This Is MS Multiple Sclerosis Community: Knowledge & Support

You are indeed fortunate that your thrombosis was able to reverse itself while on coumadin. Often, occlusion of the jugular vein is a permanent thing. You might not have had such an outcome if this vein had been the second vein treated rather than the first one.

I think that the ultrasound examination is the best screening test. Cheap, accurate and to the point.

Now you want to know how much flow there in within the vein? I would personally want to perform a venogramto assure that the vein interpreted as the IJ, actually was the IJV. Sometimes collateral vessels get quite large and may look very much like the internal jugular.

If the vein is narrowed significantly, I would try angioplasty with the expectation that a stent might be needed.

What possibly could be causing all the thromboses that we hear about. I wonder what percentage of patient treated develop IJ thrombosis.

I know that the cases of thrombosis that i have been involved with come in two forms.1. Overdilation of veins and very high pressures in relatively normal veins. Choosing vein diameter is much more precise using IVUS. I havent had a thrombosis since changing my procedure. The other association is with thrombosis resulting from treatment of hypoplastic veins. That is the reason that I have backed off aggressive treatment of hypoplasias..

Outside of your practice, is it common or uncommon for ccsvi IRs to image the azygos in different angles like this?

My patern has been to develop hyperplasia within 6-8 weeks each time. You choose to installed 2 layers of mesh stents inside my actual stents over ONE covered stent. Why? there must be some disadvantages to the covered stents.
Is there enough room to insert a covered stent? that would make it 4 layers?

I ask my question here for the benefit of other patients with similar problem.

Thanks for answering my question.
I guess what you're suggesting to me is that I should have a venogram done if I'm not satisfied with the US interpretation and the results I recieved with the procedures I had done. I have a feeling that an 18mm balloon was probably bigger than what should have been used due to not having the accuracy of IVUS, thus possibly causing the thombosis that occurred. When I looked at the before and after size of the LIJ, it looked quite larger after the first procedure. I'd post them with snagit, but don't know how to.

So far, what percentage of patients are you finding with azygous stenosis?

Forgive me if you've already talked about this, but I am curious if you have found a pattern in your own procedures that correlates with disability. You mentioned about 25 percent azygous abnormaility. Do you find that azygous dysfunction means more severe disability? Or that particular patterns of abnormalities correlate with patterns of disease/disability? Or even recovery or procedure effectiveness?

I'm sorry if I'm throwing too much into one post here. It's so exciting to think anything might make sense in this crazy disease. Thank you for any insight.

i havent noticed anyone speak about it.
That azygous is a real challenge. We have talked about it before.

i used to do 0 degrees, 20 degrees, 70 degrees, 90 degrees until i had a decent understanding of which views offered the most information.

My standard routine currently is to perform an inhalation breathhold, AP view to look at the ascending portion of the azygous vein. I do an upper and a lower view trying to see the entire azygous, hemiazygous and connections to the renal vein. Then I do a 70 degree oblique. With a 70 degree oblique, i do not h ave to raise the arms above the head. It is good in about 90% of cases in seeing the entire arch of the azygous and giving a second view of the ascending azygous. If either the anterior or posterior arch is not well visualized or obscured by superimposition, I will do a 90 degree view. that usually suffices. Then I do IVUS because I do not trust the venogram 100% in most cases.

anticoagulation and antiplatelet therapy could help.

Intimal hyperplasia may result from endovascular intervention, vascular surgical procedures, long term vascular catheters and devices, or turbulent flow. It is not infrequently seen after angioplasty, stent insertion, around long term venous catheters, and at surgical vascular and graft anastomoses. Re-stenosis occurring 3 to 12 months after angioplasty is typically due to intimal hyperplasia.

Stenosis from intimal hyperplasia is often difficult to treat. Unlike soft atheromatous plaques, these stenoses are firm and require prolonged high inflation pressures to dilate with a balloon. The stenoses often recur; repeated dilatation causes repeated intimal injury and perpetuates the intimal healing response.

First, only a 1cm section went back to the position where it was before the operation, then a month later the IR told me that the full length restenosed. I do not know how I can find out it is a recoil or hyperplasia.

Do you have any images to post?
It's odd to hear it described as a '1 cm section' and then the full length. It does not sound like the IR was considering this a disease of the valves, since he is talking about the full vein. Do you know if he ballooned the valves? Since small balloons were used, recoil would seem like a strong possibility. Most hyperplasia cases that I can remember have involved stents.

Now, I hold out more hope for dr Sclafani's approach with ivus. I still do not understand why others do not use it, it sounds a brilliant idea.