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PE Case Intro | Management of Patients with Acute & Chronic PE
PE Case Intro | Management of Patients with Acute & Chronic PE
chapterCTPA confirmed sub-massive bilateral upperDVTembolismhypercoagulablelower lobe PE's with RV strainmichiganNonepatientpriorpulmonarystraintalkupperventricular
PE Overview | Management of Patients with Acute & Chronic PE
PE Overview | Management of Patients with Acute & Chronic PE
cardiovascularchapterdeathsDVTembolismiliacNonepatientspoplitealproximalsymptomaticveins
Classification of PE | Management of Patients with Acute & Chronic PE
Classification of PE | Management of Patients with Acute & Chronic PE
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PE Management | Management of Patients with Acute & Chronic PE
PE Management | Management of Patients with Acute & Chronic PE
anticoagulationcardiologychapterconsensuscriticaldecisionembolisminstitutioninterventionalmultidisciplinaryNoneoxygenpatientpulmonaryteamteamstelemetrytpatumorvascular
CT Imaging- Acute PE | Management of Patients with Acute & Chronic PE
CT Imaging- Acute PE | Management of Patients with Acute & Chronic PE
acuteangiogramappearancearrowarteriescenteredchapterclassiccontrastcoronalimaginginfarctluminalNonepatientperfusionpulmonarysagittalscansegmentalsurroundingtechnologistthrombolysisthrombusvesselview
Therapies for Acute PE | Management of Patients with Acute & Chronic PE
Therapies for Acute PE | Management of Patients with Acute & Chronic PE
anticoagulantanticoagulationcatheterchapterclotcoumadindefensesdirectedheparininpatientintermediatelovenoxNonepatientpatientsplasminogenprocessriskrotationalstreptokinasesystemicsystemicallythrombectomythrombolysisthrombustpa
Systemic vs Catheter-based Thrombolysis | Management of Patients with Acute & Chronic PE
Systemic vs Catheter-based Thrombolysis | Management of Patients with Acute & Chronic PE
bleedingcatheterchaptermilligramNonepatientpatientsperiodriskslowersystemictargetedthrombolysistpaversus
Catheter-directed Thrombolysis | Management of Patients with Acute & Chronic PE
Catheter-directed Thrombolysis | Management of Patients with Acute & Chronic PE
arteriescathetercatheterschapterclotcontrolholesinstitutionNonenormalpulmonarysystemicthrombolysisthrombolyticvessel
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
Percutaneous Mechanical Intervention | Management of Patients with Acute & Chronic PE
Percutaneous Mechanical Intervention | Management of Patients with Acute & Chronic PE
catheterchapterclotmassivemechanicalNonepatientpatientsPig Tail Catheterpigtailpulmonarysurgerythrombolytictpa
Rheolytic Thrombectomy | Management of Patients with Acute & Chronic PE
Rheolytic Thrombectomy | Management of Patients with Acute & Chronic PE
angioangiojetarrhythmiaaspiratebradycardiachapterclotdevicehemodynamicheparinizedlysisNonepatientsuctionthrombectomytpawebsite
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
Mechanical Thrombectomy | Management of Patients with Acute & Chronic PE
Mechanical Thrombectomy | Management of Patients with Acute & Chronic PE
amplatzcatheterchapterclotcombidevicehelpsInari DeviceInari MedicallossNonepatientsprovestudiessuctionthrombectomythrombolytictpa
Registry and Data | Management of Patients with Acute & Chronic PE
Registry and Data | Management of Patients with Acute & Chronic PE
arterycathetercatheter directedchaptercomplicationsdirectedechoheparinimprovementintermediateinterventionalmassiveNonepatientpatientsperfectpressurepulmonarypulmonary arteryratioreductionregistryriskseattlestrainstudiesstudysystolicthrombolysistpaunfractionated
PE Case Summary | Management of Patients with Acute & Chronic PE
PE Case Summary | Management of Patients with Acute & Chronic PE
angiogramarteriesarterycathetercatheterschapterdistallyechocardiogramimprovedinfusinginterventionallobelungNonepatientperfusionpressorspressurespulmonarypulmonary arteryscanthrombustpaventricleventricular
Chronic Thromboembolic Pulmonary Hypertension | Management of Patients with Acute & Chronic PE
Chronic Thromboembolic Pulmonary Hypertension | Management of Patients with Acute & Chronic PE
acuteangiogramcatheterizationchapterchronicdiagnosedhematologyHypertensioninterventionalNonepatientpatientsperfusionpostpulmonaryradiologistscansyndromethromboembolictreatment
CT Imaging- Chronic PE | Management of Patients with Acute & Chronic PE
CT Imaging- Chronic PE | Management of Patients with Acute & Chronic PE
acuteadenopathyanglesarteriesatherosclerosisbloodcalcificationchapterchronicclotdistallyDVTembolismirregularmiddleNonepatientproximalpulmonarysagittalscanthromboembolicthrombusvesselvessels
Diagnostic Criteria for CTEPH | Management of Patients with Acute & Chronic PE
Diagnostic Criteria for CTEPH | Management of Patients with Acute & Chronic PE
angiogramangiographyarterialarteriesarterycapillarycatheterchapterclassificationcurativediseasedistalflushlobesmanagementmedicationNonepatientpatientspressureproximalpulmonarysegmentalsheathstenosissurgeonsurgicalthrombustreatedtypevesselswebswedge
Pulmonary Thromboendarterectomy (PTE) | Management of Patients with Acute & Chronic PE
Pulmonary Thromboendarterectomy (PTE) | Management of Patients with Acute & Chronic PE
bypasscenterschaptercomplicationdiegoNonepatientsrequiressurgeonsthromboembolism
Case Example | Management of Patients with Acute & Chronic PE
Case Example | Management of Patients with Acute & Chronic PE
acuityafibangiogramanticoagulationarterycatheterchapterclotCTEPHdistallyDVTimagesincisionleftlobelowerNoneoperationpatientspressurespulmonarypulmonary arterysegmentalstenosisthrombusuppervessels
Medical Therapy Options | Management of Patients with Acute & Chronic PE
Medical Therapy Options | Management of Patients with Acute & Chronic PE
chapterdrugsexpensivemedicationsNoneoptionspulmonarystudiedvasodilation
Balloon Pulmonary Angioplasty | Management of Patients with Acute & Chronic PE
Balloon Pulmonary Angioplasty | Management of Patients with Acute & Chronic PE
angiogramangioplastyarteryballoonballooningbandschaptercomplicationscontrastflowHorizonimageimagesluminalNoneocclusionocclusionspatientsproximallypulmonaryradiationrecanstenosisthrombustreatedultrasoundwebs
CTEPH Case Example | Management of Patients with Acute & Chronic PE
CTEPH Case Example | Management of Patients with Acute & Chronic PE
angiogramballoonchaptercontraindicatedCTEPHdiseasedistallyglidehydrophilicinterventionalmichiganNoneocclusionspatientperfectperfusionsegmentalstenosissurgerywirewires
CTEPH Studies | Management of Patients with Acute & Chronic PE
CTEPH Studies | Management of Patients with Acute & Chronic PE
acutearterieschapterchroniccpapedemainterdisciplinaryjapanmultidisciplinarymultipleNoneoperatorspatientpatientsperformedpulmonaryreperfusionrequiringthrombolysistreatedtreatmentvascular
Q&A Pulmonary Embolism | Management of Patients with Acute & Chronic PE
Q&A Pulmonary Embolism | Management of Patients with Acute & Chronic PE
acuteangiogramassistedcatheterchapterchroniccontrastdiagnosticechocardiogramembolismisisNonepressurepulmonarythrombolysistreatmentultrasound
Transcript

