Carotid & Vertebral Ultrasound: Beyond ICA Stenosis - HD

Introduction

Hi, my name is Corinne Duan.

I'm a radiologist practicing at the University of Southern California in Los Angeles at the Keck School of Medicine.

And today I'm going to be speaking about carotid and vertebral ultrasound beyond ICA stenosis.

My talk is dedicated to Carol Middlestead, who was a pioneer in ultrasound and a true visionary, and also a pioneer for women in medicine.

Goals and Objectives

The goals and objectives of this talk include reviewing a spectrum of abnormalities in the carotid and vertebral arteries, including congenital and acquired diseases and iatrogenic changes.

We're also gonna be correlating ultrasound with MRI, CT and angiography whenever possible.

Waveforms in Carotid Ultrasound

Now, first, running out with the waveforms.

It's important to remember that each part of the carotid ultrasound has a distinct waveform.

So the CCA, the common carotid artery can have a very variable waveform of appearance.

It's typically a combination of a high resistance and lower resistance waveform.

The ICA and the vertebral artery are low resistance waveform because you want increased diastolic flow going towards the brain.

The ECA, because it's supplying the external part of the face and other structures and more superficial structures, has a high resistance wave form.

Carotid Consensus Statement

Now we all know about the carotid consensus statement that was published in 2003 where we correlate the degree of stenosis with the peak systolic velocities and the visual plaque estimate of the internal carotid arteries, the I-C-A-C-C-A ratio and the end diastolic velocity parameters are additional, supplemental or secondary parameters.

But the key parameters are the velocity and the amount of plaque that we see.

It should be noted however that the I-C-A-C-C-A, peak systolic velocity ratio can be very helpful if we can't obtain accurate velocities.

And we need to look at velocity ratios.

Case Example: Bulb Stenosis

Now look carefully at this case.

So here's a case of a longitudinal image.

We have flow in the common carotid artery extending to the left carotid bulb, and we see an area at the junction where there's some narrowing, maybe about 50% or so if you kind of gauge it on a longitudinal image and you have some color, a aliasing in indicating some turbulence.

When you look at the ICA waveform, you see that there's some delay in systolic upstroke, and this is shown as tardis parvis waveforms along the mid ICA and the distal ICA as well.

And the peak systolic velocity is somewhere around 40.

Now, it would be pretty unusual to think that it's close to 50% stenosis would be causing this much of a tardis parvis waveform.

So let's interrogate a little bit further.

So we look a little bit further, and we see that the distal CCA waveform and the left carotid bulb wave form look fairly normal.

However, there's markedly elevated velocities close to three 50 for both.

So why is that the case? Why are the velocities so elevated?

When we look at our transverse image of the bulb, we see that the bulb fills completely or does it.

Now we look at another transverse image of the bulb and we actually see that the bulb is predominantly occluded with just a little bit of trickle flow.

And the area that we saw of aliasing was actually corresponding to the very peripheral portion of the bulb, which had a little bit of flow while the rest of the bulb was essentially occluded.

So this is actually severe or critical bulb stenosis.

Now again, we initially looked at the transverse image to say, oh, it looks like there's about 50% or so narrowing of the junction of the distal CCA and carotid bulb.

Remember that this is the pitfall.

The long axis measurement of stenosis may actually overestimate or underestimate stenosis because you're not actually going through the middle of the vessel.

When you look cross-sectionally, you can actually see that most of the vessel, like we saw before, is thrombosis with just a little bit of flow peripherally.

And we correlate this with CT angiogram.

The original bulb image that showed patent bulb flow was here at the cord beefy portion of the bulb.

But at the proximal portion of the bulb, you see that there is actually very severe narrowing, almost a string sign appearance, and that's also shown here on the axial view where most of the bulb is thrombosis with just a little bit of trickle flow.

So we could have missed this severe stenosis had we not paid attention to the waveforms in the ICA.

So again, very important to look at the waveforms.

Plaque Characterization

Moving on to plaque characterization, we usually stratify plaque as being stable or unstable or homogeneous versus heterogeneous or homogeneous, calcified and then heterogeneous.

So homogeneous plaque can be mildly hypoechoic to echogenic and is typically stable.

Calcified or mixed plaque is either soft plaque that's calcified or completely calcified plaque, and that is also stable.

