DrSclafani answers some questions

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Postby drsclafani » Thu Aug 18, 2011 5:52 am

Before I go on vacation, I would like very much to complete the case of the port stenoses. Not sure I can, but i will try. I have copied the prior part of the procedural report for those who havent seen it.

After completing treatments of the left internal jugular vein, the left subclavian vein and the left innominate vein. We are now in the third hour of this marathon procedure.

Catheterization of the azygous vein was performed, thankfully without major difficulties.
The image is below:

Image

I usually start by placing the catheter distally within the azygous vein and then withdraw toward the connection with the superior vena cava. This case suggests that there are possible problems with this methodology. Let me mention (to reduce confusion) that the venograms are displayed (going left to right) as follows: the first venogram performed, a series of IVUS images performed after venography (yellow arrows pointing to corresponding venographic locations), to a composite of the entire azygous and hemiazygous.

On the left, one sees irregular narrowing of the midportion of the azgyous. The corresponding arrow on the IVUS images shows a very narrow segment, smaller than the more distal part, that then enlarges as it travels to the IVC.

Note the very long arrow comparing two different images of the midportion. It seems to me that the midvein is larger on the right picture than on the left.

Note also that there is strong retrograde flow that results in contrast filling of the hemiazygous vein back to the left renal vein.

So i am left with a quandry. Is this midazygous narrowing artefactual, perhaps caused by spasm? or is it a real stenosis of collapse?

drsclafani wrote:The patient is a 52 year old female diagnosed with MS in 1998. She was originally diagnosed with RRMS but states that she never has classical relapses but rather mostly steadily progressive disease. She says that she has difficulty finding words sometimes but states that her memory is good. She has debilitating fatigue which exaccerabates symptoms such as difficulty swallowing, balance, tightness in her arm, coordination and spasticity.

She has had therapy with rebif, amantadine, LDN and in 2007 underwent an 18 month course of low dose cytoxan for MS administered through an implanted port.

The catheter was placed in the left transverse sinus.
Dural sinus venography looked like this:

Image

These images show that the transverse sinus and the sigmoid sinus had normal diameters. However there was a prominent connection between the transverse sinus inside the skull and the vertebral vein and posterior cervical branches on the outside. These vessels are connected by a very large emissary vein traversing across the skull via the hypoglossal canal. This canal is usually a very small opening in the skull but in this patient it is exceedingly large. I think this suggests that a long standing (perhaps congenital) outflow obstruction of the internal jugular vein has existed.

The catheter was then withdrawn into the internal jugular vein.
Venography looked like this:

Image

These images show very slow flow down the internal jugular vein. The majority of the flow is through collaterals involving the vertebral veins (yellow arrows). Other collaterals extend across the midline as well involving the face, spine and neck.

Note the failure of the contrast to exit the jugular vein.

The catheter was positioned lower in the internal jugular vein and the venogram was repeated. Then intravascular ultrasound was performed. Note the location of the probe in the upper right image.
Image

The upper left image shows the area of stenosis (black curved arrow). Minimal contrast exits the IJV; Collaterals are seen crossing the midline to opacify the External jugular vein (EJV), the vertebral vein (VV) and the subclavian vein (SCV). Other collaterals are seen in the midline.

The Left bottom image is an IVUS image at the level of the probe. The valve was persistently closed. The dense white tissue represents the valve tissue, thickened and immobile.

The image on the bottom right is another view. It shows a narrowed valve (double arrow). Dense tissue is evident on both sides of the arrow.



I rely upon IVUS to plan treatment of these stenoses.

Image

I rely upon IVUS to plan my treatment. I use it to decide what size balloon to use and where to position the balloon. These three images show the valvular stenosis and an image above (LEFT) and below (RIGHT) the valve.

I think that the valve is quite thick manifested by the brightness of the echoes on the valve. I think that a somewhat larger balloon may be necessary. So on the LEFT the vein measures 84 mm2 in cross sectional area. This is equivalent to a 10 mm balloon. Below the valve (RIGHT), the vein measured 102 mm2. That is close to a 12 mm balloon (113 square mm). That means the the minimum balloon I would use would be a 14 mm balloon which has a cross sectional area of 154 mm2.

That is a really big balloon to inflate on that upper jugular vein especially on the left side where there is a angle between the orientation of the vein and the orientation of the balloon.

So IVUS tells me that i need to position as much of the balloon BELOW the valvular stenosis.

In this case, the valvular tissue is thick and will require a strong angioplasty. I have included images above and below the area of valvular stenosis because they are important in deciding what size balloon to use and how to position it.