we're gonna gonna talk this morning about pulmonary embolism and acute and chronic PE and try to put in a lot of information regarding imaging and interventions I want to start by thanking the avir Board for inviting me and the AR Rin board today as well and

of course Sam for organizing this wonderful meeting and she is one of my favorite Tech's so I also like to acknowledge a lot of people so we all have mentors in our career David Williams is one of my mentors dr. Barnes

helped us at Michigan start up our pulmonary embolism response team and since I'm talking about PE so it was great to talk about that a lot of what I talk about today is gonna be followed up with another talk on Tuesday from dr.

okey sister who's one of the world's experts at PE and so he's going to talk about managing care as well and of course to our excellent team of nurses technologists residents fellows will all help take care of patients every day so

I always like to start out with a patient so the first for our first case today it's a 54 year old male who had a prior history of a stroke hypercoagulable condition and known no known prior DVT

and PE he had increasing shortness of breath for about three days his heart rates were in the 90s to hundreds he had okay blood pressure in the 120s he had a CT that confirmed sub massive bilateral upper and lower low Pease with

right ventricular strain and then the RV strain was also seen on a TT II and had elevated cardiac enzymes so this is a very typical patient here's an image on the CT on the left and on the right showing that the patient had a large

amount of pulmonary embolism and I'm sorry I don't have a mouse to control that but in the right upper and branch points on the left you can see that there's PE so pulmonary embolism is very

common it's great

incidents of patients and up to a million a year in Europe about 200 about from PE so there are more deaths in the