And here are two examples where we have a soft plaque.

It's fairly homogeneous.

There's a little bit of heterogeneity in it, but it's overall fairly homogeneous.

We don't see any ulcerations in there and we have a nice smooth border.

We also have here a calcified plaque, which is going to be stable.

Now, when we see more heterogeneous appearance or more complex appearance, we really have to be careful because if we see koic foci within the plaque, that may indicate an unstable component such as intra plaque hemorrhage, a lipid or cholesterol deposit, and can also indicate ulceration.

So in this longitudinal image of the ICA, we see that there's some irregular echogenicity along the proximal ICA, but we really don't see well what's going on.

When we apply color doppler, we see that there is actually a reversal of flow and any a reverse flow that's going into this area of plaque.

So here's the entire area of plaque, and here's an ulceration.

This is actually unstable, meaning that this person is at higher risk of a thromboembolic event.

Sometimes if you don't see the plaque very well, because a color artifact can bleed over the plaque.

If your machine has B flow capabilities, I encourage you to use it.

Here you can see there's a little bit of blood flow under cutting a plaque indicating that there is some ulceration component and there's a blood flow coming inside or behind the plaque a little bit.

So this is an unstable plaque.

String Sign

Now, the ultrasound equivalent to a string sign, we have severe stenosis here of the proximal ICA and we have elevated velocities of approximately 230.

And the string sign, if you recall, doesn't necessarily have to mean very high velocities.

It could be anywhere along the low velocity to high velocity spectrum of for severe or critical narrowing.

And we have the angiographic image showing focal very high grade stenosis.

ICA Occlusion

Now, here's a patient who went on to develop ICA occlusion.

So here in the bulb we have a lot of calcification, we have a little bit of flow by color doppler, and then beyond that the ICA is occluded.

That's also shown on our angiographic image.

This patient actually had a left MCA distribution stroke.

Now what else happens when there's ICA occlusion?

Well, the contralateral side can develop increased velocities.

So here the right ICA is occluded beyond the proximal portion.

The left ICA demonstrates elevated peak systolic and diastolic velocities due to compensatory flow.

What else can happen in ICA occlusion?

Well, the CCA on that same side can become what's called externalized.

What happens is the CCA flow is diverted from the ICA to the ECA and because it's supplying the external vasculature, it has a more high resistance component than it did previously.

Similarly, you can also develop internalization of the ECA, which means that the ECA will develop more of a low resistance waveform with high diastolic flow if it is serving as the major collateral to the intracranial circulation.

Pitfalls in Velocity Assessment Post-Procedure

Now, what are some pitfalls that we encounter with looking at velocities post carotid endarterectomy or stent placement?

Well, because we have surgically altered the carotid or endovascularly altered the carotid, their velocity thresholds may change and it's important to look for change over time in these patients, not an absolute value.

For example, when a patient has had a carotid endarterectomy, because the plaque has been scooped out, the wall may demonstrate increased compliance, maybe softer, easier to move, and also may have a larger diameter.

As such, the peak systolic velocity that can be obtained in that vessel is going to be lower.

Therefore, you may not reach a threshold of 1 25.

If you have recurrent plaque in the ICA, that's significantly ed.

Your velocities may be in the 100 range or 105 range, for example.

So you have to look at what the velocity is and look at the change over time.

Conversely, with stent placement, this, a stent will essentially decrease the compliance of the carotid vessel, which makes higher velocities than expected.

So your peak systolic velocity for stenosis may actually, your threshold may actually be a lot higher.

For example, it may be 150.

There are articles in the literature even going up to 2 75 as far as having a threshold for stenosis post stent placement.

So again, establish a baseline and look for change over time.

Other Velocity Pitfalls: Bradycardia, Tachycardia, Arrhythmia, and Low Cardiac Output

Other pitfalls include patients with bradycardia where because the heart rate is slow, there's a higher blood volume moving through, and as such, your peak systolic velocity may be higher and your end diastolic velocity may be lower.

That is the example we're showing in this case of patient with bradycardia very slow heart rate has an elevated peak systolic velocity of 1 44.

Conversely, with tachycardia, the opposite happens where you have less blood volume and your peak systolic velocities may be lower.

