Interactive Transcript
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Thank you everyone for joining me. Today. We're going to take a
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look at a handful of cases that utilize head CT perfusion.
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Now this session is going to be intended for
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the intermediate to Advanced learner somebody who already has
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some fundamental understanding of the concept of CT perfusion
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that we're not going to go through in detail. And
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really this is more focus on a case-based review
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of the possible indications and uses of
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CT profusion both. Well establish and emerging indications
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for CT perfusion and hopefully
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it'll allow you to gain some more confidence with your
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interpretations of brain CT perfusion. So
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let's begin with our first case the provided
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history is stroke like symptoms and I'm sure
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if you're practicing radiologist, you'll understand
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that the provided history is often inadequate in these cases
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that and so we should take every opportunity we can to dig
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a little into electronic medical record find any
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useful clinically relevant information that we can to
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help us with our interpretation and so in this
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As we learned that this patient is 81 years old. They
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have a history of atrial fibrillation. They're not on anticoagulation.
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So that's a stroke risk factor their last
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known well 16 hours ago. And now they're presenting with
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right-sided hemiplegia and a left gaze deviation.
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So with that information we're going to really scrutinize the
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left scribble hemisphere for a causative lesion, and
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they're NIH stroke scales 24, so it's quite high.
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It's likely this is going to be a debilitating large vessel.
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stroke if present
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So the first thing we're going to do is examine our
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non-contrast head CT the first step of any stroke
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Imaging workup to distinguish hemorrhagic stroke
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from ischemic stroke. And once we've excluded intracranial
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hemorrhage, we're going to now focus on where is
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the ischemic stroke?
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How extensive are the early scheme exchanges and
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how do we best communicate the
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location instant of that ischemic change.
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So now is a good time to launch our first poll
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question, which is about how extensive
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is this infarct as expressed
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with the aspect score. So
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I'm going to talk while you guys answer the question
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by first pausing at
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the level of the basal ganglia here to tell
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you that the aspects score is the Alberta Stroke
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Program early CT score for
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expressing the extent of infarct in a middle super artery
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territory stroke. Okay, so that is
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scored on images of a non-con has CT at
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level the basal ganglia and at the level of above the
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basal ganglia. So at the ganglionic level we score
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areas of the cerebral cortex the basal
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ganglia the insula and internal capsule and then
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above the level of easy ganglia. We score multiple areas
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of the cortex here.
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So take a few seconds. Look at the area of high potency
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gray white differentiation loss here and
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come up with your expression on non-con
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head CT. What is the aspects score?
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All right, so it looks like the
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Scores are all over the place. Yeah, a
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plurality chose two and that
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tied with five the correct answer
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here is one and let me tell you why so
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the maximum score you can have when giving
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an aspect stories 10 and
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that means a completely normal head CT without any gray white
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differentiation loss in the FCA territory and you subtract
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a point for each of the following areas that
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are involved at the ganglionic level. So frontal
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curriculum is called the M1 territory. So that's
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lost here M2 territory is the anterior part
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of the temporal lobe that's affected here. And three is
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the posterior part of the temporal lobe and like the lateral
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occipital lobe. So that's affected here.
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The caught it nucleus is another that's
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affected here.
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Part of the putanium is affected here. The
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insular cortex is affected here. The
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internal capsules. The only part of the aspect score that's
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not affected in this situation and then above the basal ganglia
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level. We have the M3. Sorry the
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M for M5 and M6 cerebral cortex. That's
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roughly dividing to thirds this MCA territory
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that are all affected by this ischemic
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stroke in addition to the MCA territory,
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which has an access for of one
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in this case. There's also in Far involving
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the ACA territory. We see this medial part
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of the frontal lobe being involved with this
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loss it very differentiation. So overall this
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is a very large territory inpark involving nearly
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the entire MCA territory sparing some
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of the butane internal capsule and also enviral
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involving a large portion of the ACA territory
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as well.
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So the next step in
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imaging is a CTA and CTP,
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but we can already make a lot of conclusions based on non-con scte
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alone, which is why I wanted to emphasize that
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evaluation and providing an aspect
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score with that regard. So the next
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part of our Imaging evaluation is
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that we're going to look at is our CT perfusion
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and the CT perfusion. We can see
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on the summary map provided by the vendor rapid that
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the cereal blood flow in that left
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Circle hemisphere is very low the CV of
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less than 30% is segmented out at
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a volume of 287 milliliters. And once again, this includes
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the MCA territory the ACA territory sparing
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some parts of the deep kind of
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lenticulous right region.