P from PE in the u.s. than aids motor vehicle accidents and breast cancer combined so it's a very high cardiovascular more rate it causes about 15% of all in hospital deaths as well it's seen in 40

to 50 percent of patients with symptomatic proximal DVT so in the above the knees so the femoral veins popliteal veins and iliac veins and recurrent PE is a very substantial risk a lot of patients have missed diagnoses of PE so

they come into the hospital with some chest pain shortness of breath maybe a light a low-grade fever they're seen in the ER and then they're thought that they maybe have pneumonia they have a viral bronchitis and it turns out that

they have pulmonary embolism so the

original classification of PE is important to know because it man it helps dictate treatment so it used to be classified as massive which is about 5% of PE patients these are the ones that

we all know how to treat they're usually coding essentially when they show up to the ER or to the angio suite or in the ICU they have a 58% ninety day mortality rate so these patients are doing very poorly they're in hemodynamic collapse

which is the diagnostic factor there that sort of makes that diagnosis because of cardiogenic shock sub massive PE is the biggest group that we'll talk about last I'm sorry the most important group we'll talk about last so

minor PE are about 55% of PE patients those are the ones that show to the ER that just don't feel right and they turns out that they have PE so it was really not even anyone's differential diagnosis and most of these patients do

just fine with outpatient anticoagulation monitoring and monitoring so the main group that matters in that most of the talks about PE are about are the sub massive group which is about 40% of patients and these

are the ones that show up with a moderate amount of clot and some right ventricular strain these are the patients who are able to tolerate their PE but they're not doing very well so they come in with shortness of breath

some chest pain and although they're not in hemodynamic collapse they are the ones who require inpatient monitoring or their good it goes to an ICU and that's really the patients that we worry about those are the ones that we're going to

do an intervention on or systemic TPA so that was the sort of the old way of classifying PE and this is the new way of classifying PE so this is the Europeans Society of Cardiology they had a

consensus in 2014 talking about PE and what we look at now and the way we stratify these are high risk PE intermediate which is intermediate high and intermediate low and then low risk PE so this is

important because it in fact it utilizes patients actual biomarkers imaging as well as their clinical symptoms all in one and so what we look at if you look at a patient with high risk PE they have to be in shock or hypotension that is

one factor that has to be there and actually everything else doesn't matter but the things that we look at are the PE severity index or the PES e score if you google PES e PE SI it's basically a bunch of things it asks for the

patient's age whether they have cancer what their heart rate is if what they're owed to sat and on what oxygen content they're on and it gives you a score and that classifies it in 1 through 5 and basically 5 is really bad which means

that you have a low or you have a higher mortality as an outpatient and 1 is really low some things like cancer give you a lot of points so that sort of pushes it over to automatically kind of 2 3 then you look at the signs of our V

dysfunction and really with PE that's really the thing that that kills you is your right ventricular dysfunction and if your right heart fails then your left heart fails and then you die and so that's really where the issue is

and then the cardiac laboratory biomarkers are what will sort of give you a blood test that you can figure out and see if that patient is going to do poorly so high risk PE shock or hypotension

low risk Pease the other end where you really don't have any of those things but you do have a PE diagnosed either usually on a CT scan but it could be on an echo as well intermediate high and intermediate low is where we all spend

all the time talking about that's what we kind of do all the studies on is really the intermediate high and low groups and what we should do for them and sort of how we can affect their lives but the main point here that I

want you to see is that they don't have shock or hypotension but they do have positive right ventricular strain either on an echo or a CT scan and they have positive biomarkers if you have positive biomarkers and imaging then you have

intermediate high risk PE and those are the patients who may benefit from some sort of intervention or some sort of further ICU monitoring and anticoagulation so I'm gonna just

briefly mention this because dr. sista

is gonna talk more about this on Tuesday but this is a slide from MGH where they started the pulmonary embolism response team and this is sort of how things used to be and I think most hospitals across the country and still exist in some

places where a patient shows up with PE and then about 20 different teams are consulted and kind of wait for everyone to say what they think you know vascular surgery may if they're involved may say something cardiology is gonna say one

thing ir is going to be involved and say something the critical care teams are going to say something and you're waiting for everyone to sort of get consensus which you may actually never get and all the while a patient is

sitting in the ER finding it difficult to breathe maybe probably an oxygen maybe not on a heparin drip and then what are you gonna do with that patient well what's the right treatment and then where are they going to go afterwards

and how are we gonna monitor them in their future well after the pulmonary embolism response teams have started showing up throughout the country it's a much more streamlined process patient shows up with a knee to the ER at our

