0:00

Next case has a history of stroke. Okay digging

0:03

further you find that there are 67 year old they have

0:06

a history of atrial fibrillation. They were found down their lasting

0:09

one week ago their Glasgow Coma Scale is eight

0:12

so we know from this vignette, they're not really a candidate or hypercute

0:15

interventions, but nonetheless the what we

0:18

call the brain attack team was activated. They were started on the

0:21

pathway that includes CT CT perfusion

0:24

and CT angiography. So

0:27

let's take a look at the first Imaging study

0:30

in our group.

0:32

So this is going to be a little bit complicated.

0:39

So we have our non-conhead CT.

0:41

That identifies bilateral abnormalities bilateral

0:44

hypodensities and strugal hemispheres

0:47

on the left side. We

0:50

see these gyrofoam hyper densities that may

0:53

represent MRI to transformation of this larger

0:56

area of infarct. What is this infarct territory

0:59

corresponds to corresponds to the MCA inferior

1:02

division as well as posterior super artery

1:05

Division and there's also an

1:08

area of hypodensity involving the right insula and

1:11

temporal cortex.

1:13

There are some areas of hypodensity that seem a

1:16

little older in the luxurable hemisphere and a smaller

1:19

one the right Servo Hemisphere. Okay. So that's what the

1:22

non-con had CT shows. There's already swelling there's midline shift.

1:25

There's so cool effacement. So we know that some of

1:28

this is going to be somewhat established.

1:31

Look at our summary Maps the CBF less than 30 volume segmented

1:34

by rapid as 0 milliliters.

1:37

The TMax square and then six seconds is segmented

1:40

at 127 milliliters. And what

1:43

is it highlighting here? It's highlighting parts of the superior divisions

1:46

of both Middlesbrough artery territories as

1:49

well as part of the inferior division of the

1:52

left middle server artery territory so we

1:55

can load the pole now while I pull up a

1:58

couple more images

1:59

Asking what is the closest estimate that

2:02

you have to the volume of infarcture? That is

2:05

either acute or Subacute?

2:08

Is it zero is a 127 or is

2:11

it 120?

2:15

And pull up these images side by side for the TMax and the

2:18

non-conhead CT as I

2:21

explained my rationale once we see the answers

2:24

and you guys have finished answering.

2:29

Okay, so a plurality of you chose

2:32

127 milliliters.

2:34

But the correct answer is 270

2:37

milliliters and here's my rationale why

2:40

so the 127 is coming from the summary

2:43

map of the TMax elevation. Unfortunately, what

2:46

is represented by the TMax elevation here

2:49

is not exactly corresponding to what is

2:52

a parent as infarct on a non-con head CT.

2:57

In this situation we want to use the

3:00

non-continhect to our advantage in

3:03

defining the areas of Subacute established in

3:06

fart. Okay, these are areas that are not

3:09

being caught on the CBF map because they

3:12

have reproduced already or there are

3:15

so hypodents that the rapid software is considering them

3:18

chronic infarct or something along those lines. And

3:21

so in order to do this analysis and you

3:24

know, I would break it down into vast segments. Okay.

3:27

So if we look at the left middle sobriety territory, what

3:30

we know is in fact it is this inferior Division

3:33

and that is hypoperfused. Well we

3:36

know is not infarctic is this Superior division

3:39

involving the frontal lobe and that is hypo perfused

3:42

as well.

3:44

In this posterior cerebral artery territory. We know

3:47

that isn't far too based on non-con head CT, but this is actually hyper perfused

3:50

based on the TMax map. We see a deep blue here.

3:53

That's a decrease in TMax.

3:56

But just because that is decreased doesn't mean it's not already irreversibly infected

3:59

we can tell that on a non-con head CT.

4:03

On the right middle super artery inferior division territory. We

4:06

see similar picture of high per

4:09

profusion meaning decreased team act here, but

4:12

we know that area is infarcted because it's hypodense and blurred

4:15

out on our non-con CT. Okay, and then

4:18

Superior division there is an elevation of Team

4:21

act. So he's hypo perfused but non-con CT we

4:24

do not see establishing far there. Okay. So we

4:27

kind of repeat this analysis for all the different vascular territories. It's

4:30

come to our conclusion of what is in far did and what

4:33

is not in far did so you can make it two by two table using your

4:36

team acts estimating. What is hypo perfused and

4:39

what is hyper perfused?

4:41

And what is established infarct and

4:44

what is nine-farted? Okay. And so

4:47

we're going to use these kind of perfusion abnormalities

4:50

for Advantage when we review the CT

4:53

angiogram. Okay. So we saw hypo

4:56

perfusion both Superior inferior divisions of the left MCA. So

4:59

we're going to look for approximal left MCA occlusion

5:03

indeed. We find an MCA M1 occlusion

5:06

on the left side that accounts for that hypo perfusion team

5:09

acceleration in both Superior and impure division

5:12

territories.

5:14

On the right side. We don't see a large vessel occlusion the right MCA, but

5:17

we know that there was hypoperfusion in

5:20

that right Superior division territory. So if we kind

5:23

of scroll in the Satchel myths to that area we can

5:26

see there's an area of severe stenosis of

5:29

one of the M2 branches here that supply that

5:32

frontal lobe where we saw that region of high Volvo

5:35

perfusion. So this is like steno exclusive disease is severe that

5:38

may account for that area of hyperfusion. Okay,

5:41

but we don't see persistent occlusion

5:44

that would account for the infer that we

5:47

see so presumably it infarcted and Rec analyzed

5:50

and you know, we don't see the persistent occlusion there anymore.

