Non-Atherosclerotic Pathology of the Carotid Arteries - HD
Introduction
Hello, my name is Leslie Scout.
I am chief of ultrasound at Yale New Haven Hospital,
and I'm a professor
of diagnostic radiology at Yale University School
of Medicine, where I also serve as medical director
of the non-invasive vascular laboratory.
And today I'm going
to be discussing non atherosclerotic pathology
in the carotid arteries.
Today we're going to be talking about non atherosclerotic
pathology of the carotid arteries.
Objectives
And the objectives of this talk are
to discuss the diagnostic ultrasound features
of non atherosclerotic vascular pathology in the carotid
arteries, particularly focusing on carotid artery
dissection, arterial venous fistula, pseudo aneurysm,
and different types of vasculitis.
Carotid Artery Dissection
So we'll start first with carotid artery dissection.
Now whatever the etiology, the way this occurs is
that blood enters into the wall
of the carotid artery separating the different layers,
and this starts with a tear of the intima,
and then the intima plus
or minus the medial layer are lifted off the adventitial
outer layer of the vessel wall.
And the thickness of this flap depends upon whether
or not the media is lifted off in addition
to the intimal layer
and whether a mural hematoma develops versus whether
or not free-flowing blood persists in the false lumen is
dependent upon whether or not there is a reentry point.
In addition to the proximal entry point,
there are a variety of things
that can cause dissections in the carotid arteries.
These include, trauma, which could be just exercise,
rapid neck motion or seatbelt injury.
And in fact, the trauma may be quite minor
and may not in some cases even be noticed by the individual.
Another common way
that carotid artery dissections occur are due
to extension from dissections in the aortic arch,
but many are spontaneous occurring likely due
to weakness within the vessel wall.
Thus predisposing risk factors include anything
that will weaken the vessel wall.
And some of the most common predisposing risk factors
include Marfan syndrome, aler Danlos syndrome,
fibromuscular dysplasia, cystic medial necrosis
and hypertension.
Approximately 70% of spontaneous dissections occur in young
to middle aged patients.
In this situation, they occur equally in males
as well as females.
And the clinical presentation is a little bit different than
those who have traumatic dys dissections
or dissections from the aortic arch.
And these patients may present with headache, neck
or facial pain, hemispheric symptoms, cranial nerve palsy
and Horner syndrome.
Carotid dissections are actually a relatively common cause
of stroke in young patients,
and this is something you should consider in the young
patient who presents with stroke.
Other causes of stroke in young patients include cardiac
disease, tumor, and, vasculitis.
Carotid dissections differ a little bit also in terms
of whether or not they occur in the common carotid artery
versus the internal carotid artery.
Common Carotid Artery Dissections
And dissections
that occur in the common carotid artery are typically the
result of extension from a dissection within
the aortic arch.
These typically occur in older patients
and are very easily seen on ultrasound.
They're often relatively asymptomatic
and typically stabilized such that,
treatment may not be required.
It's estimated that strokes occur in only about three to 7%
of patients who have dissections that are limited
to the common carotid artery.
Internal Carotid Artery Dissections
On the other hand, carotid dissections
that occur predominantly in the internal carotid artery
are typically due to trauma or spontaneous dissection.
And these tend to occur in younger patients
and they most often start at the skull base
and dissect down towards the bifurcation.
In other words, dissect approximately.
However, in
some cases they do originate at the carotid bifurcation.
These are harder to see on ultrasound and unfortunately
or more likely to result in stroke.
And because they're more difficult to see on ultrasound,
these are actually better evaluated on MRCT
or cut film angiography.
The appearance on ultrasound does depend upon whether
or not there is a false lumen or a mural hematoma,
and if a false lumen is present very often you will see very
bizarre flow patterns,
particularly on spectral doppler interrogation.
A patent false lumen,
is more common in a common carotid artery dissection,
but the appearance really does,
or the waveform really does depend upon the size
and the length of the false lumen.
Often you might see retrograde flow in the false lumen
and sometimes the false lumen is large enough
that it compresses the true lumen resulting in decreased
flow within the true lumen.
A mural hematoma,
is more common in dissections involving the
internal carotid artery.
It often,
spirals
around the true lumen causing compression
and may result in a stenosis leading
to an increase in peak systolic velocity.
Since these stenosis are often long segment, often that
increase in peak systolic velocity
is somewhat lower than you might expect given the degree
of stenosis.
The ultrasound appearance of course, is going
to depend a lot upon whether
or not there is a mural hematoma and whether
or not the,
false lumen is patent.
