Past medical history of hypertension. He was working at the tire shop when he started feeling dizzy and nauseated. He went to the local ER and when he presented there he suddenly developed this dysathria, weakness on his right side with left eye deviation. They did a none contrast head CT it was negative for bleed or any
other pathology that gave him tPA and they transferred him to our institution, when we arrived he was intubated, they did that because they were concerned about his airway and he was on Propofol for sedation. That in it of itself raises a whole another question.
But we can address that a little bit later. The neurologist saw him and found that he got no response to any voice. But he did have spontaneous movement in both of his legs, he was withdrawing to pain in his right arm and both legs but his left
arm was flaccid with no response to painful stimulus. His pupils were mid line, negative doll's eye, right corneal reflex but none on the left and he had symmetric reflexes in his extremities. So here's the head CT and you can see he's got a robust right vertebral and a very small distal left vertebral and this is the problem
right here. Embolise in the distal basal artery. Initial angiogram, I got into the left just to see if there was any way to get up there but you can see as you follow this up it is very tiny. The right side was occluded which raises a challenge.
You know if you tandem occlusions in the carotid. That's some that at least in our population, we see that a lot. And it seems like it happens every other time that we're doing stroke interventions. But, it's probably not that high.
I was actually able to get through that but not from below. I tried from below from the arm from the groin, the only way I could get there was actually to run a micro catheter wire up this way down the [INAUDIBLE] snare it after getting through started it from the arm and then I was able to get through and stent this.
You can see a micro catheter after getting through it had a lot of filling defect in here already. Like Ken said, when you have got an ICA occlusion and an MCA clot, it's rarely filled up with clot.
The radiology resident or the neurologist or the ER physician will call me and say, oh yea, we've got an ICA occlusion from the origin all the way up to the MCA and it's never like that. Once you get through, you'll see that.
I should say, it's not never, it's rarely like that. So I was able to open that up and then from the arm it would restore this. I actually did this with the original Penumbra Aspiration system in a separator and I was able to get some of the clot out with
that but then I think it just barely gotten the solitaire device in and so I used that and I was able to open it up. He had a little embolist that went out to the right but otherwise did pretty well. This was his MRI afterwards. It took him about three weeks in the hospital,
to really he wasn't fully recovered by then, but he did spend three weeks in a hospital. After a few months when I saw him in follow up, he had some trouble with his balance and his coordination.
But otherwise he was pretty remarkably well. So one of the reasons I wanted to show these case is because with tendon occlusions in the posterior circulation it's possible just like with the anterior circulation but you might have to get creative about how you get there, especially like in this situation with
the tortuous approach from the right vertebral artery. You know you might have to find another way.
Second case, and by the way if anybody has a question while I'm going through, don't hesitate to raise your hand. I don't want to get to the end and have people forget their questions, they might
not get answered. Second case was a 49 year old female with hypertension who arrived at work one morning at 8 o'clock complaining about a headache. She came out her office about half an hour later and her co-workers said that she appeared different. She was mute tremulous.
They called 911 and when she arrived at the ER, she had weakness, on the right side was aphasic, not following commands, and gaze deviation to the left side and NIH stroke scale is 24. No contraindications to TPA,
and when she arrived at our institution this was her CTA. You can see the M1 occlusion but she also had this filling defect right here in the left ICA origin. This was the perfusion map with the blood flow, up here showing decreased flow,
the blood volume, there is some infarct here but overall when you look at the mean transit time, a very large area of at risk territory. This was the first angio. This is the fetal PCA and of course your M1 occlusion. This is the initial angiogram.
