Budd Chiari Syndrome|Budd Chiari Syndrome|80|Male
Budd Chiari Syndrome|Budd Chiari Syndrome|80|Male
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The second case, quick case. It's a old man, 80 years old. virus C, he had a TIPS two years ago

and now he starts developing a small ascites for three months. And he had a new episode of bleeding, endoscopy showed that it was a hypertensive gastrophaty. All the ultrasound that he performed showed patent tips, that this tip was patent.

So we decided to evaluate the stent, through the angio suite. Through the jugular approach we could categorize the hepatic vein here, we inject. But it was really impossible to get into the stent. The angle here is not

good, so we inject here. We can see it on stasis of the contrast. We cannot see the outflow of the hepatic veins and we try to introduce stent without success. We try to frame our approach and again we cannot enter the stent. We can't put through femoral or jugular approach, it was really impossible

to get into the stent. To check if the stent was really open we did an injection, there's a leak/g trunk. Here's the spleen vein, here's the portal, and here's the TIPS.

Again we see the images of the hepatic veins here, the same image but we cannot see very well the outflow from those veins. So here we could not understand what's going on, and we decided to measure the gradient and see that it was working like a Budd-Chiari

syndrome. The stent is against the wall, against the top of the wall of the vein, and it's blocking the outflow of the hepatic veins. So what to do?

We cannot enter the stent as I told you, cannot enter through jugular or femoral approach. So we think about to put a stent here, just a stent through the right vein to the cava, or we decided to make a transhepatic puncture of the

right branch of the portal vein, and put a wire here to the right hepatic vein, and is [UNKNOWN] to the jugular and we withdraw everything and make a through-and-through technique. So now we have the guidewire going through the jugular and the transhepatic approach.

Now we can put a balloon here. We put a 10 millimeters balloon, this image is after the angioplasty but we see that stenosis/g are very important [UNKNOWN] so we decide to put a stent. We used an express 10 millimeter stent, a balloon expandable stent, and here is the final image. We have no more hepatic veins and the shunt is working properly.

So the patient had a good recovery. I also stopped bleeding, it was a successful case. Thank you very much. Unfortunately the system does not work. I'm sorry. Thank you. >> [APPLAUSE]

Randomized trials... I'm not going to go

through all those that we looked at... but here are a couple of big ones. So ACT 1 was a interesting trial in the fact that it was done on acceptable risk patients. And I hate the term low risk because if you have a carotid lesion you're not low

risk for anything. So acceptable risk for surgery patients. And the bottom line is CAS - carotid stenting - clearly established as a safe and effective procedure. And I think the shift really was away now from and that's why we're here today

talking away from carotid stent vs and endarterectomy. But can we actually optimize carotid stent outcomes. So can we pick the right patients to do carotid to offer carotid stenting to. And here's the composite endpoint for years not

statistically significant obviously between CAS and CEA. But remember again composite endpoints in all of the stroke in all the carotid stent trials include stroke death and myocardial infarction. Because if you take the MI picturing

out of it carotid endarterectomy is clearly a... excuse me... if you take the MI out of it carotid endarterectomy clearly has a lower stroke risk. So the other big trial was CREST. Looking at again

endarterectomy vs stenting and here again is your composite endpoint of death stroke or MI not statistically significant 5.2 vs 4.5. Primary endpoints equivalent. But again all strokes at 30 days were significantly

higher in carotid stent cases. And that continued out to 4 years. So equivalent if again if you add MI into it. But again this is now a technology that continues to improve and the progression of EPD or embolic protection devices has gone

from distal protection... so here and you know there's seven or eight of these filters now available... to proximal protection. This is a big device that you have to get in and occlude the common carotid

artery so you have no antegrade flow as your protection. And then what is the newest and I suspect is probably going to stay transcervical access with flow reversal which were going to talk a little bit about. Again to show

you the embolic risk is the big issue. And there is a 2x peri-procedural stroke rate for transfemoral CAS when you compare to carotid endarterectomy. So if you look at stroke 4% in the

transfemoral CAS group. 2.3% in the CEA group. And the peri- procedural stroke in patients that are over 75 look what happens here and we're going to talk about why. So the in the endarterectomy group a little bit

higher but not much but in the stent group goes up very significantly. And here's the the bottom line day 0 stroke is the culprit. If you make it through the procedure without a stroke you're probably not going to have one or

a very low risk and not much different than endarterectomy. But here's the issue so its procedural embolic strokes that were trying to avoid. So how do we

complications because these are some of the things that I do believe that you all help us with. And I will say that the one thing I love about the cath lab that it's really it is a team.