So when you consider dissections in the common carotid
artery, which are those
that are most easily evaluated on ultrasound,
the first thing that you're going to look
for on the gray scale imaging is the presence
of the inal flap.
This flap is typically quite echogenic on ultrasound.
The thickness, as I've mentioned previously,
is variable depending upon whether just the intimate layer
is lifted off or the intimate layer plus the media is lifted
off the advent tissue
and the luminal flap may be mobile, so it may
pulsate or move during,
the cardiac cycle.
If instead of a patent false lumen,
one has a neural hematoma,
the most common gray scale ultrasound appearance is
of long segment,
wall thickening causing a smooth stenosis
of the common carotid artery.
This often spirals around the true lumen
and this homogeneous thickening,
of the carotid wall typically involves both the anterior
and posterior walls.
When two lumen are present, the doppler wave forms are
typically quite different.
In each lumen, you might see an increase
or a decrease in peak systolic velocity flow might be
bi-directional or reversed,
and it is very, very common
to see very bizarre flow patterns within the false lumen.
So here is an example on a transverse
and longitudinal image of the left common carotid artery.
You can clearly see this very thin
echogenic intraluminal flap.
When color doppler is used, you can see
that there is flow both within the true and the false lumen,
and you can see in fact the flow is reversed
or blue within the false lumen.
On Doppler interrogation, you can see
that the waveforms in these two lumen is quite different.
The waveform in the true lumen, which is antegrade
as you see here, is somewhat abnormal in
that you see decreased diastolic flow
and a little bit of a delay in systolic upstroke,
but certainly looks much more normal than the waveform
pattern in the false lumen, which is very irregular
and actually bidirectional
as you see on the spectral doppler waveform.
Here is another example where on the gray scale on the sagal
as well as the transverse view, you can see this echogenic
intimal flap and noted that this is quite lifted off
and is actually folded upon itself.
And you can sometimes see very bizarre patterns of the
intimal flap as in this particular case.
In this case, you can see
that the intimal flap on the sagal gray scale image is
somewhat irregular in configuration,
but very, very thick walled.
And notice that within the residual lumen you have a very
bizarre waveform pattern that is very spiky
with absent diastolic flow.
Here is another example where on the
frozen single frame film here,
that intimal flap actually looks quite thick
actually on real time it was thin.
And the reason that it is thick is that it was so mobile
and we couldn't,
capture a single image where it looked,
thin as it did on real time imaging.
Notice that their,
true
and false lumen are both patent
with flow going in opposite directions.
In this particular case, the color scale has been,
reversed and you can see
that the more normal appearing waveform is in the deeper
or more posterior lumen,
which is color coded blue in this image.
And the false lumen is color coded red
with a very bizarre bidirectional waveform pattern.
The pattern really depends upon the length of patency
as well as the relative size of the true and false lumen.
But as you can see in these
two, this case here,
you can really see very bizarre waveform patterns.
And although the waveform pattern is most commonly bizarre
within the false lumen in this particular example,
you can see the waveform is abnormal in both the true
as well as the false lumen.
When dissections,
occur secondary
to extension from dissection of the aortic arch,
it's important that you look as approximately as possible.
This is a patient who had Marfan syndrome who presented
with a known dissection in the aortic arch,
and we were asked to evaluate whether
or not the dissection extended
into the common carotid arteries.
And when we initially did the examination,
we didn't see any evidence
of dissection within the common carotid arteries.
However, when we went
and looked with the hockey stick transducer
and really looked as inferior,
as we could notice way down low in the left common carotid
artery, you can actually see this
dissection.
And here you can see it not quite to
as good advantage on the,
sagittal image as well,
but initially it was not seen
because we didn't look,
proximally enough.
And in this particular case,
the right common carotid artery was completely normal
and the dissection had only extended into the left common
carotid artery, but had not extended into the origin
of the right common carotid artery.
This is an example of a patient
who has a thrombosis false lumen
or aural hematoma noticed that when the thrombus is acute,
often it is very anti coic
and you can see clearly here
that it is compressing the true lumen, causing a little bit
of,
aliasing.
Where the vessel,
lumen is most
narrowed.
Here is an older case demonstrating
very smooth homogeneous thickening of the wall
of the common carotid artery.
Notice that both the anterior
and the posterior walls are involved.
And very often when you have a intramural hematoma,
it will cause this very,
smooth long segment stenosis.
And you will note that the hematoma spirals around the lumen
of the carotid artery, again involving both the anterior
as well as the posterior wall.
Ultrasound Appearance of Internal Carotid Artery Dissections
Now, the ultrasound appearance
of dissections in the internal carotid artery are
typically very, very different from
what I've just described in the common carotid artery.
