Upper extremity DVT|Upper extremity DVT|56|Male
Upper extremity DVT|Upper extremity DVT|56|Male
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thrombosis. There're different flavors of radio, probably get to see another one

later from my colleague Dr. Saad. History and physical, 56-year-old male, who had recent diagnosis of small cell carcinoma, with some mediastinal adenopathy, and a small subsegmental PE. And he was initially started on Lovenox with transitioned to Warfarin.

Not sure how they did that, although there was a known diagnosis of malignancy. But that's how it is, when they go into the, not away from the main campuses, they go to the suburbs. People don't know the importance of having these people on, low

molecular weight heparin, who's a known candidate with cancer, and use DBT. He later presented with left upper extremity swelling, and severe pain. Physical examination showed that, he had swelling all the way from his shoulder, down up to his hands. And he had severe pain associated

with that, when he presented to the emergency department. And for some reason, a counsel was not sent to us initially. And his INR, at that time of admission in the emergency, was 3.1. And the Doppler evaluation was done at that time, which had shown upper extremity vein, you'll see the findings, upper extremity veins, Doppler was done. And for some reason, he was started on oral anticoagulants,

they're not sure why it was done that way. But Pradaxa was started, thinking that, okay, patient was on Warfarin, developed this possible venous thrombosis. So somebody decided in the ER, start him on Pradaxa, so he was already on Pradaxa. He did not improve. And this was the left axillary vein,

color Doppler ultrasound imaging, which shows some hyperechogenic material within the auxiliary vein. it was similar in the brachial vein as well. Is not a good color flow throughward, and it was not compressible. So all the findings consistent with deep venous thrombosis in the upper extremity. So based on the findings in ultrasound, and when the counsel came

through finally, with his symptoms not getting any better, we planned for doing a mechanical thrombectomy, to remove the clot burden. Since he was already on Pradaxa, with it's half life being anywhere between 17 and 21 hours, and we still don't have prax buying the antidote that, to reverse in these people right away, although it's available now, and

it's approved by FDA in October 2015. So we were in a bind, how are we gonna do lysis who's already on Pradaxa, with history of lung malignancy, and you don't know what's his status in the brain? We were a little bit reluctant, to kinda of do lytic infusion, or use a lot of lytic straight away. So it was not done on the initial

day. We stopped the Pradaxa, changed him to unfractionated heparin, while he was in the hospital. Then realized that he had some, kind of hit with some thrombocytopenia developing. He was changed to Argatroban. But once he came

to us, we did an angiogram through the left basilic vein, which was still patent, and a venogram was done. And initially, we did some mechanical aspiration thrombectomy with the CAT6, we didn't have CAT8 at that time. Like I said, we decided against lytic infusion catheter through the clot, because the effect of Pradaxa had not worn off.

This is the initial images. Here you can see access from the basilic vein. The initial angiogram showed that ready appearance, of the left basilic continuing as the axilla. And then the central veins were something like this. There's irregular eight years of filling defect within the vein. And then some irregularity

in this area, and a large filling defect in the left brachiocephalic vein. Here you can see the CAT6, going through the separator coming right here, We worked on for it for quite some time, without much improvement of

the appearance of the clot, in the central veins. You have to believe me, the actual CT sections did not show any mass lesion right here. There was some mediastinal adenopathy,

but there was none around the left brachiocephalic vein, to explain for this. So it was not just extrinsic compression causing this whole problem. It's cancer induced thrombosis, but he was symptomatic, so you're trying to help him

to relieve the clot burden. So once we did this on the first day, and Pradaxa was stopped there, we didn't do a lytic infusion. We were able to clear, most of the clot from the axillary region. And then at the end, only some part of the left brachiocephalic vein, and little bit in the subclavian vein

remained. Further work the next day, things seems to have gotten better. And at this point, he was off Pradaxa. We did an Angiojet pharmacal mechanical thrombectomy. At this point, since he was off Pradaxa for more than two days, we were a little bit more positive. And we did a little bit of lytic in a

pulse-spray fashion, with up to 68 milligrams here, and it cleared out more clot. And finally, this part in the left brachiocephalic vein, was very difficult to just suck out the Angiojet. We didn't have the ZelanteDVT at that time. So what we did was, we managed to use a cleaner, and hopefully because of the fact. that it was a little

bit soft. And although it didn't come out, with the help of Angiojet only, it kind of cleared, and the patient got better with that. And we were able to operate up completely. So now for the samp question. Which of the following is a finding in the setting of deep venous thrombosis?

