PE (Submassive), Pulmonary Infarction|Thrombolysis (Catheter-directed)|60|Male
PE (Submassive), Pulmonary Infarction|Thrombolysis (Catheter-directed)|60|Male
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this is a case one. A 60-year-old man with hypertension CAD presenting to ED with disorientation. In the setting of progressive exertional, shortness of breath and chest pain over the past week.

PE particles CT was obtained, shows bilateral central thrombus extending into the lumbar vessels. Bilaterally there is also an infarct in the pear/g segment to the right lower the lobe. Taking a look at the heart here so obvious left axis deviation measuring from endothelium to endothelium,

or however you do it really. There's a mercury elevated RV to LV ratio. Just reviewing the AHA criteria for submassive PE, this patient had a submassive PE, not only on CT, but also on echo where there

was RV dilation and evidence as to start this function. And there were also EKG changes consistent with RV dysfunction and evidence with myocardial necrosis, with an elevation of [INAUDIBLE]We elected a D catheter directed thrombolysis. These are the initial agiographic images.

Redemonstrating the CT findings of central colladics/g and low volume/g and segemented vessels bilaterally. The initial PA pressure was a mercury elevated. We kept the catheter on the right side and 24 hours later, the central heparine/g had essentially resolved.

There was a little bit of, not occlusive thrombus really in sentimental vessels in the- and also the lopa/g vessel and right lower lobe. PA pressure was improved. We swung the catheter over to the left side,

to consider continuing thrombolysis but we found that the central [UNKNOWN] had also essentially improved there. With the exception of the segmental thrombus in the left of her lobe. So, given these findings and also symptomatic improvement of the patient,

we decide to stop on the second day there. The patient had an echo on the third day that showed reduction in RV size. Normalization of RV systolic function from baseline. And also PA systolic pressure improvement from 67 to 29. Patient was discharged on the

fourth day on anticoagulation and remained asymptomatic at four

Okay, next case. 60 year old male, history of multiple vascular surgical procedures, he had aortobifem, a couple of fem-fems,

a couple of fem-pops on both sides and had multiple thrombectomies performed. But never thrombolysis. This is an amazing case. This guy had actually extensive vascular history but never had an angiogram. I don't know why went for all this.

But I think it was actually Hopkins. I know, amazing. So he presents with very little information first of all, and cold legs with right more so than left but obviously it's thrombosed, something centrally.

We They did come with an outside CT luckily but unfortunately not much else. So we really didn't have much idea about his surgical history. And this can be challenging obviously. This looks similar to the other case but it's a different case but it's a different case. But that proximal end looks pretty similar.

This case of course both limbs are thrombosed. And I think in In this case you can make a pretty strong argument for surgical thrombectomy probably, right? This guy has an aortobifem, both of them are down,

there's a fem-fem below that. So one of this probably chronically down cause you've got a fem-fem So there he's got a couple of fem-fems there. All right, brilliant And then as you go down he's got like three

grafts on the right and a couple on the left. This is totally absurd right? Yeah. [LAUGH] So what do you access?

>> [LAUGH] >> Any ideas? >> [INAUDIBLE] >> Send him away, exactly. >> Stick the fem-fem. >> How do you know which one is the bad fem-fem? Palpation?

>> Yeah, well with ultrasound you can often see what's more acute. >> Right. >> Right? So the echogenic one is probably more chronic right?

So that's what we did. We ultrasounded, got an idea which fem-fem is more acute and stuck it. Oh wait, sorry. I've one thing before the CT scan. So as you it go it down,

you can see that obviously he's got all these grafts that are all occluded apart from this one here that looks it comes up a profunda and it goes down. And this thing is actually patent and then comes then and touches down the AT. So that's the amazing thing about vein grafts. When you get a good vein graft,

those things are really good. And this thing stays open despite this incredibly poor inflow. So yeah. We stuck the fem-fem. This is the angiogram. But we stuck the fem-fem here going in this direction.

And I'm not sure why we went in that direction, probably because his right leg was worse. This was easy so it's not clearly acute. We were able to catheterize the aorta easily, do an angiogram and you see that obviously the aortobifem limbs are both down.

And I'm assuming the left is the down chronically and this fem-fem was placed at some point. And then you see a lot of collaterals reconstituting the profunda, and then here is the proximal anastomosis of his vein graft of a profunda branch. It's pretty amazing. And that looks actually pretty good

And the AT is up below that. What was interesting about this guy is that he didn't seem to have a lot of pain. It was out of proportion with his vascular findings. I don't know if that was just from multiple surgeries maybe.