And in fact, sometimes the ultrasound findings are
completely normal because the dissection begins at the skull
base up above your field
of view when you do your carotid ultrasound
lower down in the neck.
And if it doesn't particularly compress the lumen,
the proximal waveform and proximal gray scale
and color imaging may be completely normal.
So if there is strong clinical suspicion
of a dissection in the internal carotid artery
and your ultrasound exam is normal,
you should consider referring that patient to either MRCT
or angiography to look further,
despite the presence
of a normal carotid ultrasound.
If the lumen is significantly compressed
by the dissection in the internal carotid artery,
you may see a high
resistance waveform in the internal carotid artery.
And so if you see such a waveform in a young patient
who has no evidence of stenosis
or plaque at the carotid bulb, you ought
to be thinking about a distal dissection.
You ought to think about this diagnosis
and a patient who presents with an acute occlusion
of the ICA who is very young,
and sometimes you'll see a smooth tapering stenosis
of the internal carotid artery in a young patient.
And similar to the ultrasound appearance
of the mural hematoma
that I just described you in the common carotid artery,
this,
stenosis will be hogene,
the wall will be homogeneous in echo texture,
relatively hypo coic,
and you will not see underlying evidence of atherosclerosis
or calcified plaque.
Typically, this narrows the residual lumen
and you will see increased peak systolic velocity
at the site of this smooth tapering stenosis.
So this is an example of a young 24-year-old female patient
who presented with a headache.
And when you look in the right common carotid artery here
and the right internal carotid artery,
down
below you will see that the waveforms look totally normal.
Upstroke is sharp
and there is a normal amount
of diastolic flow both in the common
and in the internal carotid artery.
However, when you look on the left side,
you will see both in the common carotid artery as well
as the internal carotid artery
that there is no diastolic flow.
And in fact, there is a little bit of reversal
of early diastolic flow.
This is a very high resistance waveform suggesting
that there is a proximal obstruction.
In addition, there is marked asymmetry in
peak systolic velocity.
The peak systolic velocity in the right internal carotid
artery is 107 centimeters per second,
but is only 21 centimeters per second in the proximal left
internal carotid artery.
When you look on the gray scale, you'll notice
that there is no evidence of thrombus
or plaque in that proximal internal carotid artery.
It looks wide open, no underlying atherosclerosis,
but again, the spectral Doppler waveform is very abnormal
with decreased peak systolic velocity,
no end diastolic flow,
and actually frank reversal of flow in early diastole.
And the this constellation
of findings should make you consider the possibility of a
obstructing lesion up higher outside of the field
of view of your ultrasound.
And in a young patient,
the primary thing you should be considering is a carotid
dissection at the skull base.
This patient went on to,
have a CTA
and noticed that the right internal carotid artery,
although tortuous appears completely normal,
but on the left, although the internal carotid artery is
completely normal at the bulb
and bifurcation, as you follow it up towards the skull base,
you can see that it becomes extremely
attenuated and narrowed.
And when you look at the
contrast images,
you can see again that on the right the common carotid
and internal carotid artery are normal all
the way through the skull base.
But on the left you can see that there is a smooth tapering
of the distal internal carotid artery
as it enters the skull base consistent with a dissection
of the distal internal CID artery dissection.
Here is another example
where you can see on the sagittal color image
of the proximal right internal carotid artery
that it looks completely normal.
There's complete fill in of the lumen.
There's no abnormality of the vessel wall at all,
but when you get your spectral doppler waveform,
it is extremely abnormal, very, very high resistance
with significant reversal of diastolic flow
and early diastole, no end diastolic flow.
And once again, the peak systolic velocity is extremely low,
1718 centimeters per second.
This has been described as a thump wave form
or a knocking wave form,
and again, is indicative of a distal,
obstructing
phenomenon or distal obstructing etiology.
And in a young patient, the thing that is most likely
is a distal carotid artery dissection.
This patient,
went on to have a,
CTA several days after the ultrasound.
And here you can see this smooth tapering stenosis at,
just beyond the level of the carotid bifurcation.
This obviously had extended from the
stenosis
that you see up higher in the intervening two days.
Note that there is no evidence
of underlying atherosclerosis.
Occasionally you can actually see blood in the wall
on a CT or an mr
corresponding
to hypo coic thickening,
on the ultrasound.
So again, correlation
with the history is extremely important
and this etiology should be considered in a young patient
or a present patient presenting with neurological
symptoms following trauma.
Here is a,
different kind of appearance
of A ICA dissection.
Here you can see that while the distal ICA luminous patent
notice that there is smooth,
tapering of this vessel.