The image on the LEFT is above the injury. The cross sectional area is 84mm2. This is slightly larger than a 10 mm balloon. The image on the RIGHT shows the vein BELOW the valve.The cross sectional area measured 102 mm2, slightly less than a 12 mm balloon. So we surely will have to start with a 14mm balloon which has a cross sectional radea of 154 mm2. That is more than twice the cross sectional area of the vein above the stenosis. On the left jugular, because of the angle of the vein compared to the balloon, this is a bit riskier for dissection.

It because critical that I position this balloon so that the majority of the balloon is below the stenosis where the vein is of a dimension that can more easily accomodate the 14 mm (and possibly a 16mm) balloon.

This next sequence shows that decision in action.

Image

The uper row again shows the IVUS exam. The middle row (Left) shows the IVUS probe at the level of the valve stenosis. It is just below the second rib. I attempted to place the upper shoulder of the 14 mm balloon (note the black dot at the waist on the balloon) exactly at the valvular stenosis (MIDDLE). Unfortunately I cut it too close and the balloon slipped below the stenosis. (RIGHT) The balloon was deflated and repositioned.

The lower row shows the new position of the balloon. Thus there is a small amount of upper vein that will be subjected to a fairly large distension (double in cross sectional area). The waist on the balloon (indicative of resistance to dilation) was overcome with 18 atmospheres of pressure. The post dilatation venogram shows a really nice diameter.

Unfortunately, there was still slow flow....

But that is a story for another day

Any questions so far?
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Re: IVUS Images

Postby drsclafani » Thu Aug 18, 2011 6:02 am

NHE wrote:
drsclafani wrote:nhe

here is the answer from the manufacturer's engineers

Greg -
This question was more up my alley than Ross’s so he passed it over to me.

I spoke with Engineering about this and got the following:
The ‘length’ (in ILD view) is variable and determined by pullback speed, catheter stretch, or other movements in the vessel.
Within a single slice (tomo view), the wedge angle is fixed, but actual chord dimension will vary with distance.
Within a single wedge, (and this appears to be the dimension of interest) the distance is determined primarily propagation speed.
The average value is 0.138mm, our maximum tolerance values are 0.170mm upper and 0.074mm lower.

If there is more detail required (for instance research paper, etc.), let me know and I will get the answer out of Engineering.

Thanks
-Jim


I hope that this answers your question.


Dr. Sclafani,
Thanks so much for sharing that information. I recall reading about pullback speed and the image stacks in the IVUS Made Easy book, but had forgotten the details. The book is now back at its home library 2270 miles away. The dimmensions quoted above at 74-170 µm help to put images such as this into perspective. In effect, although it appears that we're looking down at the valve, we're really looking at a cross section through the valve.

Thanks again, NHE


I wonder what it is like to have a library 2270 miles from home. Thanks for the internet! It surely shortens the distance between your home and mine.

I think that the valve is larger than any one image, so there is a sequence of images at the valve as the probe is pulled through it. Some of the valve is not visible on these images because is it so thin and not holding still for the IVUS camera.
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Postby Cece » Thu Aug 18, 2011 9:10 am

drsclafani wrote:Before I go on vacation, I would like very much to complete the case of the port stenoses.

A well deserved vacation. May it refresh and restrengthen. There is so much yet to be done, when it comes to CCSVI! And you have done so much already. Thank you.
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Postby ErikaSlovakia » Thu Aug 18, 2011 9:33 am

drsclafani wrote:Before I go on vacation,...

Have a nice vacation and do not forget to come back :) We will be waiting for you :wink:
Erika
Aug. 7, 09 Doppler Ultras. in Poland, left Jugul. valve problem, RRMS since 1996, now SPMS,
- Nov.3,09: one stent in the left jug. vein in Katowice, Poland, LDN, never on DMDs
- Jan. 19, 11: control venography in Katowice - negative but I feel worse
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Postby MikeInFlorida » Thu Aug 18, 2011 11:31 am

drsclafani wrote:mike
do you have the image yet?

I made the mistake of requesting the entire packet. They were waiting on chart copies, etc. But they do have the images. I'm leaving to pick them up now. If ok, I'll email them to you, and you post the salient images. My wife also put your name on the "authorization for release" form (I'll email you a copy of that also).
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Postby munchkin » Thu Aug 18, 2011 2:38 pm

Have a wonderful vacation and return with renewed energy.
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Postby Cece » Thu Aug 18, 2011 2:57 pm

drsclafani wrote:Catheterization of the azygous vein was performed, thankfully without major difficulties.
The image is below:

Image

I usually start by placing the catheter distally within the azygous vein and then withdraw toward the connection with the superior vena cava. This case suggests that there are possible problems with this methodology.