I mean I can't do what I do without you all and the honest truth is that if you move into the admin world when we talk about standardization of care right that reduction of variance. The only way we really do that is we do

that with the sonographers the technicians those in the cath lab those in the in the CAT scan. We standardize care actually through you all. It's actually because the doctors do what doctors do right. You know they

can't... three doctors in a room and we get four opinions because they keep changing their mind. And so the fact is that we standardize care specifically in this instance reducing complications actually with you telling us that something is

going on. So there are there are three things that I want to talk about. One was the high risk contrast induce nephropathy. So we know that nephropathy can be defined by a

number of different ways but the ACCNCR - the American College of Cardiology Cath Registry - defines it a 0.3 rise and the creatinine. Which is actually I'm gonna tell ya not very much. Most people believe that if it's a twenty-five

percent rise its significant. But the highest risk patients interestingly enough... acute coronary syndromes chronic kidney disease volume depleted low cardiac output diabetics heart failure older patients hypertensives - this is the STEMI

patient. This is the STEMI all the...all factors. So what do we normally do well. We we prevent it with hydration we prevent NSAIDS we wait 48 hours for another

contrast load right. Because this is the ED did a CT scan already careful catheter wire manipulation. And guess what happens in a STEMI all that's out the door. We have no chance to pre hydrate we don't get a chance to stop

their Motrin or their Feldene that they took beforehand. And we are rushing to get this stuff done. So things are going very quickly. So STEMI patients unfortunately have a greater than two-time risk for having contrast-induced nephropathy. So

there are a couple of ways which is IV bolus therapy up front. Again sodium bicarb is not. But this is actually what I've been talking to the cardiologists about. Is that if you measure the filling pressure of the heart and I realized

most of you are not in the coronary world. I'm trying to get you here... talk to me.... is that we can bolus it based upon a measurement of intravascular volume and it will reduce the risk of contrast-induced nephropathy. So and there

are some guidelines for that. Obviously you want to minimize the bolus if they're volume overload but notice how there's still a volume bolus. And the reason is the heart is stiff after an acute MI. Pre-procedure high dose statins which

is actually part of our protocol is what we do. There is a maximum contrast dose that I'm just going to quickly go over. And I'll just tell you basically it's... there's a couple ways of calculating it... but probably the easiest way is if you know their

GFR are you can calculate that. There are there are levels at which point you should not exceed. There are weight-based contrast loads but it's not as accurate as the GFR right. Because if somebody is big and has a creatinine of 1.5 or

2 you can give them more contrast but that creatinine of 2 usurps their weight. So isn't just weight based. It should be based upon a GFR. And I will tell you unfortunate you go from risk of 6% if you go two and a half times to greater than

35% if you give them the maximal contrast dose. And I'll tell you the 5mL per kg we do that commonly. And I'll say that's probably more of a problem in the peripheral vascular world news in the coronary world. Ok access site complications that was a

great segue Dr. Vignen. Thank you. Basically yeah we get these ugly things that look like that. But we don't get that with radial access site... radial access. I'm not going to cover this. you all know how to get great access.

Unfortunately this is still a pretty common problem right. They hit the SFA they go to the external iliac. Its a problem. Hematomas retroperitoneal bleeding pseudoaneurysm. The rate of these are

actually still pretty high regardless of what kind of closure device you use. Closure devices unfortunately do not affect the rate of access site complications. A retroperitoneal bleed is going to occur regardless of what

kind of closure device you use. So radial site... radial artery access I won't cover that because that was covered by the last lecture... that was a great segue by the way... There is a bias against using radial arteries in the acute MI setting. And

that mainly is because we are under the gun for time. So if there is a conflicting interest. I wish there was going to be change in that there probably will not be. Abrupt closure dissection. Usually it's at the

balloon or stent edge. And I will tell you that it's not as obvious as it appears sometimes to the cardiologist because they are looking... and actually this is probably true across the board... this is really targeted therapy. You look at

what was bad and you look at what you did and you don't look what happened upstream or downstream. So this is where you want your eyes can really help us. This doesn't project really well but i'm going to I'm just going to tell you. This isn't

is going to project well. Okay so this is the initial lesion. This is the final. Unfortunately there's a problem right. Right at the take off of the septal and the diagonal ... it looked normal before... it doesn't look normal now.

So the doctor I am looking right here I go awesome high-five let's get out of the room. And there's something wrong right there. It's very easy to miss. You know where

you're going to figure this out. 30 minutes later when the patient occludes the artery they come back. So it's also actually... oh yeah so see I missed even in my own slide.. and so downstream here this caliber of the artery

is smaller than it was here. So there's a problem. It's easy to miss. And again I think part of it is because you know doctors being paged. They've got two other things to do and you know they're hungry. Actually we're all hungry. They gotta pee.

And then the next thing you know you're ready to get out of the room but there's a problem. So there are a couple of things. If you see something I want to hear something doesn't look right. One of the

hardest things is that when you're doing this and you're under the gun we don't do a lot of the quantitative measurements that we do do. I know the IR world you guys do a lot of quantitative measurements. How many times have you

seen a cardiologist actually say go out and measure that. The answer is none. Because it takes too long. Marginal dissections are very common the problem is it tends to occur at the edges.