The wall is thickened, it's very homogeneous.
It is very, very hypo coic.
And again, in a young patient where you don't see evidence
of underlying atherosclerosis,
but you see this very smooth
homogeneous hypo coic wall thickening, you ought
to be thinking about a dissection as well
as a mural hematoma when the
pulse oler waveform was obtained in this particular patient.
Again, this confirms what you saw on the color image,
namely the lumin is narrowed velocity is increased
to 225 centimeters per second.
There's some spectral broadening,
actually increased diastolic flow.
This is the type of waveform that you see at a stenosis,
but what's atypical here is that there's no evidence
of atherosclerosis
and the wall is diffusely thickened in hypo coic.
This patient went on to have an Mr.
Notice that you can see increased signal intensity within
the wall of the vessel confirming the presence of blood.
And this is an intramural hematoma due to a dissection
of the internal carotid artery.
I want to point out, as you can see from the cases
that I've just presented, that the most typical appearance
of a dissection involving the internal carotid artery is
either that of a high resistance waveform,
without evidence of stenosis due to the distal obstruction
or a intramural hematoma
with hypo coic homogeneous thickening
of the wall causing a tapering of the vessel lumen.
But it is very, very uncommon
to see a dissection flap itself in the
internal carotid artery.
This is probably because the vessel is so small
and it tends to occur distally.
So unlike in the common carotid artery,
when you most often see a dissection flap, visualization
of the dissection flap is quite rare, rare in a patient
with a dissection of al in the internal carotid artery.
Arteriovenous Fistulas
Well, moving on to,
artery venous fistulas,
this is a connection most commonly seen
between the common carotid artery
and the internal jugular vein.
This is almost always due to trauma.
It could be blunt trauma or penetrating trauma,
and unfortunately the trauma is iatrogenic.
So we often see this in
our institution following an attempt to place a,
central catheter in the internal jugular vein.
And sometimes we see this in post,
surgical
patients.
However, occasionally it can occur in patients,
who have an underlying cervical malignancy
or have been treated with high dose radiation therapy in the
neck and either the,
fibrosis from the radiation therapy
or erosion from the malignancy may cause erosion into these
two contiguous vessels resulting in a fistulas
connection,
between them.
Extremely rarely a connection
between the common carotid artery
and internal jugular vein can be,
congenital,
but this is actually most usually referred to
as an arter venous malformation rather than an
arterial venous fistula.
These patients clinically present with a neck hematoma,
a bruery, sometimes a palpable thrill
if there is a very large shunt
of blood from the common carotid artery
to the internal jugular vein.
This sometimes can cause overload of the right heart
and patients may present in congestive heart failure
and sometimes one will see on physical exam distension
of the internal jugular vein
and can note that it is extremely pulsatile.
In today's practice, treatment is usually,
placement
of a carotid stent
and occasionally now surgery is still,
required
On ultrasound, you're going to see color sene within
the connection between these two vessels,
and sometimes the increased velocity
of flow will actually cause
a perivascular soft tissue vibration,
which one ultrasound will appear as a color brewing.
You'll see increased systolic
and diastolic velocity in the feeding artery.
Though sometimes we don't always note this in the common
carotid artery because peak systolic velocity
and diastolic velocity are quite elevated,
baseline.
But you should see pulsatile flow in the draining vein
that has higher than expected velocity.
Note that the artery up
above the fistulas connection should have a normal waveform.
And similarly, the waveform in the internal jugular vein
above the fistulas connection
most commonly has a normal waveform,
although occasionally you might see retrograde flow.
Another interesting phenomenon is
that if an arterial venous fistula is small,
it may collapse when a patient is supine.
And so in order to visualize it, you may have
to have the patient in an upright or sitting position.
So if there's strong clinical concern
for an arter venous fistula, a patient has a palpable brill,
for example,
thrill for example.
And if the,
patient presents with,
pain following,
an attempted line placement,
you don't see anything when you're doing
the patient's supine.
It probably is worth it to have the patient sit up
and take a quick look,
as well.
This is an example of a patient
who had had a carotid endarterectomy
and presented with a brewery in the neck as well
as a palpable thrill.
And notice on the color doppler ultrasound, you can see
what we describe a soft tissue brewery, this color mosaic
or speckled pattern in the soft tissues
between the common carotid artery as well
as the internal jugular vein.
This is due to the fact that increased velocity
of blood flow through
that small fistulas connection causes vibration
of the surrounding soft tissues.
And on color doppler, this,
results in this color mosaic.
The problem with this, of course, is
that it obscures visualization of the underlying structures.
So what should you do in order
to improve your visual visualization?