Let me mention (to reduce confusion) that the venograms are displayed (going left to right) as follows: the first venogram performed, a series of IVUS images performed after venography (yellow arrows pointing to corresponding venographic locations), to a composite of the entire azygous and hemiazygous.

On the left, one sees irregular narrowing of the midportion of the azgyous. The corresponding arrow on the IVUS images shows a very narrow segment, smaller than the more distal part, that then enlarges as it travels to the IVC.

Note the very long arrow comparing two different images of the midportion. It seems to me that the midvein is larger on the right picture than on the left.

Note also that there is strong retrograde flow that results in contrast filling of the hemiazygous vein back to the left renal vein.

So i am left with a quandry. Is this midazygous narrowing artefactual, perhaps caused by spasm? or is it a real stenosis of collapse?

I am not sure what possible problems there would be with the methodology of placing the catheter distal and drawing it back. Is it that the catheter blocks the flow? The azygous is pretty small, in general.

Retrograde flow is taking the contrast to the renal vein, which is not the normal direction of flow. That would seem to indicate a problem.

You have not often seen a midazygous stenosis that is a legitimate one in need of treating.

Did you look at the possible stenosis in different stages of respiration?
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Postby drsclafani » Thu Aug 18, 2011 7:20 pm

Cece wrote:
drsclafani wrote:Catheterization of the azygous vein was performed, thankfully without major difficulties.
The image is below:

Image



Did you look at the possible stenosis in different stages of respiration?
there was no change in the diameter with respirationhowever, putting the catheter distally may cause spasm in the vein and the appearance of stenosis.
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IVUS measurements

Postby ttucker » Fri Aug 19, 2011 8:22 am

The IVUS measurements under discussion are a potentially direct means of determining any haemodynamic standing pressure waves created by venous obstructions. If such pressure waves can measured by IVUS, then through the application of computational fluid dynamics, the amount of hypertension in the area of periventrical lesions could be computed. If this hypertension is sufficiently acute to cause blood-brain barrier breakdown this would provide an explanation for the transport of iron and leukocytes into the cerebral parenchyma. It would also provide a means to estimate the amount of capillary bed ischemia, hence hypoxia, hence loss of oligodendrocytes and hence deterioration of myelin. Leukocytes meet weakened myelin and - voila - MS. If IVUS pressure waveform measurements (systolic and diastolic would suffice) could to be taken at a number of positions going up the vein (IJV?) with a measure of the distance from the obstruction, this could demonstrate that both neurologists and vascular scientists are right. It is an autoimmune disease, but its root cause lies in the venous obstruction causing acute hypertension in the BBB at the venule end of the bed.
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Re: IVUS measurements

Postby MikeInFlorida » Fri Aug 19, 2011 9:38 am

ttucker wrote:The IVUS measurements under discussion are a potentially direct means of determining any haemodynamic standing pressure waves created by venous obstructions. If such pressure waves can measured by IVUS, then through the application of computational fluid dynamics, the amount of hypertension in the area of periventrical lesions could be computed. If this hypertension is sufficiently acute to cause blood-brain barrier breakdown this would provide an explanation for the transport of iron and leukocytes into the cerebral parenchyma. It would also provide a means to estimate the amount of capillary bed ischemia, hence hypoxia, hence loss of oligodendrocytes and hence deterioration of myelin. Leukocytes meet weakened myelin and - voila - MS. If IVUS pressure waveform measurements (systolic and diastolic would suffice) could to be taken at a number of positions going up the vein (IJV?) with a measure of the distance from the obstruction, this could demonstrate that both neurologists and vascular scientists are right. It is an autoimmune disease, but its root cause lies in the venous obstruction causing acute hypertension in the BBB at the venule end of the bed.

Hi ttucker,
If I understand you correctly, you believe that, not only do venous obstructions increase the static venous pressure, but the resultant turbulence (from reflux) creates standing waves, the period of which could be measured with the IVUS equipment. Then using sophisticated mathematics, these wave parameters could be predicted (or translated into) the DCVs?

I love the standing wave idea, but measuring them in the IJV and using that to calculate the DCV wave freq and amp seems... prone to error (but I'm no expert on this).

Regardless, wouldn't it be great if the measurements could be made in or near the DCVs? I wonder how far into the (e.g. straight) sinuses you can safely put the IVUS, using the smallest available catheter sheath? Dr. Sclafani previously said that the sheath used for this patient was 10 french (3.3 mm)... are smaller sheaths available?