If you have a patient with an arrhythmia trying to measure the peak systolic velocity after the most normal cardiac cycle.

So if you have a very irregular heart rate or heartbeat, it may be hard to measure the true peak systolic velocity, but just try to figure out what is the most normal looking waveform I can see and measure off of that.

If that's not possible, then you know, measure the peak systolic and end diastolic like you would, and you may end up having to use the rely on the ratio a little bit more than you would have otherwise.

Similarly, in a patient with low cardiac output as we'll see soon, you may not generate high enough velocities to indicate stenosis.

So again, the velocity ratio may be a better bet as far as estimating stenosis.

So again, we know that the primary parameters of velocity and plaque for significant stenosis exists.

And in critical stenosis the velocities may vary.

But with CCA stenosis, we don't really have good criteria.

There's a lot of variation in the literature as far as how we can assess CCA stenosis and one theory is that we can look for change in the peak systolic velocity of 50 to 75% across a lesion to assess for CCA stenosis, it should be also noted that CCA stenosis is 15 times less common than ICA stenosis.

Case Example: CCA Stenosis

So here's a an old case that is from my chairman which has left proximal CCA elevated velocity of 250 centimeters per second.

And in this case you see a lot of spectral broadening.

And the ICA though in the mid CCA, there is a delay in the systolic upstroke.

It almost looks like a little bit of a TARDIS parvis or perhaps early TARDIS parvis waveform with a delayed systolic upstroke with a mid CA velocity of 32 centimeters per second.

The contralateral CCA though on the right side has a normal systolic upstroke normal CCA wave form of 70 centimeters per second.

But when you look on the angiographic image, you can see that severe CCA stenosis to account for the initial high velocity with spectral broadening that we see proximal to a stenosis and the delayed systolic upstroke that we can see distal to a stenosis.

Here's another case of a CCA stenosis, and here's the plaque formation that can cause some aliasing.

As we see in this vessel, the most common cause of CCA stenosis is atherosclerotic disease.

However, trauma fibromuscular dysplasia, tassos arteritis and radiation therapy are also contributors.

Bilateral Abnormal Waveforms: Global Diseases

Now, what are some things we can look at as far as assessing when our waveforms are abnormal bilaterally?

So a global disease, something that is affecting the entire body.

What are some diseases that can affect the waveforms bilaterally?

So here's a 46-year-old male with ischemic cardiomyopathy, ejection fraction of 10 peak systolic velocity left less than 40.

When we look at the right ICA and left ICA waveform, they're pretty irregular, and the velocities, as we said, are less than 40.

So why is this the case?

When we look at the chest x-ray and we see massive cardiomegaly, this patient has low cardiac output, they simply can't generate enough volume to have a velocity peak systolic velocity of over 40.

And also, because of the low cardiac output, their waveform is abnormal.

Here's a patient with high velocity in the proximal right CCA of two 60, mid right CCA of 200 distal CCA velocity is normal.

But looking at the waveform, there was a delayed upstroke in the mid CCA and the distal CCA and we had similar findings on the left side.

This patient had an MRA neck, which showed no caratitis stenosis.

So what could be causing this appearance?

Well, the patient has a murmur, and it turns out that this is related to aortic stenosis.

So if you have delayed systolic upstroke in the common carotid circulation, especially if it's bilateral, explore for the possibility of a murmur, possibly aortic stenosis.

Here is another case where we see bilateral TARDIS parvis waveforms in the right carotid and vertebral circulation, and also on the left side again consistent with the history of aortic stenosis.

Here's another patient who has basically a systolic notch, or this called mid systolic retraction evidenced by the or pointed to by the red arrow.

This entity can also be seen with cardiomyopathy.

However, on the ultrasound, there was no evidence of stenosis.

The patient does have a murmur and the yellow arrow had that you're seeing as a normal dichotic notch.

So what can cause this quote, mid systolic retraction?

This entity is called puls serrin and it's related to aortic insufficiency.

So this appearance, if you see this, think aortic insufficiency and in other cases may be related to cardiomyopathy.

Here's another patient who has rapidly reversed early diastolic flow, so-called water hammer pulse.

This is related to more severe aortic insufficiency, so again, more severe from the case that we saw earlier.

Here's another patient who has bilateral tardis parvis waveforms.