You can increase your scale
or your PRF, you can increase your wall filter
because typically this perivascular soft tissue vibration is
a very low frequency.
And the other thing that you can try to do is
to image in diastole.
So in this particular case,
we increased our PRF and our wall filter.
We eliminated that soft brewing,
and then you can see both with a color
and on the gray scale quite clearly, this connection
between the internal jugular vein as well
as the common carotid artery.
And on the spectral doppler tracing within the fistulas
connection itself, you can see a very
low resistance waveform pattern characterized
by an increase in both peak systolic as well
as end diastolic velocity.
And in the draining vein, namely the internal jugular vein,
you can see very high velocity flow nearly,
440 centimeters per second.
And it is also very pulsatile as you see here.
Notice though that there is still some respiratory variation
increase in peak systolic velocity in diastolic flow in the
common carotid artery,
is seen most commonly in patients
with arterial venous fistulas,
but occasionally can be seen in patients who have distal
cerebral arterial venous malformations.
And very rarely you can see this in a patient
who presents very early in the course
of an acute
stroke.
However, in this particular case,
you typically see only an increase in diastolic flow.
You don't typically see a significant increase in peak
systolic velocity, and this occurs really only very early,
following an acute stroke,
and it's usually in the setting
of a very extensive,
stroke.
Pseudoaneurysms
Well, the next thing I want to discuss is,
pseudo aneurysms arising from the carotid arteries.
And the most common,
pathophysiology here is that there
a hole develops in the arterial wall allowing extravasation
of blood, which becomes encased by compacted,
surrounding soft tissues.
However, in the setting of a carotid dissection,
the adventitia plus
or minus the media may be all that remains
of the arterial wall, and this wall therefore is weakened
and sometimes can bulge.
And this,
also is described as a pseudo aneurysm.
A true aneurysm is surrounded
by a full thickness vessel wall comprised in the intima,
the media as well as the adventitia.
So it's important to remember that
occasionally a pseudo aneurysm may be encased
by the adventitia and sometimes it,
however, is encased by
just compacted surrounding soft tissues.
A variety of things can cause pseudo aneurysms.
The most common is trauma, either,
typically penetrating trauma, though it can be iatrogenic.
Occasionally you can see this following infection
or malignancy, which causes erosion of the vessel wall,
but anything that weakens the arterial wall can cause
that second type of pseudo aneurysm, which is bulging
of this very,
thickened a wall,
particularly if the intima is lifted off.
So consider this diagnosis in patients
who have received radiation therapy to the neck
who have a known carotid dissection,
fibromuscular dysplasia, other types of vasculitis,
a aler Danlos syndrome and Marfan syndrome as well.
And the risk of course of a patient
with a pseudo aneurysm in the car,
carotid artery is a rupture.
And so these patients are typically treated with placement
of a carotid stent or surgery.
On ultrasound, you're going
to see on gray scale a cystic mass adjacent to the
vessel, which will fill in,
with color flow on color interrogation
unless it is completely thrombo.
When you see color flow within the patent pseudo aneurysm,
the flow swirls
around causing atypical ying yang appearance.
And if you interrogate the neck,
and if that neck is thin, you'll see the classic two
and fro flow within the,
neck of the pseudo aneurysm.
And this is described as flow, which is two
or towards the pseudo aneurysm in systole and away
or fro from the pseudo aneurysm in diastole.
But whether or not you see that two
and fro flow really depends upon the size of the neck.
And you will only see this if the neck is small.
If the neck is very wide, as in this particular case,
you will not see that to and fro flow.
This particular,
individual presented three years following carotid
endarterectomy telling the referring physician
that she had a palpable,
hard mass in her neck
that had been,
increasing in size over the past year.
And here you can see this outpouching from the
common carotid artery.
Notice that approximately half
of the pseudo aneurysm is thrombosis.
You can see the intraluminal echoes here.
And on the color Doppler image, you can see the swirling,
pattern of blood flow,
namely the ying and the yang pattern.
And this is the spectral doppler appearance of the ying
and the yang pattern as it just swirls around
and changes direction,
throughout the cardiac cycle.
In this particular patient, as I mentioned,
because that neck is so wide, you would not see the two
and fro pattern within the neck.
This patient,
went on to have a stent placed
and had an angiogram, as you can see here,
and very faintly,
an outline of the fill in of the,
pseudo
aneurysm.
This is a,
28-year-old IV drug abuser who presented
with neck pain, and you can see on the initial scans
evidence of a hematoma within the neck.
It's very echogenic.
This,
thrombus was,
subacute with a more hypo coic,
peripheral component, just reflecting the fact
that hematoma will have,
different levels
of echogenicity depending upon the time course
since the bleeding occurred.