institution a page is sent out after they're seen by the ER team and that involves a medical team usually vascular medicine or the pulmonary critical care IR interventional cardiology if they're involved the critical care services and

whatever whatever service initiated that and then it sort of goes through that process where the patient gets gets a consult from a multidisciplinary team much like a tumor board and we make a general consensus in our institution

this happens within 30 minutes of the patient hitting the door at this point so there's no longer like a two or three-hour wait to make a decision it may not always be the right decision but if that patient for example gets worse

over there the next two hours if we decide we're going to just treat them with anticoagulation and oxygen and telemetry in 30 minutes they may get worse and then we have another call and we make another decision and then we may

say you know what push TPA or they need to come to IR to get a catheter based intervention and again dr. or sisters can talk more about this but it really helps us with disposition and treatment

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

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

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

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

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

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

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

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

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

used another main mainstay and PE

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

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

access reowww lytic thrombectomy or the angio jet device which is the most frequently used device for this what it does is basic disrupts the clot by shooting out TPA

embeds it into the clot and then you suck it up using suction thrombectomy using the venturi effect and you aspirate some of the clot and you can see that here that's a picture from I think the angio jet website the benefit

is that it can be you can use it without TPA and just use the suction thrombectomy mode with heparinized saline and that can be helpful to help break up some clot the drawbacks is that it has a black box warning from the FDA

so we do this every once in a while in the right patient but this is definitely not recommended by the company or anyone for that matter but it does work in some cases and the main reason is that the the vibrations caused by the device can

cause significant bradycardia in addition to the bradycardia that you get from red blood cell really lysis that you get with these devices so you actually couldn't cause arrhythmia on top of bradycardia which sounds like a

bad a bad combination and these patients can get hemodynamic collapse and die right on the table just cuz you turned on the device so that being said we've all I think done it once or twice I've seen I've only done it once and I never

do it again because a patient coded one of my colleagues did it on a patient because the patient was already coding said well what's the harm and that patient survived they did better actually because we were able to break

up the clot so I will say that if you do it and the patient doesn't do well you really don't have a leg to stand on because right on the cover of the packaging it says do not use in the pulmonary arteries aspiration

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

another device that's new in the market

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

all the thrombus is gone so what happens

after after years in these patients so I'm gonna kind of change gears here from acute PE to chronic PE and this is actually something that I'm very interested in is actually what happens

in these patients so chronic thromboembolic pulmonary hypertension or CTF which I'm going to say for the rest of the talk because that's a lot easier is really what happens in some patients whose pee never really goes away another

term you may hear is post PE syndrome but that's the same thing essentially so post PE syndrome or CTF occurs in about 3 to 5 percent of patients with acute PE and it's a it's higher in patients with recurrent PE so if patients have some

sort of blood clotting disorder where they keep getting a clot they may get CTF we have no idea as to who is gonna be the patient who's gonna get it so we don't know right now who the patients

are and that's sort of a focus in the cardiology and IR and hematology and sort of worlds to figure out who's gonna get post PE syndrome it's one of the leading causes of pulmonary hypertension and it's really under diagnosed because

patients just don't know so patient has a PE they go through the system they go they get discharged they're alive and well and then they just never recover they're still fatigued they're just really never able to get back to their

life they think it's you know that they have this chronic bronchitis again or common or frequent pneumonia it turns out that they have post PE syndrome or CTF and it's never been diagnosed so CTF has this very complex algorithm and it

involves a lot of different teams but a patient who has PE and clinical suspicion what actually has this walk-test so they walk down a hall which is a known length and it sees how far they can get on a sir

of time and that's the six-minute walk this these patients if they have a positive six-minute walk test which requires no intervention really they go on and have a VQ scan or VQ scan with some other sort of imaging if they's

find if these tests come back with findings suggestive of CTF then they get a pulmonary angiogram in a right heart catheterization for every patient because then you have to make a decision as to what you're gonna do

surgical treatment medical treatment or now an interventional treatment so this is a VQ scan I'm a board-certified radiologist and I am NOT an expert at reading these anymore but what you what you want to look at is that if there are

areas that look abnormal that don't match so in a VQ report you're looking for areas of mismatch which means that ventilate that the that ventilation is happening but there's no perfusion so we're looking for VQ deficiencies this

has a very high sensitivity for PE but not a good specificity it's a lot less radiation exposure than CT but as we all know in a patient who has a VQ scan for a qpe we're really not sure if it's real or not but in chronic PE a VQ is a gold