Here's that filling defect. And this was after I put in a stent. The way that I did this was I had a nine French sheath at the groin put the moment device up there for [UNKNOWN] protection. I actually used the moment quite a bit for carotid stents if I'm worried at all about knocking off stuff that could embolize to
the brain. And in retrospect I wish I would not have stented, but I'll get to that. I mentioned before that we see a lot of tender occlusions and in the heat of the moment I was like okay there's something there in the coratal/g origin,
I'm just gonna stent and go and, got up there, used my micro catheter run showing no extravasation and after two passes this was the result. There's a lot better flow, but I grade as a ticky 2A. I wasn't really more aggressive at giving more of the frontal lobe here
because I knew that there based on the perfusion imaging that I had in fact of this general vicinity and I didn't want to open that up and increase the risk of hemoragic conversion. This was her MRI afterward, I think that we had these images within an hour.
So there is plenty of out of stroke. Here it's scattered around the MCA territory. The next morning this was her head CT. And most of the MCA had gone on to infarct. She also got an ultrasound.
I don't know if I can show arterial, here we go, and that stent had occluded. This is the only instance where I've had a carotid stent occlude on me afterwards in that 30 day period,
>> [COUGH] All right. Thank you. Next case. 68 year old female presented to be an outside hospital with right visual feel depth set like weakness. And she was admitted for a stroke there.
She had a left PCA in fact. But she also had a critical left vertebral steneosis. Three days later, they were about to transfer her to a rehab facility when became unresponsive and both the upper and lower extremities. She was transferred to our institution, where a non contrast CT
was negative. And the DWY was negative. This was her MRA. You can see the basal artery coming up and then just stopping. Here's the angiographic images. The problem here though is that the left vert/g was occluded.
These are actually images from one of my colleagues who did this part of the case. And, he went up the right side, he was able to get a really good flow. Maybe a little a distal embolis here in the left but I think if
i remember right that's where her impact was. Early the next morning i think it was about, was it 4 AM? The actually nurse noticed that she was a fasic She was pasturing intermittently following commands and so they got a head CT thinking that she had a maragic conversion but she hadn't reacluted her
basil artery with that hyper dense right there and there's a filling defect on the coronal/g nips, So at this point I was on call and when I got the whole story I was looking the imaging asking maybe there's something at the proximal right vertibral but really nothing, not even stenosis not
at the section. Again here is the Basilar Occlusion is able to get it open fairly quickly, this was using I think it was a either five max acer or A64 up into the basilar artery with a solitaire using that stent retriever and aspiration, the first time around was also a solitaire
and once I got it open I thought let me check and see if there is anything at all in that right vert again even though the chance of something being there maybe there's got to be something what if she throw another clot within 24 hours and this three four days after she'd already thrown a big clot. This was her MRI.
And you can see that she has a fair bit of brain stem infarct with all of this and a fairly poor prognosis. Her family decided to make her comfort measures and she passed away three days later. And somehow I did not include a video of the left vertebral artery because after I looked at the right again on the way out,
I looked at the left, and you can see this little trickle getting through there. And there was plenty of collateralization coming from costocervical, thyrocervical whatever.
And you could see a bunch of clot seating there in that V2 segment. So that had to be where it was embolizing from. >> Yeah. I had a case like that six years ago and we actually there was enough flow that we were able to identify the thrombus there. I actually went after we took the clot out of the buzzler there
were several residual clots that actually went up and over and coiled it to just sacrifice it, make sure we were done and there were no additional embolizations from there. And that's what afterwards when I was talking to my colleague about this that's where we were both thinking if we need to,
depending on how she does, we can certainly go back and do that. So any questions or comments?
All right, case number two. A 64 year old right handed male, left MCA syndrome, NIH was estimated
to be between 24 and 26, last seen normal at 09:45 hrs. WAWA EMS was called, the patient was transferred to an outside hospital. The patient was given IV TPA without improvement
one hour post ictus. Non-contrast head CT at baseline was a 10. Again, we were able to look at these films from the outside hospital. CTA showed a one centimeter left M1 occlusion. The patient has a large vessel occlusion, got IV TPA, they call
us, we say just ship them. There's a very low chance this patient is gonna improve because of the size of the clot alone. Past medical history. Hypertension, no allergies, alcohol abuse, patient lives alone.
