeons as well as

you know those who are involved in the vascular interventional space as far as the ir docs and and in this setting they would do generally general anesthetic and a longitudinal neck incision so you've got that and the need for that to

heal ultimately dissect out the internal carotid the external carotid common carotid and get vessel loops and good control over each of those and then once you have all of that you hyper NIH's the patient systemically not unlike what we

do in the angio suite and then they make a nice longer-term longitudinal incision on the carotid you spot scissors to cut those up and they actually find that plaque you can see that plaque that's shown there it's you know actually

pretty impressive if you've seen it and let's want to show an illustrative picture there ultimately that's open that's removed you don't get the entirety of the plaque inside the vessel but they get as much as they can and

then they kind of pull and yank and that's one of the pitfalls of this procedure I think ultimately is you don't get all of it you get a lot more than you realize is they're on on angiography but you don't get all of it

and whatever is left sometimes can be sometimes worse off and then ultimately you close the wound reverse the heparin and closed closed it overall and hope that they don't have an issue with wound healing don't have an issue with a

general anesthetic and don't have a stroke in the interim while they've clamped and controlled the vessel above and below so here's a case example from our institution in the past year this is a critical asymptomatic left internal

carotid artery stenosis pretty stenotic it almost looks like it's vocally occluded you can see that doesn't look very long it's in the proximal internal carotid artery you can see actually the proximal external carotid artery which

is that kind of fat vessel anteriorly also looks stenotic and so it's going to be addressed as well and this is how they treated it this is the exposure in this particular patient big incision extractors place and you can see vessel

loops up along the internal and external carotid arteries distally along some early branches of the external carotid artery off to the side and then down below in the common core artery and ultimately you get good vessel control

you clamp before you make the incision ultimately take out a plaque that looks like this look how extensive that plaque is compared to what you saw in the CT scan so it's not it's generally much more

impressive what's inside the vessel than what you appreciate on imaging but it's the focal stenosis that's the issue so ultimately if yet if the patient was a candidate stenting then you just place a stent

across that and he stabilized this plaque that's been removed and essentially plasti to that within the stent so it doesn't allow any thrombus to break off of this plaque and embolize up to the brain that's the issue of raw

it's the flow through there becomes much more turbulent as the narrowing occurs with this blockage and it's that turbulent flow that causes clot or even a small amount of clot to lodge up distally within the intrical in

terrestrial vasculature so that's the issue here at all if you don't take all that plaque out that's fine as long as you can improve the turbulent blood flow with this stent but this is not without risk so you take that plaque out which

looks pretty bad but there are some complications right so major minor stroke in death an asset which is a trial that's frequently quoted this is really this trial that was looking at medical therapy versus carotid surgery

five point eight percent of patients had some type of stroke major minor so that's not insignificant you get all that plaque out but if you know one in twenty you get a significant stroke then that's not so bad I'm not so good right

so but even if they don't get a stroke they might get a nerve palsy they might get a hematoma they may get a wound infection or even a cardiovascular event so nothing happens in the carotid but the heart has an issue because the

blockages that we have in the carotid are happening in the legs are happening in the coronary so those patients go through a stress event the general anesthetic the surgery incision whatever and then recovery from that I actually

put some stress on the whole body overall and they may get an mi so that's always an issue as well so can we do something less invasive this is actually a listing of the trials the talk is going to be available to you guys so I'm

not going to go through each of this but this is comparing medical therapy which I started with and surgery and comparing the two options per treatment and showing that in certain symptomatic patients if they have significant

stenosis which is deemed greater than 70% you may be better off treating them with surgery or stenting than with best medical therapy and as we've gotten better and better with being more aggressive with best medical therapy

this is moving a little bit but here's the criteria for treatment and so you have that available to you but really is

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

thanks everyone appreciate it [Applause] [Music]

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

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

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

are in the room here's a case of an 80

year old with a previous mi had a left hand are directing me and it's gonna go for a coronary bypass graft but they want this carotid stenting significant card accenting lesion to be treated first there's the non-invasive blow

through this but there's the lesion had a prior carotid endarterectomy so had that surgery we talked about first but at the proximal and distal ends of that patch has now a stone osis from the surgical fix that's developed so we

don't want to go back in surgically that's a high resolution we want for a transfer Merle approach and from there here's what it looks like an geographically mimics what we saw on the CT scan you can see the the marker and

the external carotid artery on the right that's the distal balloon and then proximally in the common carotid artery and they're noted there and then when you inflate the balloons you can see them inflated in the second image in the

non DSA image that's the external carotid room carotid artery balloon that's very proximal the common carotid balloon is below or obscured by the shoulders and ultimately when you inflate the common carotid balloon you

just have stagnant blood flow then we treat them you can see both balloons now and the external carotid and common carotid in place we have our angioplasty balloon across the lesion and then ultimately a stent and this is what it

looked like before this is what it looks like after and tolerated this quite well and we never had risk of putting the patient for dis Lombok protection or to salamba lusts overall I'm not gonna go over this real

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

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]

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

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