DrSclafani answers some questions

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drsclafani
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Re: DrSclafani answers some questions

Post by drsclafani »

Cece wrote:
drsclafani wrote:pelopidas
thanks

why should we treat something that is not constant. afterall, venous drainage from the jugular veins is absent when the patient is erect.
My understanding is that jugular flow is not absent when erect, but reduced by 90%?

Have you ever seen a patient where muscular compression is the only problem? No valve issues or hypoplasias or anything but muscular compression? I am guessing this is an unlikely scenario.
i wont quibble about the ten percent., normal flow of 375 ml per minute going to 37.5 ml is pretty big drop. But those phasic narrowings are probably physiological. . wearing a tight collar might slow the flow down a lot. i think there is a difference betwen o bstructions and these types of compression.

i hav epersonally not seen such a condition. One could argue that in the absence of valvular stenosis causing obstruction, these compressions might not even be visible.
Salvatore JA Sclafani MD
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Re: DrSclafani answers some questions

Post by drsclafani »

Cece wrote:Ok, that is a surprise! There is flow in the jugular but it is upward flow. Wrong direction. Such are the tricks our CCSVI veins play....

It's reminiscent of the subclavian stenosis that we saw previously, which was due to chemotherapy damage. This would appear to be an innominate vein stenosis. With no chemotherapy in the patient's history, perhaps it is due to a thrombosis. The guidewire and catheter were able to access the vein, so it is not a full occlusion. Treatment options would be ballooning followed by a stent?

I am presuming that during the prior procedure this stenosis was missed. The other possibility would be that the innominate vein stenosed after that procedure.
There are a few obstructions of the innominate vein. The first as you quickly mentioned is traumatic stenosis after catheterization. Another is a tortuous innominate artery compressing the vein against the clavicle and sternum. That is my bet.

treatment is stenting and angioplasty. I am likely to deploy the stent first and then do angioplasty.

i think it is likely that the innominate obstruction was missed and this was probably the reason that a stent was placed in the IJV.
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Re: DrSclafani answers some questions

Post by Cece »

drsclafani wrote:i think it is likely that the innominate obstruction was missed and this was probably the reason that a stent was placed in the IJV.
And now the stent in the IJV has intimal hyperplasia and needs to be managed. :(
Unnecessary stents are the worst. Right after migrating stents and occluded stents. Third worst.

And the innominate is another vein that can be compressed, to the patient's detriment. Are there any other compressions to think about? Renal vein compression by the aorta, iliac vein compression by the iliac artery, azygous compressed by the aorta, muscular compression of the jugular, carotid artery compression of the jugular, innominate vein compression by the innominate artery.
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Re: DrSclafani answers some questions

Post by NZer1 »

Hi Team,
Something that Cece said earlier reminds me of discussions we had way, way back.
If we are looking at Jugular flow and other veins that are draining when we are lying down, what are we working towards fixing?

Is the symptom group that is improved by PTA caused by problems when we are asleep? Sounds rare or pointed, but we have to look at the bottom line here!

The PTA is effecting a group of symptoms that occur when we are certain body postures, in the same way that Dr. S is showing us that head position is effecting flow.

Is all of this symptom group and maybe other symptom groups based around our body position and the physical body itself. If we have vein design, skull design, trauma, injury, and a host of other factors such as diet and environment combining at times and in such a way that there is an outcome that is loosely called MS?

Are these symptoms caused in an on off sense, that we affected by body position, time of day etc, etc?

Because none of us are effected or affected by the same treatments and remedies is there a need to also focus on 'upright posture' before there is a 'full' understanding?

Food for hungry minds,
Nigel
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Re: DrSclafani answers some questions

Post by NZer1 »

I put a survey on this site a while back about when do symptoms become obvious, trying to define if there was a time of day for RRMS people, unfortunately there was little response.
I was interested to hear if RR people have a moment in time when they notice the onset of a relapse or more correctly a change in symptoms.

If we are working with veins that have a purpose related to body position, are we also looking at symptoms and a connection to body position and or time?

Regards Nigel
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Re: DrSclafani answers some questions

Post by NZer1 »

The differences that are happening from PTA treatment are IMO a clue to fluid function within the brain.

The capillary bed that is being stressed and leaking across the BBB by reflux would not recover that fast to see symptom improvements on the table. Over time and I have no idea how long, there would be changes to the issues caused. I would assume that lesions would be a visual effect of BBB leakage and to some degree, some of our permanent symptoms would occur because of lesion and axonal damage.
So I would consider this to be one type of our multifactorial disease.

The second effect of PTA that seems to be overlooked or misunderstood is the changes in fluid flow and the corresponding pressures in and around the skull. Changing the flow of blood is directly changing the flow of CSF and the function of CSF.

Brain cushioning and brain position is dictated by CSF as well as the skull design. If you change fluid flows in the brain you are re-positioning the brain in its capsule. If the brain is contacting the skull, or the brain stem is in contact with the foramen magnum because of lack of CSF cushioning you will have immediate symptoms and these symptoms I believe are what we are hearing about immediately after PTA.