Here's the NIH stroke scale, and I guess this was from earlier this month. Seventh, NIH stroke scale was 24 on presentation, so no significant improvement. ASPECTS score was 10, looking at this occlusion and don't see any changes in the non-contrast head CT.
The CTA, I just showed these. I basically used them, axial imaging, but then I go through the MIP imaging. If films are available, so all the patients
getting transferred over here. I'm looking at these three critical portions to plan my procedure. Pull all the equipment, have it ready to go. I'm looking at the arch first, making sure there's no ostial lesions, looking at the proximal tortuosity. Second thing I'm looking at very carefully is where did this stroke from?
Is it a artery to artery embolism? I'm looking very carefully at the bifurcation. And then finally I generally will use stent retrievers with balloon guides. Where am I gonna put the balloon guide catheter? Is it feasible or should we consider aspiration. This patient does have a pretty nasty little 360 loop here in
the distal ICA, so I'm keeping that all in mind when the patient comes in. Here's the MIP reconstruction, you can see that the clot is at least 12 millimeters. I do see some suggestion of collateral vessels, but it's not great. But again, when I'm talking to neurologists,
I can tell them that this is a good patient to just helicopter over because he's probably not gonna get better. Here's a patients wake, general conscious sedation, 8 French sheath, and then I used a VTK glandular/g advantage, and then navigate the balloon guide catheter as high
as I think it can be done safely. Like I said, there's a 360 degree loop which I already know about, and I don't even try to mess around with that loop. Once I'm in the internal carotid artery I'm pretty satisfied. So you see no flow to the left MCA distribution. Really good
look at the ACA. On the late arterial phase I'm always hoping, and you can see really robust leptomeningeal collaterals. And when I don't see it, like this patient, I kinda get bummed out
cuz there are some collaterals, but they're not that great. And they don't get all the way back to the back surface of the clot. So already feeling a little bit pessimistic about this. [COUGH] Again I want the guide catheter at the skull base, but I would prefer safe over ideal, and so I'm putting it here as low as possible. And before I access this, a lots of times I'd prophylactically give them a
little bit of verapamil, like five milligrams intra arterial verapamil, before I start putting devices in here. So trevo is deployed. This marker represents the distal under the trevo.
And here you can see the trevo pretty clearly here. Here's the proximal end of the trevo. And you can see how much I've loaded the device so I unsheath, probably about a centimeter or two. And this is all very, very, very active load.
And when I say load, I mean I'm pushing the device and gently withdrawing the micro catheter rather than passively unsheathing it. So here's the trevo device is deployed, then I'll do a little angiogram to see what it looks like, and it looks terrible. Like
there's no antegrade flow, so I'm getting more upset here. Take trevo after that pull, second pull I kind of repositioned it a little bit more proximally. Same thing really loaded the device. You can see right here that's where the clot is sitting.
Unsheath and then load the device. Here with the device up we've restored antegrade flow. And this is what the trevo looks like. After pulling out the trevo second time, no improvement. So anybody next step would do have a flow gate
0.084 and then I have a trevo open already. Anything you guys would do next? >> [INAUDIBLE] >> Yeah, yeah. Aspiration at this point,
see if you can get engage the clot. >> Yeah. >> Just get it- >> I agree, I do that. Usually I'll do two passes and if it doesn't work in two passes I'll add aspiration.
Before I would basically have to take out the flow gate, or use a very small aspiration catheter so striker guys will come out now with the CAT 6 which will fit through the balloon guide. It's an 0.060 aspiration catheter. And basically, here's the distal
end of the balloon guide catheter, and then now with the CAT 6, I was able to quickly track that CAT 6 all the way intracranially. Now the CAT 6 which is designed to work with the flow gate pretty much makes perfectly, and now I feel much more comfortable getting the balloon guide higher. So now you can see I've pushed the balloon guide higher,
here's the CAT 6 device. And now when I deploy the trevo device, here's the CAT 6 which is sitting right at the M1, here's the trevo device.
