0:00

Moving on to the nonatherosclerotic cases in our list.

0:05

So the first we're going to talk about is Raynaud's phenomena, which is an

0:09

exaggerated vascular response to cold temperatures or emotional

0:12

stresses. It most commonly affects digits like the

0:16

fingers, but can also affect toes and knees, tips of ears and

0:20

nose. It's characterized by sudden episodes of vasoconstriction

0:24

followed by reperfusion, and is really

0:27

a transient arterial constriction that reduces blood flow.

0:31

The causes include primary causes as well as it can be seen in the setting of

0:35

connective tissue disorders such as CREST syndrome or drugs.

0:39

Now, this kind of vasospasm can be distinguished from vascular injury, A,

0:43

in the presence of clinical history, but also a repeat imaging,

0:47

particularly at 48 to 72 hours, would show a normal caliber

0:51

vessel, and so it can help differentiate thrombus or a high grade

0:54

stenosis versus vasoconstriction or Raynaud phenomena,

0:58

so that we don't over call these.

1:02

The next disease that we're going to talk about is the Buerger disease, also known

1:06

as thromboangiitis obliterans, which is a non-necrotizing

1:09

inflammatory vasculitis that affects small and medium-sized

1:13

vessels, most commonly of the extremities.

1:16

The diagnostic criteria include history of smoking, very highly

1:20

associated with that history. It occurs in young

1:23

males. Typically, the onset is below the age of 50

1:27

years, typically has an infrapopliteal involvement,

1:31

lack of traditional atherosclerotic risk factors other

1:35

than smoking. And although there are no pathognomonic imaging

1:39

features as such, segmental occlusions with normal intervening

1:43

segments, collaterals which have a corkscrew appearance.

1:47

The age and the history all can kind of point us towards the

1:51

diagnosis as being Buerger disease rather than the typical peripheral

1:55

arterial disease.

1:56

There are, however, definitely other entities that can have an

2:00

imaging overlap with these, such as peripheral arterial disease, of course,

2:04

connective tissue diseases, SLE, and scleroderma.

2:09

The next pathology in nonatherosclerotic disease is

2:13

vasculitis. Now, giant cell arteritis is really one of the most common

2:17

forms of large and medium cell vasculitis, and the most common

2:21

site of involvement is the aorta and upper extremity branches, such as the

2:25

subclavian arteries, the axillary and the brachial arteries.

2:28

And the lower extremity arteries are not that

2:31

typical to be involved. But when they are involved, the most common

2:35

vessels that are involved are the superficial femoral and the popliteal

2:39

artery. Claudication is really how these patients present,

2:43

and because lower extremity claudication is not uncommon in elderly

2:47

patients, which is also the population that gets affected by giant cell arteritis,

2:51

that can be mistakenly attributed to the same.

2:54

So imaging can certainly help play a role.

2:57

Predominant lower extremity involvement is an unusual

3:00

pattern, which is what we're going to see in our case that we're going to discuss

3:04

in a bit. And really, the aorta arch,

3:08

arch branches, and the temporal vessels are really when it's more

3:12

symptomatic and involved.

3:14

So this is looking at that same patient whose CT we just saw with the

3:18

vasculitis.

3:20

And we can see corresponding to the findings that we saw on the CT,

3:24

there is significant FDG uptake along bilateral

3:27

superficial femoral arteries. And looking at that in a more axial view, you can see

3:31

there's no uptake in that aorta iliac artery branches.

3:34

But as soon as we come to the level of the superficial femoral arteries, there's

3:38

marked FDG uptake bilaterally. All of these signs point

3:42

towards vasculitis, and this person landed

3:45

up having giant cell arteritis.

3:49

The next disease that we have in the nonatherosclerotic section is a

3:53

vasculopathy. Fibromuscular dysplasia is one of the more

3:56

common non-inflammatory vasculopathies.

3:59

It's a non-inflammatory, nonatherosclerotic disease that affects small

4:03

to medium-sized arteries, but the most common arteries being

4:06

involved are renal, carotid, and vertebral.

4:10

Characteristically, the arteries have a beaded appearance,

4:14

although reportedly, there can be a lower extremity involvement of the

4:18

arteries in up to 6% of patients.

4:22

Moving on to arteriovenous malformation, which represents an anomalous

4:26

direct arteriovenous communication that bypasses a capillary

4:30

system. Now, typically, arteries and veins are interposed by high resistance

4:34

capillary beds. And if these are absent, this results in a

4:38

high-flow system from an artery to a vein, and venous

4:42

walls are not designed to handle this arterial blood pressure.