From a multi-factorial point of view I believe this concept stacks up and the use of Upright MRI and ways of monitoring CSF will give a wider understanding of what is happening with PTA treatments.

CSF has many functions that are not well understood and it is hard to test the necessary pressures and flows.

Dr. Flanagan has spent years studying this and I think he has many insights to PTA outcomes as well. Getting all minds together is getting the learning further, the involvement of Trev Tucker, M Beggs has been an excellent example.
Re-involving Frans Schelling may be another winner.
The work of the Fronar team on Upright MRI is discovering outcomes relating to CSF and MS as we speak so they would be starters for a think tank as well.

Enjoy you weekend, I will,
Nigel
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Re: DrSclafani answers some questions

Post by NZer1 »

And I must add a special heartfelt thanks to Cheer for her incredible work and time commitment. Finding and posting the volume of articles and writing about them as well as communicating to the world on her findings is a huge amount of effort.

Thankyou Cheer.

Nigel
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Re: DrSclafani answers some questions

Post by Cece »

I think the impact of CCSVI on cerebrospinal fluid is underexplored, and will remain underexplored, until more neurologists see evidence of the significance and/or existence of CCSVI and get working. We need more Dr. Salvi's.....

Questions for Dr. Sclafani: It would seem that three stents are indicated for this patient. Compression of the innominate and compression of the renal vein are not treatable by balloon alone, so that's two stents, and a stent inside the stent in the jugular might take care of that intimal hyperplasia. But is it true that this particularly charming, lovely, and kind patient did not want stents? In such a situation, would you balloon the innominate or renal veins anyway? Or is the benefit not worth the risk? I know renal veins can be treated surgically instead of endovascularly; can an innominate vein compression be treated surgically? I don't know that I would want that option, but it is good to lay out the options.
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Re: DrSclafani answers some questions

Post by Cece »

here is where I got the figure 10% for jugular flow when upright:
http://www.medscape.org/viewarticle/522597_3
Valdueza and colleagues[45] used color-coded duplex sonography to measure cerebral venous outflow in 23 healthy human volunteers, and found that internal jugular flow decreased from 700 mL/minute in the supine position to 70 mL/minute at 90° elevation. They also found a corresponding increase in vertebral vein flow from 40 mL/minute at 0° elevation to 210 mL/minute at 90°, with the remainder of the unmeasured flow probably passing through the internal vertebral venous plexus, which was inaccessible to Doppler measurement.
I find it fascinating....
When upright, when you subtract out 70 ml/min going through the jugulars and the 210 ml/mn going through the verts, you are left with about 400 ml/min going through the internal vertebral venous plexus.
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Re: DrSclafani answers some questions

Post by drsclafani »

Cece wrote:I think the impact of CCSVI on cerebrospinal fluid is underexplored, and will remain underexplored, until more neurologists see evidence of the significance and/or existence of CCSVI and get working. We need more Dr. Salvi's.....

Questions for Dr. Sclafani: It would seem that three stents are indicated for this patient. Compression of the innominate and compression of the renal vein are not treatable by balloon alone, so that's two stents, and a stent inside the stent in the jugular might take care of that intimal hyperplasia. But is it true that this particularly charming, lovely, and kind patient did not want stents? In such a situation, would you balloon the innominate or renal veins anyway? Or is the benefit not worth the risk? I know renal veins can be treated surgically instead of endovascularly; can an innominate vein compression be treated surgically? I don't know that I would want that option, but it is good to lay out the options.
i think that this illustrates the problems of extrapolating one situation into another. I am finding it particularly difficult to educate patients of differences between the jugular vein response to stenting to other areas such as the iliac, the renal veins that have consistent persistent and high flow and seem to have better outcomes that stents in the jugular vein.

In this particular situation reluctance also involved financial considerations as well as the fear factors.

We will have to see how she responds to the two angioplasties that were done and go from there. This is, after all, a lifelong effort
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Re: DrSclafani answers some questions

Post by Cece »

The patient would also have an accurate diagnosis now, of both the innominate stenosis and the renal stenosis. That is a very important something gained.

All our knowledge as CCSVI patients is of stents used in jugulars. Extrapolation is normal, even if in this it turns out to be wrong. How to educate on the difference.... To take it back to the plumbing analogy, if you have a pipe that is running 24/7, it will sweep away debris. The flow itself will keep the pipe walls healthier. If you turn the pipe down to a trickle for 16 hours of every day, debris might build up. And these are fancy flexible pipes, that collapse together when turned off....