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Now looking at the TMax greater than six seconds
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math. This is essentially that entire territory as
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well and it probably artifactually counts
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some of the contralateral, you know
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ripe Bridal region. So we're going to you know, mentally
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take off a little bit of this volume when interpreting
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these numbers so your cvf less than 30% is
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going to be your ischemic core your TMax career
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then six seconds gonna be your critical hype
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who perfusion volume and the mismatch
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in between of these and between these they have
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38 millimeters, but that's probably an overestimate is what
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would you you would consider your penumbra or
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tissue at risk that could be salvaged if
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you were to intervene. Unfortunately what
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we can see from these parameters summary Maps is
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that the core is large. It's essentially most of
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the lesserable hemisphere, you know, except the PCA
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territory, and this is a matched defect
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in terms of
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The comparing the TMax the CBF less than 30
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territories.
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Some other things we can derive from these summary Maps we can
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see that there's a hypoperfusion index which is the ratio of
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TMax greater than 10 seconds to tmaxxary than
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six seconds volume. And this is quite High meaning that
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this tissue is severely ischemic greater
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than 0.4 is considered high
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and that indicates that there's poor collateral.
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flow into this hypoperfused territory
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Another thing we can observe on these summary images
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is that there's a flattening of this
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arterial input function on this time attenuation curve. We
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see that it starts going up around 15 seconds and doesn't come
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back down towards Baseline until after 45 seconds. So with
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this curve is greater than 30 seconds, which is
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strongly suspicious for cardiac output failure
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cardiac dysfunction causing
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a widening of this arterial input
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function curve. So that's something that I think is relevant
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to mention because sometimes you may be the first
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to suggest that possibility because the patient doesn't come with
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pre-existing diagnosis of cardiac disease.
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So the
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last thing that we're going to take a look at so in you know
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in summary the CT perfusion shows large
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core essentially matched defect
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for collaterals or cardiac output and now we're
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going to examine the CT angiogram just to
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see what are the
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Vessel deficits that are concomitant with this perfusion deficit
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so as expected there is a cutoff of
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this left MCA at the distal M1 segment. That's
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after giving off an anterior temporal Branch.
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But you know, most of the MCA territory is Downstream of
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this large vessel occlusion. In addition.
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There's a cutoff here of the ACA the
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left ACA right at the a1a2 junction.
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So that accounts for that ACA invark we
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could have predicted all this just based on looking at our CT
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perfusion parameter maps and using that to inform
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our evaluation of the CT angiogram.
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Okay distally, we see
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their it's a relatively decreased density
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of vessels and the distal territory indicating poor
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collateralization. The rapid software
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does highlight this area as suspicious for large
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vessel occlusion. And you know, it has highlighted
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that for us based on this decrease density of blood vessels.
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So back to our slides, we have A2 and
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M1 occlusions on the left. We have believed in collaterals. This
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patient was outside of the TPA window.
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So they were not receiving from lysis. The infarc
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was too large to
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Be a good candidate for mechanical thrombectomy because the
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benefit would not be realized in this situation.
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There's essentially no tissue left
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to save if you were to take out that clot.
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They were admitted to the neurological Intensive Care
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Unit where they underwent intensive care for swell watch
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they receive hyperosmal or therapy. They
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considered how many cranic to me if it was within the goals
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of care. But unfortunately this patient progressed to
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have cerebral swelling herniation. They were
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put on comfort care and died within a few
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days.
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So what we learned from this case, so this is a case of a completed
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stroke. They were within the so called late window
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late hyperacute window. That's 6 to 24 hours after stroke
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on set. But the CT perfusion imaging
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basically showed no penumbra of salvageable tissue
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at risk. They were not a hyperacute
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intervention candidate based on the findings these, you
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know, non eligibility for you know
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mechanical term back to me could be made on a non
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contrast CT alone because they were so obvious and
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that there was a large territory in far
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however, not all cases are as obvious
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and in those cases CT perfusion can help
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I wanted to show you an obvious case just so you can match up the non-con
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CT findings with that of CT perfusion.
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Does anyone have any questions on the first case? If you
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have any questions, please drop them in the chat and we'll try
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to address it after each case.
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If not, we'll move on.