When we look carefully at the common carotid artery,
you can see actually the,
track
of blood flow from the common carotid artery
to the more medial proximal part of this,
largely thrombo pseudo aneurysm.
You can see some color aliasing within the neck,
and again, that ying yang pattern
of swirling flow within the residual patent.
Component of the pseudo aneurysm
here is a spectral doppler waveform
obtained within the neck, demonstrating that classic two
and fro pattern with flow heading towards the pseudo
aneurysm in systole
and away from the pseudo aneurysm in diastole.
This is another example of a pseudo aneurysm obtained,
or that,
occurred following a drug addict's attempt
to inject in the common carotid artery.
Here you can see on the power doppler image the pseudo
aneurysm arising from the distal common carotid artery just
below the bifurcation.
And here on the angiogram,
you can see the pseudo aneurysm exactly
as we saw it on the power Doppler image.
This is a,
patient who presented
with a neck mass in the intensive care unit following an
attempt at placing a central line.
This is the common carotid artery near the bulb.
This is the pseudo aneurysm adjacent to it,
and here you can see this very thin neck
between the common carotid artery
and the paint and pseudo aneurysm.
This is the,
angiogram,
confirming the ultrasound,
findings and notice that in,
this neck again,
you had the classic two and for away form pattern,
but as I have said, you will only see
that pattern if the neck is thin.
If it's wide, you're going to have a very,
bizarre flow pattern.
This is a patient who had a mycotic pseudo aneurysm
demonstrating that you see just a bizarre way form pattern
in the neck because again, that neck is very wide
and typically you see a wider neck in a patient who has a,
mycotic pseudo aneurysm.
When the pseudo aneurysm occurs
because of penetrating trauma, it's typically
a narrower more pinhole neck that has the two
and fro wave form pattern.
This is a patient who presented actually five years
following carotid endarterectomy.
She actually had a TIA and
therefore had a CAT scan, which suggested a vascular
abnormality actually,
up fairly high
above the bifurcation,
when she had her ultrasound
to further evaluate what they'd seen on the CT notice,
you can see evidence of the,
crowded endarterectomy.
The bulb is,
distended, and here you can see the patch,
but the distal com internal carotid artery actually looked,
pretty normal, but up higher well
above the operative site.
You can see this focal outpouching,
which represented the pseudo aneurysm
that they'd seen on the CT scan,
and this probably was due to clamp injury.
Here on the color Doppler, you can see
that swirling blood flow pattern described as a ying
and the yang appearance, again, this is a wide neck,
so it would not have a two and fro pattern within the neck.
This patient went on to have an,
angiogram
because they were going to try
and exclude this by placing a stent across this.
And again, you can see the very wide base of this,
pseudo aneurysm, again, well above the operative side,
probably related to a clamp injury.
And it's kind of an interesting case
because as they attempted to place the stent,
across the pseudo aneurysm,
it actually got coiled within the pseudo aneurysm.
They weren't ever able to retrieve this,
and this had to be convert, converted to an open,
operative procedure,
to retrieve the stent
and to,
fix the pseudo aneurysm.
True Aneurysms
True aneurysms are actually very uncommon in the carotid
arteries and occur more commonly in the common carotid
artery than in the internal carotid artery.
Causes can include atherosclerosis
and underlying connected tissue disorders,
and these are differentiated from the pseudo aneurysm,
of course, because the lumen is encased by a
complete,
arterial wall that includes the intimate media
as well as the advent tissue.
But I've only seen a few examples of these cases,
and these would not show that swirling ying yang appearance
as you see in a pseudo aneurysm.
Vasculitis
Well, I'm going to talk briefly about several connect,
types of vasculitis.
And the most common type of vasculitis
that one sees in the United States is
fibromuscular dysplasia.
Fibromuscular Dysplasia
This is an arterial disease of unknown etiology.
It's been postulated
that deficiency in alpha one antitrypsin,
might,
be a cause of this,
but other etiologies
that have been postulated include ischemia,
hormonal changes, and even mechanical stress.
The incidence has been estimated in the general population
as being only between about 0.6 and 1.1%.
It's most common in,
women of middle aged
or younger women between age 25 and 50,
and it is,
three times more common in women than in men.
This typically involves medium
to large arteries causing the so-called string
of beads appearance on an angiogram or an ultrasound,
and it is the renal artery that is most commonly involved.
However, the internal carotid artery is the second most
common artery to be involved.
And if a patient has this beaded appearance
of the internal carotid artery, it's estimated
that about a third of these patients will also have
involvement of the renal arteries.