Choice A, a non-compressible vein on ultrasound evaluation. Choice B, no detection of flow on color Doppler. Choice C, filling defect on direct venography. Choice D, presence of multiple enlarged

collateral veins. Choice E, is all of the above. Time starts here. [BLANK_AUDIO] Okay. everybody got it right, hurray, 100%. Okay, that

was a simple question. So little bit about the upper extremity DVT. Catheter-associated upper extremity DVT accounts for vast majority. So I'm talking here, only about the secondary forms of upper extremity DVT.

There is a primary form which you already know, it's a Paget-Schroetter. The secondary forms, it results mainly from indwelling central venous lines or portacads/g, and less frequently from pacemaker or defibrillator leads. Systematic screening however in these patients, reveal thrombosis in up to

two thirds of cancer patients, with central venous catheters. And patient-related risk factors include the presence of cancer, especially ovarian or lung adenocarcinoma, presence of distance metastases, and also a history of thrombosis or thrombophilia in these patients. Cancer

related upper extremity DVT, even in the absence of central venous catheter, it is usually the cause of secondary upper extremity DVT, because there are cancer-induced prothrombotic states or venous stasis, resulting either from venous compression, or from some kind of infiltration as the contributing factors.

So early thrombus removal and restoration of the patency, it aims at reducing the risk of post-thrombotic syndrome in these patients. And catheter-based therapy is recommended for patients, with proximal upper extremity DVT of recent onset, and with severe symptoms, and in patients who have low risk of bleeding complications with a good functional status.

the specific treatment options available in IR specifically, starting with sclerotherapy.

Sclerotherapy closes off a malformation by injecting sclerosant into the sacs filled with the venous blood or lymph until the sacs collapse and so this will be direct puncture of the malformation. Sclerosant irritates the vessel wall resulting in clot formation.

The clot stops blood flow through the vessel and the inflammation of the inner wall will destroy the vessel, which the body will replace with scar tissue. Patients often do require repeat treatments to block all of the abnormal vessels.

We do expect that the area will swell and the patient will have pain once the treatment is completed which is good to know, you know, when we go to discharge them. We expect this to swell, often it'll become a lot larger than it was before, which is completely normal.

Swelling typically lasts about three to five days post treatment and then often times it's treated and the patient may go several periods of time without needing to come back. So I'm going to talk a little bit about the sclerosants that we use at UNC for treatment,

starting with venous malformation sclerosants, we use STS, Bleomycin and Ethanol. And the mechanism of action generally speaking of all sclerosants, they damage endothelial cells leading to inflammation and fibrosis. Effect depends on the concentration of sclerosant used

and contact with the endothelial cells, they are generally bound to blood proteins rendering them ineffective. The process to treat venous and lymphatic malformations is very similar and there is overlap in the sclerosant that may be used. So STS is three percent sodium tetradecyl sulfate.

Mechanism of action, it causes direct endothelial cytotoxicity, it disrupts the cell membrane causing thrombosis, leading to occlusion of the injected vessel. The benefits of using STS, less swelling and neuropathy and no cardiac toxicity. It's minimally invasive and generally safe and effective,

but we have to talk about possible complications. And I will preface this by saying that I have not seen any of the complications that I will show you, but, you know, if they extravasate or, you know, get into surrounding tissues it can cause skin ulceration.

If it's, if you're doing arterial access it could cause necrosis, DIC and swelling. Swelling we are going to, you know, obviously be particularly careful with our patients that are having like the tongue sclerotherapy, so. All right, the next sclerosant is ethanol,

we use 100 percent ethanol which, again, causes direct endothelial cytotoxicity, disrupts cell membranes, denatures proteins, causes a thrombosis, it's pretty effective and inexpensive. Possible complications, a lot of the same kind of stuff, ulceration, especially with

arterial access, microemboli, DIC, swelling. Bleomycin is another agent that we use, Bleomycin is an antineoplastic and an antibiotic agent. It inhibits DNA, RNA and protein synthesis, it's pretty inexpensive and it's got well known effectiveness, minimal

and controllable side effects. Because it is an antineoplastic we obtain this from our Chemotherapy Pharmacy and you need to use, you know, precautions because it is a chemotherapeutic agent. So when you're handling it and delivering it

you just have to use those precautions. Possible complications, fibrosis, alopecia and you can see there is flagellated hyperpigmentation. This is an actual patient that we treated, this is the lip venous malformation. She was treated with Bleomycin and this is

a picture of her five days status post the sclerotherapy with the Bleo. Mom was concerned about the swelling which we looked at the pictures and we said this is completely normal for it to swell like this after treatment.