In the CCA, we previously mentioned that this can be seen with aortic stenosis, but in this case, the patient has an aortic dissection, and that can also cause the bilateral TARDIS parvis appearance.

In this patient we have variable systolic peaks.

In the ECA, we have inconsistent peaks.

We have high and lower systolic velocity peaks.

Also in the ICA this patient has pulses ultras, basically the peak systolic heights are alternating and it can be caused by a myriad of diseases.

And this patient has some irregularity in their heartbeat that have alternating systolic heights, not so much alternating like the previous patient, but more variable appearance, both the ECA and the CCA.

This is called pulses paradoxes.

And this can occur with a big drop in blood pressure with inspiration.

And the etiology of this is debatable, but it has been associated with COPD, cardiac tamponade and also with deep breathing.

Now, if this doesn't take you back to your A CLS course, when you're looking at this wave form, this should trigger a thought of atrial fibrillation.

Again, just correlating with what we see by EKG.

Now, here's a patient who has bilateral monophasic waveform.

So both these are the right CCA and ECA waveforms, but the same findings were seen on the left side where you don't have that normal arterial waveform.

You have basically a more monophasic appearance.

And this is seen with patients who have a ventricular assist device such as this patient having has an LVAD.

Here in this patient we have alternating systolic peaks with flow going below the baseline.

And we see this in patients with an intraaortic balloon pump where we have the unassisted peak followed by the assisted peak.

And so when you're assessing the velocity, assess the initial velocity, which is the lower velocity, that should be the true unassisted peak when you're assessing for peak systolic velocity.

The second peak is going to be the assisted peak.

Rare Cases and Congenital/Acquired Abnormalities

Now more fun stuff, more fun cases that we don't see too commonly, but it's good to know about.

Here's the patient who has longitudinal image of the carotid circulation, and we see antegrade flow in the ICA and retrograde flow in the ECA, and we have confirmed that on spectral doppler, antegrade ICA, retrograde ECA.

So what causes this appearance here we see ec increased echogenicity within the left CCA consistent with thrombus.

So we have an occluded CCA in this patient.

In this patient. We have both antegrade flow and retrograde flow within the CCA as confirmed by the spectral waveforms.

Why is this? Well, here on these images you can better see that we have an intimal flap along the CCA and we have normal antegrade flow in the true lumen, and we have reversal of flow in the false lumen.

Again, carotid dissection, sequela carotid dissection and include stroke.

So here we have a patient with an acute infarct that we see on MRI.

Here's a 30-year-old male who has a left carotid brewery, family history of hypertension, history of left-sided tingling and numbness.

So when we image this patient on the carotid, we could see the left carotid bifurcation, but we only see the ECA.

We don't see continuity with the ICA.

This was confirmed with power doppler and also with spectral doppler.

All we were able to see beyond the CCA was a high eec, high resistance ECA waveform.

We did not see an ICA.

So this patient actually has absent left ICA.

So we see on the MRA neck on the right side, you can see the common carotid with the internal and external carotid.

But on the left side, all we see is continuity with the external carotid with the branches, we don't see any internal carotid artery.

Here's another patient with a history of TIA.

When we examine this patient, we only saw a left ECA beyond the bifurcation.

We did not see an ICA, we again saw a high resistance waveform compatible with an ECA and on the CTA head, we had absence of the carotid artery and a small carotid canal in contrast to the contralateral side.

So again, this patient had an absent or hypoplastic left ICA.

Iatrogenic Complications

Now, here's a patient who is status post line attempt in the internal jugular vein who developed neck swelling.

So we scan this patient.

So when we initially scan this patient, we didn't know if this was the IJ or if this was the IJ that was thrombose.

We thought that this was probably the CCA and there was a hypoechoic foci.

It looked like it was emanating from the CCA.

Then when we put color doppler on it, we realized that this is indeed the thrombo internal jugular vein, and this is the common quaded artery with a yin and yang appearance emanating from it, compatible with a pseudo aneurysm.

So this is iatrogenic complication of line placement because the IJ was occluded, the line was put inadvertently into the CCA causing a pseudo aneurysm and subsequent hematoma.

Innominate Artery Steal

Now this is a patient who demonstrates incomplete flow reversal and the right CCA as you can see, right ICA and ECA and the vertebral artery demonstrates complete reversal of flow.