There's about a 10 to 20% incidence
of spontaneous carotid artery dissections, probably
because,
the vessel wall is weakened
and about 30% of patients
with fiber muscular dysplasia will have
intracranial aneurysms.
So it behooves the referring physician to,
order a study
to look at the intercranial arteries as well.
Patients with fiber muscular dysplasia involving the
internal crowded artery may present with TIA hemorrhage
or stroke, but very often they're asymptomatic.
And on ultrasound, just like on an angiogram, you're going
to see a beaded,
or scalloped appearance of the internal carotid artery.
Power doppler has the best edge resolution
or of,
the,
different types
of color doppler imaging.
And so we often use power doppler in order
to best bring out this beaded appearance.
The,
finding will be bilateral in up to 65% of cases.
Very often it involves a relatively long segment
of the internal carotid artery
and it will narrow the
lumen.
Here's another example where you see this beaded
or scalloped appearance involving quite a long segment
of the right internal carotid artery.
If the lumen is substantially narrowed,
you may see an increase in peak systolic velocity.
However, sometimes as in this case,
the peak systolic velocity may not be quite as high
as you expect because this is a long segment stenosis,
what you really have is a series of tandem lesions.
And in that case, particularly when you look
distally,
you may not see an increase in peak systolic velocity,
though sometimes you do see a tardis pars waveform,
as you did see in this particular individual.
Takayasu Arteritis
Tatsu, arteritis
or a arctic arch syndrome is a fairly rare type
of arteritis in the United States.
This is sometimes also referred to as pulseless disease
because patients,
most often present
with absent pulses in the upper extremities.
This is an inflammatory disease of unknown etiology.
One sees granulomatous,
inflammation
that predominantly affects the wall of the aorta as well
as the major branches at the origins.
This inflammation will result in thickening of the,
walls of these branch vessels at the origin,
resulting in arterial stenosis, sometimes progressing
to thrombosis, and occasionally patients may present
with aneurysms as well.
This most commonly occurs in young women between the ages
of 15 and 30.
In fact, it's estimated to occur eight
to nine times more commonly in females than in men.
And although this is very uncommon in North America, it's a,
has a very high incidence in,
Asia.
In fact, it's in India, it's the most common cause
of renal vascular hypertension.
These patients are treated with steroids.
Although this is not always terribly effective.
On ultrasound, you are going to see wall thickening
of the proximal common carotid arteries resulting in
narrowing of the lumen.
You will see increased peak systolic velocity at the
site of the stenosis, and this is often
but not always bilateral, though, even when it's bilateral,
it can be asymmetric.
And so here you see an example
where you see diffuse wall thickening
of both common carotid arteries.
Note that it is more prominent proximally
and improves as you go distally.
Here is a different patient though,
where you can see actually that the wall thickening extended
all the way to the carotid bone.
On spectral doppler interrogation,
you can see a relatively normal waveform pattern,
but the varsity is increased
because the vessel wall is narrowed.
Radiation Arteritis
This is a patient with a different problem.
You can see that there is diffuse thickening
of the left common carotid artery,
but notice that it begins in the midcom carotid artery.
The proximal common carotid artery is normal, extends up
to the bulb and the
right common carotid artery looked relatively normal.
Here you can see another patient with the same,
pathophysiology, where you can see diffuse,
relatively homogeneous wall thickening
that involved predominantly the midcom carotid artery.
And while this looks very similar to a patient
with taki issue's arteritis, the difference is
that the origins of the common carotid artery look normal,
and this predominantly affected the midcom carotid artery.
And this is a patient who has wall thickening due
to underlying radiation arteritis.
This is a well-known delayed effect
of high dose cervical radiation therapy.
We see this most commonly in patients who've been treated
for Hodgkin's disease
or squamous cell cancers of the head and neck.
And the underlying pathology is indeed an accelerated
atherosclerosis characterized by significant inflammation
as well as fibrosis.
In addition to the problems
that I've just described in the vessel wall itself
surrounding scar tissue
and soft tissue fibrosis can also contribute to,
compression of the common carotid artery causing stenosis,
and even occlusion.
It's estimated that there is an occurrence rate of as high
as 30 to 40% following high dose cervical radiation therapy.
It does take about five to 10 years
to develop radiation arteritis
after the cervical radiation therapy.
The stroke rate is estimated to be as high as 7%
in these patients, and often
therefore, treatment is recommended.
And the, in today's practice,
the optimal treatment therapy is considered to be,
stent placement in the common carotid artery,
which brings up a very interesting question.