So in this guy, we lysed. And I had nothing to do with the fact that it was 4:30 in the afternoon. So we stuck a catheter in there, one of those long Uni-Fuse catheters. I tend not to use Ekos in the arterial system,

and yeah we've discussed thrombolysis I guess, right? Came back, looks pretty good, right? So this limb is all opened up. I mean thrombolysis works great.

If it weren't for thrombolysis, we couldn't do any of this stuff, right? So this is open, this is open. It's got some strictures here, but all in all pretty good apart from the outflow on the right.

So obviously now we're gonna redirect our access down the right leg and see what's going on, right? So we get into the profunda branches and get the A Jet out and start buzzing around a little bit, trying to find the connection to that bypass.

We end up ballooning here. And then that kinda opens things up and now we can see this branch which gives off that bypass. And in the interim what's funny is we've started filling some of these old fem pops, which look all degraded.

I mean I considered embolizing that. That doesn't look so good, right? >> [LAUGH] >> And on this side, this all looks pretty good, apart from

one little dislembles/g that we had which is very annoying. So we went after that and I think we might have used A-Jet or aspiration, I'm not sure but it ended up here. So as you can see this is open here and now it's occluded the distal anastomisis. So we went back down with a Spider, and I did my swat spider thrombectomy

trick, which is where I deploy a Spider below the lesion and then pull it back. And sometimes this works and you can actually pull out. And this is one of those cases that I actually pulled this out and got lucky, and he has a patent AT below that.

So we ballooned the distal anastomosis, got a decent result that reconstitutes peroneal, I think that is. And then we did end up actually getting access going in the other direction to work on the left side. So it's fairly a lengthy case.

And we haven't seen him since, so who knows what happened to him. >> Back at Hopkins. >> Back to Hopkins for some more surgery. And here is the seg and non-invasives. This is pre and post, so pretty much what you'd expect right? [BLANK_AUDIO]

Okay, questions? >> [INAUDIBLE] >> I think he was on anti-coagulation. Yeah. But I'm not entirely sure. But that's a good question. Like how do you treat these? I prefer not to give anticoagulation if possible and just go with antiplatelet.

But sometimes, a lot of patients guys who come back every year and get lysed get the same stupid ex-fem or whatever lysis and stuff. They end up basically being on anticoagulation and dual antiplatelet and they still come back so yeah.

ask the question. Anybody here feel comfortable looking at a 12-lead EKG raise your hand. Good. For those of you who are not comfortable how many of you actually get a chance to

look at it before you actually get into the room. For those are going to STEMIs. And answer is probably not too many. You can predict what the doctors going to need by looking at that EKG. So that's the part of the reason I'm going to go over

this. Beyond the fact it's really cool because I'm a cardiologist. So this is a 12-lead EKG and I'm just going to go over these are the limb leads and these are the precordial leads. And fundamentally the leads tell us where

things need to go. So this is in your handout don't take any notes. Um just look. So the inferior wall... the red... supplies the back of the heart most of the posterior descending artery. And if you see changes in the EKG PQRST

wave the ST segment is where we hinge our therapy. So the lateral wall which is in blue... is actually not well seen out here... but it's on this margin right here. The anterior septum which is yellow here is in these leads v1 and v2 this is

the precordial leads. The anterior wall... so this is where usually the money is if you will cause of survival vessel... involves this green area here. Its the front of the heart the left anterior descending. So when they talk about the

"widow-maker" this is it. Lateral wall again is blue which is a little bit more of the lateral margin. Somewhere between green and red...I'm sorry green and yellow is going to be the other blue.

Ok so you're like I really don't understand that. Well let's take a look at some EKGs. So

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.

>> 65 year old female who in 1998 had hysterectomy. Her left iliac vein was ruptured. It was ligated by the surgeon because they could not repair it.

So she had extensive left lower extremity DVT. She was put on anticoagulation and compression for 12 years. She couldn't stand at the stove for more than five minutes, couldn't play with the grand kids, she was very very miserable.

And here she is. Here's this actualization looks great. However, at the pelvis it occluded and you can see that there is a clip right here. So we were actually able to get through the femoral vein, do the

EKOS overnight, serial dilated and stented centrally and got this very ratty irregular femoral vein. However, the flow was very brisk. Here she was essentially open. Five years out she has a normal coactive vein.

She's extremely happy. She no longer wears compression stocking. She does treadmill cycling, very rare, minimal symptoms at all and her villalta score went down to a two. And here's her Doppler study.

Again these veins recover, they remodel, they become normal coapting vessels. So the goal here again is to establish direct inline flow, you wanna get from the calf to the thigh, thigh to pelvis, pelvis to the

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