4:45

So over time, this affects the vessel wall structure that

4:49

becomes weakened, and that's why they're at a higher propensity

4:53

for hemorrhages and ruptures, and they can present with a wide

4:57

varying form of symptoms, all the way from skin discoloration

5:01

to ischemia in distal tissues and heart failure from

5:05

arteriovenous shunting. They can be progressive and

5:08

congenital that expand into adolescence and adulthood.

5:11

They can occur sporadically, or they can be syndromic as part of Cobb

5:15

syndrome or Osler-Weber-Rendu syndrome or

5:18

hereditary hemorrhagic telangiectasia syndrome.

5:22

The next pathology is the cystic adventitial

5:26

disease. This is generally seen in young middle-aged men.

5:31

More commonly, it's the popliteal artery along which where we find this,

5:35

and we see these as cystic lesions that are in the wall of the

5:39

artery, which are basically mucoid cysts, and can result in

5:43

compression and even thrombosis in the vessel where they are at.

5:46

Again, the most common artery is the popliteal artery.

5:50

MRA can help identify that cystic nature, so T2

5:53

hyperintense and non-enhancing after you give contrast are all clues of

5:57

cystic adventitial disease.

5:59

The last set of cases that we have are popliteal artery

6:03

entrapment syndrome. This is an uncommon entity, commonly

6:07

seen in young athletic individuals, more common in male.

6:11

And there's repetitive popliteal artery insult, which results in

6:15

damage and aneurysm and thrombosis.

6:18

Typically, these patients present with calf claudication, and they have an

6:22

anomalous relationship of the muscle to the artery in the popliteal fossa

6:26

that causes an extrinsic compression that leads to all of the insult.

6:30

Normally, the popliteal artery is adjacent to and lateral to the medial

6:34

head of the gastrocnemius muscle.

6:37

And the gastrocnemius muscle attaches just superior to that

6:40

medial femoral condyle. And so there are different types of

6:44

popliteal artery entrapment syndrome.

6:46

Again, we're not going to be looking at all of them in detail,

6:50

but just knowing that it is important to look at

6:54

the relationship of that gastrocnemius muscle to that popliteal

6:58

artery is really important. So popliteal artery can

7:01

run medial to that medial head of gastrocnemius.

7:05

The medial head of the gastrocnemius can be more laterally attached.

7:09

That can cause mass effect on that popliteal artery.

7:12

There can be an accessory slip of the gastrocnemius muscle or just an accessory

7:16

bundle that can cause compression of the popliteal

7:19

artery. The popliteal artery itself might have an abnormal

7:23

course and pass below that popliteal muscle.

7:27

That can also involve not just that artery, but there can be venous involvement as

7:31

well, and then there can be functional entrapment as well.

7:34

Now, diagnosis for this typically involves dynamic imaging, either in the

7:38

form of ankle-brachial index, where there's a drop in

7:42

the ankle-brachial index values.

7:44

With exercise, ultrasound, where again, there can be an increase in

7:48

systolic values or significant stenosis or thrombosis

7:52

on dynamic maneuvers, which basically means we scan patients in neutral position

7:56

and then either dorsiflexion and plantar flexion,

7:59

whichever maneuver is the one that the patient complains about

8:03

and is symptomatic on.

8:05

And the same dynamic maneuvers can be done in an MR as well as a catheter

8:09

angiogram.

8:11

So this is the follow-up imaging of this patient that we just saw,

8:15

where we raised concern of popliteal artery entrapment on the CT.

8:19

We did a MR in both the neutral and the plantar flexion, and we

8:23

can see how nice and wide and patent this popliteal artery is on

8:27

the MR. This is in an axial view, whereas this is on a sagittal

8:30

view. Compare that to scanning this patient in plantar flexion, and we can see

8:34

there's a significant anteroposterior flattening and a reduction in the

8:38

caliber of that popliteal artery, nicely seen here as a tubular

8:42

area of moderate to severe stenosis of that popliteal artery on dynamic

8:45

imaging. So really, a change in caliber of popliteal artery on dynamic

8:49

imaging can be seen on both CT or MR.

8:52

MR is technically preferred because, again, these patients tend to be younger.

8:56

Looking at attachments of muscles is better on an MR compared to a

8:59

CT.