Given the fact that this,
has a very high incidence
and that these patients,
about 7%
of them will develop stroke
and that there is good therapy for it,
should we screen patients
who have had high dose radiation therapy,
in order to,
prophylactically treat these patients
before complications,
develop
the ultrasound appearance mimics the appearance,
as I've mentioned, of takayasu arteritis, except
that this diffuse wall thickening
of the common carotid artery typically involves the middle,
part of the common carotid artery.
It may be very severe,
but is,
typically very, the stenosis is very smooth
and long segment.
Occasionally it can ulcerate
and it can be severe enough that a occlusion occurs,
and very rarely,
it can lead to the development
of pseudo aneurysms
and even rupture of the carotid arteries.
Here's another example where you can see that
although there is some underlying atherosclerosis,
you can see this echogenic plaque out at the wall
of the common carotid artery.
Notice the vast majority of this stenosis,
which is very long segment and smooth walled,
or
with a very smooth,
luminal interface, is due
to this very long segment homogeneous hypo coa, thickening
of the wall of the midcom carotid artery.
Here's another example where you can see that,
the wall is a little bit more irregular,
but again,
very homogeneous
and,
hypo coan
Moyamoya Disease
Moya Moya disease
is a uncommon type of vasculitis.
This is believed to be inherited, tends to be progressive,
and this typically involves the internal carotid artery
as well as the middle and anterior cerebral arteries.
Ultimately, this vasculitis will cause significant
constriction of these vessels and occlusion.
It tends to be bilaterally
and once occlusion occurs, it is the basal artery
that will ultimately supply most
of the blood flow to the head.
This is a very severe,
disease, often symptomatic
with patients presenting
with stroke, hemorrhage or seizures.
And there is no known,
medical therapy.
This tends to occur in children
and young adults in the third to fourth decade.
It is also more common in women,
and there's an increased incidence in individuals
with down syndrome, neurofibromatosis
and sickle cell disease.
On angiography, you will see occlusion of the internal,
carotid arteries in the,
skull as well as occlusion
of the middle and anterior cerebral arteries,
and the so-called puff of smoke appearance.
Due to compensatory dilatation
of the striate vessels on ultrasound, you won't see
that puff of smoke appearance,
and obviously you don't typically interrogate the
intracranial internal carotid artery or the middle
or anterior cerebral arteries.
But because of this occlusion of these distal vessels,
you will see a high resistance waveform in the more proximal
ICA as well as common carotid arteries.
Temporal Arteritis
The last type of arteritis I want
to talk about is temporal arteritis,
which is sometimes referred to as giant cell arteritis.
This is a chronic systemic inflammatory arteritis
and tends to occur in older women over the age of 50.
These women typically present with headache,
visual abnormalities, systemic myalgias or arthralgias,
and sometimes the temporal artery may be painful.
On physical examination,
it typically involves a superficial temporal artery,
which is a branch of the external carotid artery,
but it can involve any medium to large artery.
You'll see thickening of the vessel wall sometimes
with obliteration of the lumen,
and if it involves the internal carotid artery,
this can result in stroke,
though this is relatively uncommon, diagnosis is made
with biopsy of the temporal artery,
and these patients are relatively effectively treated
with steroid
therapy.
This is an example of a patient
where you can see a high resistance waveform in the common
carotid internal carotid artery, as well
as the external carotid artery.
Note that there's no diastolic flow in the
common carotid artery.
There's very reduced diastolic flow in the internal carotid
artery, and there's actually reversal
of flow in the external credit artery.
So again, a high resistance waveform pattern in
all the vessels on the neck.
This was a very extreme case,
but notice that the abnormality is more,
exaggerated in the external credit artery
because that's the vessel that is typically involved first.
Conclusion
So in conclusion, don't forget to look
for non atherosclerosis related pathology in the carotid
arteries during your Doppler ultrasound examination.
Ultrasound is an excellent way
to diagnose common carotid artery dissections,
artery venous fistulas, and pseudo aneurysms.
It is certainly not as accurate for detecting a pathology,
such as what I've just described in the internal carotid
artery or in the vertebral artery, particularly
vertebral artery dissections.
And so you may need an angiogram for complete evaluation
or STEM placement in patients who you think have disease,
particularly dissections involving the internal carotid
artery or the vertebral arteries.
I think ultrasound has a limited role in the evaluation
of vasculitis,
but consider the diagnosis of vasculitis dissection
or radiation arteritis in patients who present
with long segment smooth wall thickening,
particularly in the common carotid artery.
And I do think that we should consider screening patients
who've,
had high dose cervical radiation therapy
starting about five to 10 years following completion
of their cervical radiation therapy.
Thank you very much.
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