5:54

So those are the findings

5:57

of how we use the C2

6:00

profusion to our benefit when seeing these

6:03

multifocal infarction multiple of asset

6:06

territories. We're going to suggest an embolic etiology

6:09

and supporting that is actually looking at

6:12

the arterial input function on our time with attenuation

6:15

curves. We see that it starts going up around like

6:18

12 seconds doesn't come back down to Baseline until well after

6:21

40 seconds. So the time it takes to go up and come

6:24

back down as greater than 30 seconds which again should suggest in

6:27

your mind the possibility of cardiac dysfunction underlying all

6:30

this and we know this patient has a history age for fibrillation. It's

6:33

unclear whether ejection fraction is

6:36

but that was evaluated by a bedside echocardiography and

6:40

that was found to be depressed supporting this conclusion.

6:46

So what are some teaching points to get away from to take

6:50

away from this CT case? So when you have

6:53

bilateral perfusion abnormalities or Subacute infarcs,

6:56

these are often not picked up on the rcbf summary

6:59

Maps when you have reperfusion of

7:02

imparks. You may not meet the TMax thresholds

7:05

that you typically use to define hypoperfusion of

7:08

infarctic or potentially infarctic territory

7:11

on your summary Maps as well and these

7:14

cases of Subacute infarctica really rely heavily on

7:17

your non-con CT to determine what it's matched versus mismatched

7:20

non-con CT determine what is infarct

7:23

core and your

7:26

team active determine what is

7:29

kind of hypo perfused tissue use the

7:32

CTP to your advantage to look for a medium vessel

7:35

abnormalities that are difficult detect on CTA by itself. We see

7:38

a large region of hypervision. We're going to really scrutinize the

7:41

medium vessels that supply that area for standard occus

7:44

disease.

7:45

So the next part is

7:48

really just an MRI that confirms some

7:51

of the abnormalities that we saw in CT just

7:54

to convince you guys that you know, I'm not making this stuff up

7:57

that when we look on the DWI. We

8:01

see these areas hyperintensity. It's not really hyper intense

8:04

like a hyper acute infarctica. It's

8:07

kind of a mild signal intensity and

8:10

that's because it's now a Subacute in Far a lot

8:13

of asogenic edema in the area as well in that

8:16

left MCA inferior Division and then posterior

8:19

cerebral artery territory as well a more

8:22

recent in far from the right temporal insular region

8:25

of that right MCA inferior Division.

8:28

And then we see that chronic infarct in

8:31

the left Superior server hemisphere more recent

8:34

important, right Superior server atmosphere and the

8:37

GRE confirms the suspicion

8:40

for particular hemorrhagic transformation in this gyrofoam pattern

8:43

in that area of subway.

8:46

Optical hemisphere

8:50

So MRI confirms our suspicion that

8:53

we could identify on close analysis of the CT including

8:56

areas of particular Hemorrhage and

8:59

this Subacute infarct. This patient was managed

9:02

with anticoagulation for their

9:05

presumably cardioabolic source of stroke in

9:08

summary was this case about this is

9:11

a case of bilateral late acute or sub acute infarcts.

9:14

The pitfalls to know about is

9:17

at hyper perfusion can exist in these cases because of

9:20

luxury perfusion after either treatment of clot

9:23

or spontaneous rebassadorization due

9:26

to clot autolysis or recruitment of

9:29

collateral flow.

9:33

The rcbf summary Maps can be falsely negative

9:36

when the abnormalities are bilateral as

9:39

and in these cases you got

9:42

to rely heavily on your non-con CT to

9:45

delineate what is established infarct or not?

9:49

So we have any questions on that.

9:52

Yes, we've got two.

9:54

Are you performing the perfusion before or after the CT angio?

9:57

Does it make a difference?

10:00

I don't know that it makes a difference. I think either can be done depends

10:03

on the protocol at your institution what

10:06

you have set up on your scanner.

10:10

This might be more General on stroke protocols. What

10:13

do you perform first CTP or CTA? Is there any difference

10:16

performing one or the other first?

10:20

Yeah, I I am not an expert on the technical

10:23

factors there. I think

10:27

both have been done. I don't

10:30

know which one is preferred.

10:34

That's it for the case. Yeah, and my old institution. We

10:37

did CTA followed by

10:40

CTP.

10:43

You did have to wait a couple minutes after a

10:46

CTA to let that contrast equilibrate. So

10:49

you get back to Baseline before we start your CTP.

10:52

And so it does add a few minutes before we

10:55

have a reliable signal for CTP. But

10:58

usually you're doing your

11:01

technologists are doing stuff on the on the on the scanner trying to

11:04

gear out for the CTP. Anyway, so the time

11:08

passes pretty quickly, but that's how we did things

11:11

where I trained.

11:14

Got one more question for this one isn't anticoagulation contraindicated

11:17

given hemorrhagic transformation.

11:23

That's a good question. So I'm not a stroke neurologist or

11:26

neurontinence intensivists. I will say that.

11:30

The degree of hemorrhagic transformation is informative

11:33

in determining how

11:36

and when to initiate anticoagulation.

11:39

So anticoagulation is indicated when

11:42

people have a cardiabolic source such as with atrial fibrillation and

11:45

the timing of the initiation of that

11:48

anticoagulation.

11:51

Depends on how large the territory

11:54

you're infarct is and whether you've had

11:57

symptomatic hemorrhagic transformation or not,

12:00

but it's not a strict contraindication, but people

12:03

do vary about when they start anticoagulating for

12:06

this patient and atrial fibrillation

12:09

some might wait, you know two weeks after the stroke

12:12

before beginning into coagulation. So what I

12:15

indicate on the slide that the treatment was anticoagulation, I don't think it was

12:18

immediately be gone because they were suppressants

12:21

of of because there's a presence of hemorrhagic

12:24

transformation. That would be a relative contradictation to

12:27

immediate initiation of anticoagulation.