(edited: replaced my misuse of the word "harmonic" with "standing". Harmonic and standing waves are related, but not interchangeable.)
Last edited by MikeInFlorida on Fri Aug 19, 2011 10:56 am, edited 1 time in total.
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Re: IVUS measurements

Postby Cece » Fri Aug 19, 2011 9:51 am

ttucker wrote:The IVUS measurements under discussion are a potentially direct means of determining any haemodynamic standing pressure waves created by venous obstructions. If such pressure waves can measured by IVUS, then through the application of computational fluid dynamics, the amount of hypertension in the area of periventrical lesions could be computed. If this hypertension is sufficiently acute to cause blood-brain barrier breakdown this would provide an explanation for the transport of iron and leukocytes into the cerebral parenchyma. It would also provide a means to estimate the amount of capillary bed ischemia, hence hypoxia, hence loss of oligodendrocytes and hence deterioration of myelin. Leukocytes meet weakened myelin and - voila - MS. If IVUS pressure waveform measurements (systolic and diastolic would suffice) could to be taken at a number of positions going up the vein (IJV?) with a measure of the distance from the obstruction, this could demonstrate that both neurologists and vascular scientists are right. It is an autoimmune disease, but its root cause lies in the venous obstruction causing acute hypertension in the BBB at the venule end of the bed.

I like the ideas here.

Dr. Sclafani, would IVUS be useful in measuring pressure waveforms as Dr. Tucker is describing?

That last sentence - "It is an autoimmune disease, but its root cause lies in the venous obstruction causing acute hypertension in the BBB at the venule end of the bed" - leaves me hanging for what happens after that root cause (venous obstruction) is treated. Does the autoimmune disease continue or not....
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Postby ttucker » Fri Aug 19, 2011 10:46 am

Cece

My best guess is that when the capillary bed's blood flow returns to closer to normal, the BBB probably mends itself largely and progress of the disease either slows substantially or stops. However, the existing iron deposits, scar tissue and other damage remains. To me this means the earlier in the progress of the disease that venous angioplasty is performed the greater will be the impact of the procedure and the more normal life the patient will lead. If there have been a number of earlier serious exacerbations that have left many scleroses, a lot of scar tissue, a lot of damaged myelin and damaged nerves, the impact of "liberation", I strongly suspect, will be substantially less. In my view, the brain specialists, the neurologists and pharmaceuticals have a lot of work in front of them to come up with successful re-myelination schemes and a way to mop up the iron deposits. On this latter, I suspect it will be a challenge to find a chelating agent that can cross an intact BBB to mop up iron.
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Postby HappyPoet » Fri Aug 19, 2011 11:25 am

Here's a link to an article that discusses the idea of using IVUS to measure pressure waves in coronary arteries, and some of the broader ideas seem like they might also relate to veins:

http://www.cathlabdigest.com/articles/C ... confounder
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Postby ttucker » Fri Aug 19, 2011 11:37 am

MikeinFlorida

If you haven't seen it yet you might want to watch my 3 part Youtube called "From Stenoses to Fatigue and Scleroses". It provides some demonstrations of the characteristics of fluid pressure standing waves. Application of fluid dynamics to vein obstruction (for example, a thickened IJV valve) would mean that at various points along the vein the pressure excursions may be almost double that which is normal (large systolic to diastolic fluctuations) At other points there may be little fluctuation at all. So it would not be static pressure but at some points there could be localized acute hyptension - very dynamic. If you consider some typical values, an IJV might be 15 cm long and the average flow rate about 15 cm/sec. So it takes about one second for a pulse to enter the vein at the venules until it is reflected from the thickened valve and another second to travel back to the venules. If the pulse rate is 60 pulses/min or one pulse/sec the reflux pulse would crash into another one coming out of the venules, causing a point of acute hypertension. Applying Computation Fluid Dynamics (CFD) in order to match the pressure waveform distributions in the lower part of the vein would probably allow for a reasonable estimate of its value up at the venules.

To compute this in sufficient scientific detail things like the elasticity of the veins and surrounding tissue, the changing dimensions along the length of the vein etc. would have to be included. But with today's CFD technology, I am comfortable that reasonably accurate hypertension computations that could be applicable to estimating the amount of hypoxia and BBB disruption may be possible.
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Postby MikeInFlorida » Fri Aug 19, 2011 12:31 pm

ttucker wrote:you might want to watch my 3 part Youtube called "From Stenoses to Fatigue and Scleroses".

I look forward to it.
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