Now, what do you think is causing this appearance?

This is a case of a nomin artery steel.

This is a 73-year-old male patient with a history of lung cancer.

And when we did the CTHS, we saw that the right innominate artery right off the aortic arch was occluded, and this occlusion extended all the way up to the common carotid artery.

So this is an innominate artery steel.

And if you think about it, the innominate steel is very similar to a left subclavian steel.

It's just on the other side, and it's only going to affect the right-sided vessels.

So if you see that appearance, think a nominate steel on the right side as opposed to a left side, which would be a subclavian steel.

Here's another case of a nominate steel, which is more severe.

This is another case from my chairman with complete reversal of flow in the carotid circulation.

You can see here there's total reversal of flow in the CCA, the ICA, the ECA and the MRA images demonstrate an absent or occluded, I should say, occluded and nominate artery.

Takayasu Arteritis

Here's a patient, 21-year-old female with weak upper extremity pulses.

And in this patient we see a lot of thickening along the walls of the common carotid circulation.

This is transverse and longitudinal images.

We see a lot of color aliasing here suggestive of stenosis and the velocities in the CCA in this region, we're measuring at over 200 centimeters per second.

This is the same patient on the left side.

We see the same finding, we see extensive wall thickening along the CCA.

We see what looks like critical stenosis.

This is low velocity low velocities obtained in this area of sluggish flow.

The right vertebral artery and the left vertebral artery also demonstrates some irregularity of the waveforms.

This is a patient with TAUs arteritis.

TAUs is considered a large vessel vasculitis.

It frequently affects the aorta and pulmonary arteries, and in our case, it also affected the vessels coming off of the aortic arch.

It is very common much more common in females than in males, especially young Asian females, and typically presents with weak or absent upper extremity pulses.

Vertebral Artery and Subclavian Steal

Now moving on to the vertebral artery, vertebral artery waveforms, we're gonna talk about early subclavian steel.

There are actually four types of early subclavian steel.

There's type one, which is basically just a very small very transient mid systolic notch that you can see.

You can see a very small early systolic peak, then a notch, and then you see the rest of systole followed by diastole.

But the antegrade flow is maintained throughout the cardiac cycle in a type two or bunny wave form.

There's basically a deeper cleft with between the two systolic peaks In type three, there's actually a mid systolic cleft that goes below the baseline and there's rapid recovery of forward flow as diastole continues.

And in type four, the systolic cleft falls well below the baseline because there's a greater reversal of flow during systole, but there's still forward flow in diastole.

So just a spectrum of mild to more significant stenosis, which then can progress to complete reversal of flow due to more severe subclavian artery stenosis.

Now, looking at the waveforms more specifically, this is for example a type two waveform, which you have the more significant systolic cleft between the two peaks.

And this has been called, as we said before, a bunny waveform.

And it could either be like, this can be the bunny ears with the bunny hump, or this can be asymmetric ears with the bunny.

Either way it's up for interpretation.

And again, on the MRI images, we see a stenosis of the subclavian artery on the right side.

Now the subclavian steel, as we said, can progress, so it's important to look for changes over time.

Here's the vertebral artery with a bunny waveform, and we see on the CTA the subclavian stenosis and this can progress to become more severe.

And six months later, actually this patient developed bidirectional waveforms.

This went from a type two to a type four early subclavian steel since the waveforms became bidirectional.

Reactive Hyperemia Test for Subclavian Steal

A maneuver that can be done to assess the potential severity of subclavian steel is done with the blood pressure cuff.

And it's the you can inflate the blood pressure cuff on the affected arm until basically you exceed the systolic blood pressure to make the arm is ischemic and it should remain ischemic for at least two to three minutes.

Once you release the cuff, the blood flow will be directed away from the head and it will accentuate the vertebral artery abnormalities.

So sometimes you'll see a bunny wave form or bunny rabbit sign change to a complete flow reversal.

So in this case, we had a type three or type four early subclavian steel with a s systolic flow below the baseline diastolic flow above the baseline.

Once we released the cough, we ended up having complete flow reversal, so we progressed to severe stenosis indicating that this was had very severe potential.

And that being said, no bunnies were harmed in the making of this presentation, and I thank you for your attention.