You don't want it to continue past, you know, a week and a half or so. Lymphatic malformations use many of the same sclerosants as in venous. Macrocystic we use Doxycycline, STS and Ethanol, for our microcystic we'll use Bleomycin,

I've already discussed STS, Ethanol and Bleo. So Doxycycline is an antibiotic that inhibits protein synthesis, causes direct endothelial cytotoxicity, mitochondrial level cell death and it's generally safe and effective. And we have a patient here that was treated,

he was the lymphatic malformation that I showed you earlier that had the giant neck malformation. And he was sclerosed with Doxycycline and you can almost not see that it was even there. Possible complications with Doxy, skin necrosis, neurotoxicity and neutropenia.

And just generally speaking with our sclerosants, any one of them can cause skin necrosis because, especially when we're dealing with superficial malformations, if the sclerosant diffuses, causes extravasation, if you have arterial penetration or direct injection into the artery or use of a tourniquet.

So basically the physician just has to be very careful when they're injecting the sclerosant.


This is another example. This is a complex aneurysm. This is an aneurysm that's actually involved the common trunk of the SMA and the splenic artery. So we can't embolize the splenic artery. That's not a good thing.

This shows you a lot of teaching points, a lot of technical teaching points about the management of these complex aneurysms. So this is a complicated... This is a complicated aneurysm. It involves the common trunk of the SMA and the celiac axis.

So the plan is, we need, going down low, is actually the SMA, so what we need to do is to embolize the splenic artery, proximal as possible, okay, to allow as much collateral as possible to go to the spleen. Do a stint graft from the aorta into the SMA to exclude the aneurysm and then thrombose it.

The embolizing material in this case, plugs, it could be coils as well, would do the same principle of preventing back bleeding into the aneurysm. So you're kinda seeing all these principles being put together in this complex procedure.

So the first thing, we went up to the splenic artery and we embolized it with plugs, okay and that's kind of embolized, and then we went into the SMA and put balloon expandable stints and excluded the aneurysm. Here you see the aneurysm with the eggshell calcification,

see this anatomy perfectly, almost on the dead lateral. We put the stint grafts. On our follow up CT, the aneurysm had shrunk partially thrombosed, but still there is still more flow in the aneurysm. So this most likely kind of like a type 1 endo leak

into the aneurysm. The patient was on Plavix and on Aspirin. So technically, what you can do is to put another stint proximally and close that kind of type 1 endo leak. What we chose to do is actually stop the Plavix and stop the Aspirin, just stop it,

'cause they're anticoagulants, stop it for a month and follow up CT. That helps actually thrombose it. Okay so instead of subjecting a patient to another procedure, you just stop the Aspirin and Plavix for a month. Maybe that's enough to help it thrombose.

Then resume the Aspirin and Plavix, and that's all we needed to do is just stop the Aspirin and Plavix. Kind of several technical and medical teaching points

And the etiology of this is numerous, it's diagnosis of exclusion, it's diagnosed in less than 1.5% of liver transplants in the United States and Japan. For some reason it is diagnosed at 25% in Germany, so somebody's overcalling it and somebody's undercalling it.

Over the years, I can tell you, 10 years ago, most transplant surgeons in the United States did not believe in it. Now they're believing it more and more, they're calling it more and more. It probably is happening in 1-2% of transplants

in the United States, not 25%. This is a perfect example where the hepatic artery is open, the hepatic artery is so slow that the actual splenic vein catches up with it. The splenic vein actually catches up with the flow in the hepatic artery.

That's how slow and stagnant that hepatic arterial flow is. Your differential diagnosis is a fistula. It's that there's a fistula between the hepatic artery, that's kind of differential diagnosis. However, this is truly a splenic phase. You see the spleen.

Contrast has gone right through the spleen up, down the splenic vein and caught up with the hepatic artery, so this is a true, slow flow in the hepatic artery in a transplant. Initially, we thought that the best way to deal with this is to actually embolize the spleen and there are two types.

There's a GDA spleen, and a splenic artery steal. So there's a GDA steal, which is even rarer, and a splenic artery steal. So initially we thought that the best way to deal with this is just to embolize the spleen, because this is splenic steal.

The spleen is stealing flow from the hepatic bed. Simple, simple thought process. Embolize the spleen, or embolize the GDA in case if it's a GDA. But it's actually a lot more complicated than that.

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