I am not a plumber, so that is my best attempt!
(edited to add: it's a poor use of the word 'debris' ... makes it sound like plaque build-up, when I meant platelets or clotting build-up ... analogies are hard.)

edited to add: With the first image of the jugular that you showed us, with the contrast going upward instead of downward, were there any clues there that we could have picked up? Was the flow stronger than it should have been for reflux flow? What were you expecting when you then released contrast within the stent? By the time you released contrast in the subclavian, did you have the mystery solved and what you saw confirmed what you expected, or was it still coming together? You have now seen two patients with stenosis in the innominate or subclavian vein, that we know of. Are these veins that CCSVI IRs need to be aware may be involved and, while maybe not necessitating routine checking of these veins, are there any obvious indicators when the IR should check these veins? When the catheter is going through the innominate, and there is a compression, does that affect the catheter's progression through the vein so you can detect the compression stenosis at that time?

Lots of questions because I'm finding it hard to express the main point, which is: how hard is it to make this diagnosis? What could the first IR have done differently to have caught this one, or to catch the next such one? If a patient has had chemotherapy or dialysis, should that be an automatic indicator to check the subclavian and innominate veins? I know this patient hadn't had chemo, but the prior patient with the subclavian stenosis had.
Last edited by Cece on Mon Dec 19, 2011 8:50 pm, edited 2 times in total.
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Re: DrSclafani answers some questions

Post by JohnAm »

Dr S
If jugulars are (severely) stenosed do You see any pattern in the collateral veins from head and neck?
Is there any general discernable pattern in the vertebral venous plexus, emissary veins, or other veins in that case?
Can You see this on US, fluoroscopy or IVUS and if so how clearly?

Thanks.

---
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Re: DrSclafani answers some questions

Post by munchkin »

Dr S

If the jugular has scar tissue and a stent is required will the risk of intimal hyperplasis be higher due to the damage to the lumin or will the damage to the vein inhibit endothelial growth over part of the stent causing more concern with clot formation? Sorry if I am using the wrong terms.

Thanks
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Re: DrSclafani answers some questions

Post by drsclafani »

Cece wrote:The patient would also have an accurate diagnosis now, of both the innominate stenosis and the renal stenosis. That is a very important something gained.
edited to add: With the first image of the jugular that you showed us, with the contrast going upward instead of downward, were there any clues there that we could have picked up? What were you expecting when you then released contrast within the stent?
that was a clue. Once I saw contrast flow upward, the next issue was to define the abnormality in the stent. One could expect intimal hyperplasia to be the culprit, or perhaps thrombosis. So the next step would be to pull back the catheter and inject the contrast in the stent. I admit i expected the stenoses to be in the stent, but once i saw the size of the lumen filled with contrast media, i knew it had to be more proximal toward the chest. My first thought was that there was a membrane at the bottom of the stent. The next step was to pull back a bit more and see where the contrast media went. It obviously wasnt going back toward the heart!.
Was the flow stronger than it should have been for reflux flow?
absolutely! one never sees reflux above an obstruction, something was wrong.
By the time you released contrast in the subclavian, did you have the mystery solved and what you saw confirmed what you expected, or was it still coming together?
The subclavian venogram was icing on the cake.
You have now seen two patients with stenosis in the innominate or subclavian vein, that we know of. Are these veins that CCSVI IRs need to be aware may be involved and, while maybe not necessitating routine checking of these veins, are there any obvious indicators when the IR should check these veins? When the catheter is going through the innominate, and there is a compression, does that affect the catheter's progression through the vein so you can detect the compression stenosis at that time?
I think anytime i see slow flow AFTEr performing venoplasty, i must check the more central veins. Some IRs study these veins all the time. I am not sure they are wrong.
Lots of questions because I'm finding it hard to express the main point, which is: how hard is it to make this diagnosis? What could the first IR have done differently to have caught this one, or to catch the next such one? If a patient has had chemotherapy or dialysis, should that be an automatic indicator to check the subclavian and innominate veins? I know this patient hadn't had chemo, but the prior patient with the subclavian stenosis had.
i think we learn from these cases. but i think the diagnosis should have been made before reaching me..
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drsclafani
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Re: DrSclafani answers some questions

Post by drsclafani »

JohnAm wrote:Dr S
If jugulars are (severely) stenosed do You see any pattern in the collateral veins from head and neck?
Is there any general discernable pattern in the vertebral venous plexus, emissary veins, or other veins in that case?
Can You see this on US, fluoroscopy or IVUS and if so how clearly?

Thanks.

---
Great question. I am finding that the primary diagnosis of stenosis is usually made from the venogram with IVUS finding some of the cases missed by venography. i think that the collaterals are pretty unpredictable. It will depend on the volume of contrast media and how hard one injects that contrast media. The more, the more likely one will see collaterals.

I am not looking for them in particular. IVUS often shows large branch openings on the wall and this is a good sign of collaterals.

The emissary veins are very interesting. they are the most common large collateral that i see. However, having never seen them in normal patients because i did not do any dural sinus venography before this. The books say they are 1-2 mm in diameter normally. A lot of patients have veins that are much bigger.
Salvatore JA Sclafani MD
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