It's not where your eyes are going ok. I'm going to move ahead because I'm at 9:58 yeah I'm gonna go right past here. So I'm going to tell you that intravascular ultrasound is actually one of the answers to this. Again it takes time and

skill. The other thing is if you you see something this is kind of what I want to hear is what do you think about that distal edge you know the flow is not as normal.

It doesn't look like it did before. That edge is hazy. Those are common findings that we tend to see after the fact. So we're reviewing this and it's some conference and almost always there is a clue. The question is can you get it ok. So

dissections and... I'm sorry... acute thrombus tends to occur with dissections. So you know you balloon an artery and it may look ok but unfortunately in this artery this is the first picture and then all of a sudden the artery disappears. So this is

the pre stent and then the artery is down. This abrput vessel closure usually in the stent is acute thombus. Inadequate anticoagulation or suboptimal expansion of the stent is the most common cause.

So when this happens unfortunately you don't want to ever want to lose wire right. Keep that wire down there. There's a tendency to kind of say things look really good and just start yanking everything out. And everyone starting to

feel that right because it looks good enough and so you start pulling out stuff. That's usually a problem. You have to reevaluate the degree of anticoagulation. And there's a variety of

different ways to do that. Its in your handout. Its 10 o'clock. Okay I know that was

next three hours we would probably just go over all these trials if that's okay. So

obviously a lot of time and effort has and a lot of money has been spent by industry to actually look at this. And so the question is why are we still talking about this and what happened to carotid stenting. So if we

can take a lesion that looks like this which I would venture to say that most surgeons would not be anxious to approach this lesion because it goes for a very long distance high up in the internal carotid. And if you can make it

look like this why are we still talking about carotid stenting and what happened. So here's the reason. Because this is what these things look like from the inside and all surgeons know this and it

makes us nervous to put a wire and a balloon and a stent through this. And so embolic protection is the holy grail for carotid stending. And it's why we're still talking about it why is not completely replaced endarterectomy. So

current treatments really for carotid stenting... this is kind of what you all see. There's a little basket here a filter and here's a stent coming to treat this lesion. So there is a less invasive alternative. It's

patient-friendly and durable as proven... I'm sorry i keep getting wrong button... as proven in the CREST trial. But there is clearly still excess procedural stroke risk. So when you look at endarterectomy vs stenting even though

the overall risk when you add MI into the picture is equivalent. The stroke risk is clearly higher with stenting. So because the procedure itself can create thromboembolism and we're going to talk about that.

What causes peri-procedural stroke which is the real issue. Well traditional carotid stenting from a transfemoral approach requires several steps that can create and embolic risk. So you have to advance the

catheter from that femoral artery through the arch and if you follow me this catheter now potentially scraped off plaque from this arch disease into the left subclavian and the left vertebral so there's the first brain

artery at risk. When you're trying to treat a right carotid so left vert it then went by the left carotid so there's a second artery it went into the innominate which could theoretically then embolize the subclavian and the

right vert so there's a third one and here's your target lesion. So all four vertebral... all four cerebral arteries are at risk when you do a trans-femoral stents. And that's been proven in the trial so navigating and then the

last is you actually have to get through this lesion with your protection device before you have protection. So embolic

principles of vascular trauma. Makes sense right. Stop the bleeding and

restore perfusion to the affected anatomic distribution. You need to be able to diagnose this rapidly provide stability repair or ligate the affected blood vessel. Sometimes that still requires open direct repair and that's

usually where there's large contaminated wounds. Bypass can be offered to that patient depending on the particular clinical situation. We had several patients in Iraq who were Iraqi National Army and Iraqi police

forces that we were working in conjunction with and they didn't have the capability of transporting those all of those soldiers to Germany or back to the United States. So we had to do definitive bypass procedures for femoral popliteal

typical vessel injuries that they encountered. And of course endovascular repair using stents and of course coils to arrest bleeding or covering injured vessel which have started to become you know more commonly used. Of

course you know coils more commonly than stents and that's primarily because you know you can stop bleeding with the coils the stent's not always capable of stopping things with multiple injuries. This says your battery is very low seven

percent. I don't know I just didn't want to die out on us. Moving on general principles of trauma always start with your ABC's airway breathing circulation. Establish your large-bore IV lines external compression and touriquet

application. We look for soft signs and hard signs we call them of arterial injuries. Those are clinical...basically clinical identifier is that can tell us are there potentially a vascular injury. Because

you know you have an injured soldier who is hypothermic acidotic has you know multiple bullet wounds or shrapnel injuries. You don't know could you have hit an artery maybe maybe not. But obviously it's

paramount for us based on certain things to go ahead and diagnose that. And we treat everyone like they have one until we rule it out. You get the appropriate imaging where capable in level 3 and level 4. Or level 3 and higher we have a

CAT scanner. We have some sort of digital subtraction angiography to be able to diagnose these types of injuries and that's where it becomes important. Questions. Is this blunt or penetrating

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