standard actually at least in the initial diagnosis after that you get a

CT scan frequently or they actually show up with a CT scan so I want to highlight the fact that this is different these images are different than the patients

who had acute pulmonary embolism I will say that it's very hard to kind of get this into your brain but they're very different so first of all they'll have a VQ scan that'll show that they have mismatch defects after that when you

look at the scan the clot has a different appearance before it was in the middle of the vessel it was surrounded by a rim of normal contrast here it's actually wall adherent it's irregular it's got weird weird angles to

it weird margins and then distally the vessels are very small in acute PE the proximal pulmonary arteries are enlarged because they're hitting they're enlarging because they're hitting a roadblock in here in chronic PE the

vessels shrink down and shrivel beyond it because there's chronic clot they're a lot like patients who have chronic DVT in their legs when you look at that sagittal view kind of think back to the original case that I showed you

you saw that sort of with clot there's a thin lines floating in the middle of the vessel here it's irregular it looks serrated it's gotten really weird angles so this is another example of chronic PE from the literature that believe it or

not is not mediastinal adenopathy it's not a patient with cancer it's a patient with chronic PE all that thrombus sort of lines the inner walls of the pulmonary arteries you can even have calcification just like you would have

in atherosclerosis also the vessels distal to the clot become shriveled down and that's a way to tell if that's chronic PE versus acute here's another example of a patient of the image on the left is the patient years or before and

then the image on the right is a patient with chronic thromboembolic pulmonary hypertension and then a few more examples showing you that it's usually on the side of the blood vessel rather than in the middle of the blood vessel

so if you want to know just an easy way if you see clot in the middle of a blood vessel it's probably acute if you see it on the side and along the walls it's chronic more pictures kind of just to put in your brain so the diagnostic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

thromboembolism n't it's very very complex surgery we have at our institution I think 15 cardiac surgeons

and only one knows how to do this because it requires a separate training pathway almost every surgeon in America who does this trained at least did a a time at UC San Diego or at MGH where the two big centers in the country

it requires bypass they patients are put on bypass for about six hours so you have to wake them up after that two surgeons who have a higher volume of this have much lower complications but the complication rate is up to 10% the

patients who are the surgeons who have the best complication rate are still at 4.5% so that's still pretty high

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

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

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

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

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

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

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

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

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

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

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

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

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

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

real briefly about medical therapy options there are a lot of different

options with a lot of fancy medications that have been studied the problem with these medications these patients are gonna be on them life long and their disease is never gonna get better it's just gonna get maintained so there are

multiple different classes of drugs and basically what they're all doing is causing vasodilation of the pulmonary arteries so a couple drugs that we I think many of us know viagra is on their sildenafil believe it or not that has

more than one use and this is one of the main uses pulmonary hypertension there are other drugs that were created specifically for them that are prostaglandins or guanylate cyclase stimulators which basically cause

vasodilation many of these have been studied for for many years and they're very expensive as much as $1 000 a day so that's pretty expensive insurance does cover them but they're expensive drugs with potential

side effects so I'm gonna finish off the

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

improvement so this is an example that we've treated at Michigan us a 67 year old female patient who has CTF she's gone through sort of a treatment she

turned down so she was not a good candidate for surgery because her disease is distally it's in the sub segmental branches so we went back and forth for you actually on this patient when we're

starting our program and decided that she would be the right patient to start she followed instructions she was her disease was severe enough that I was affecting her life she couldn't walk from here to the back of the room she

was on medication she didn't qualify for the surgery so we said she'd be the right wand and so we started with a pulmonary angiogram you can see there's disease it's not the worst patient that you would see because those would be

surgical but well you see those arrow heads there's areas of webs there's areas of occlusions and stenosis so she's got all the different types of pathology morphology would be great for treatment so what we did as we do in all

these cases get a wire across it if we can wreak analyze it we get a wire we never use hydrophilic wires that's actually contraindicated in these so you never use like a glide wire an O and a glide wire you never use a v 18 or any

of those types of wires because those have a higher risk of perforation frequently we actually use coronary wires from the inner from our colleagues in interventional cardiology you cross the lesion and then you balloon it with

a very very very small balloon so you do not want to get aggressive in these patients we start with a two millimeter balloon even if the vessel should be four or five millimeters we always start with the two millimeter balloon and you

can bring them back and do another intervention in a few months at without a larger sized balloon so in this patient we ballooned two branches in the right lower lobe and then this is what it looks like afterwards so you have

improved flow it doesn't look perfect we're not going for perfect we're going for profusion so if you think about that same thing with acute PE you're not going for a perfect image you just want to get perfusion distally and then the

body will figure it out afterwards so

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

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]

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