Once I deploy the stent retriever, I'll pull out the delivery micro catheter. So the stent trevo is not going anywhere. I know we always are trained to never let go of the wire, but you could pretty safely remove the catheter. And the reason I do that,
is that it allows there to be more space between the transceiver and the intermediate catheter, and so this intermediate catheter I attach to a penumbra pump, and then the balloon guide catheter again, I have an assistant doing aspiration.
So once I have the stent trevo up, I'm able to pull a lot of stuff higher. So it's kinda grappling hook technique. You deploy that stent trevo now, I'm gonna take the intermediate catheter up to the face of the clot.
I don't want to capture the stent trevo, I just wanna bring it up to the phase, and when I feel a little bit of resistance, I'm thinking in my mind that I'm able to sandwich the clot between the stent trevo and the intermediate
catheter that's attached aspiration, and then somebody's manually aspirating. So that's me pushing the CAT 6 a little bit higher, and pushing it forward to kind of engage the clot. Now here's the flow gate,
again I think it works best when it's like at the skull base. Now I'm able to a little bit more aggressively move the flow gate right up to the skull base. Now I inflate the balloon guide, pull everything out and this is TICI 3 reperfusion.
Here's the AP lateral view. I don't see any non targeted emboli. Once I did everything and I pulled back, I'm gonna take a very,
very careful look because as a little bit aggressive with the carotid. I wanna make sure I didn't create a dissection and I wanna make sure I don't leave one if I did. This patient unfortunately took three passes, which is kind of frustrating. Generally it's one, one and half passes, but this
was a little bit trickier. Patient go to the room at 12:57 hrs, groin puncture was 12 minutes later. It's not because I'm good, it's because we do it with max sedation, no Foley, no art/g line and it's like a level one trauma. First pass from groin stick was 14 minutes later. Very simple, I
use the same approach every time and then modify that approach, but I try not to use different approaches every time. Final revascularization happens 49 minutes later. That's the CAT 6. Basically, I just showed this with a 5.4 French catheter and it's a 0.060 catheter.
So here's the actual clot, you can see the tip of the intermediate catheter, you can see the stent trevo, and you can see that the clot is kind of wedged between the two. It's kind of corked in there. And once I pull the intermediate catheter back,
you can see how it pinned the clot in there. But again, I only use the intermediate aspiration as second line. Here's the NIH stroke scale. Unfortunately, the patient's NIH stroke scale although improve will still a 10.
He ended up going to DTs, and having a pretty rough course. Any questions for that case?
[INAUDIBLE] So I think a lot of this has to do with how you present [INAUDIBLE] You can have a sophisticated [INAUDIBLE] with an
understands what's going on once a clear cut answer. And I think, the 40 to 50% improvement to the 10% improvement is reasonable when we're starting out. >> Yeah. And the last thing is that we can get the clot out but you can't guarantee they're gonna do better, and this patient won't fall within the trial data.
It's like well outside, and it's like kind of in the end. Okay, the last case I'm gonna show you not to end on a bummer, but, we keep this data in our mind but cases can go badly. I tell people that are asymptomatic,
I can make you worse so stop asking for stuff to be done to you, cuz you'll find somebody to do it. This is a 84 year old, right handed, Indian American male, makes me feel even more sad.
Patient presenting with malignant right MCA syndrome with a complete occlusion of the right ICA. ICA/MCA occlusion. Right there angiographically, we're looking at a very bad outcome. And then you have an 84 year old. You have an 84 year old with a right ICA/MCA and an NIH greater than 18.
I mean, I'm not gonna tell them they're gonna have a 50% chance of a good outcome on this one, I'm gonna be like 10%, 15% chance of a good outcome. This is the non-contrast CT of the head, this patient's already
suffered prior stokes. Here is the right PCA distribution stroke, and I don't see too many early ischemic changes but you do see, let me see I think I blew this up, here you go. The putamen, insular and it's hard to tell if this is a new M2 for ASPECTS, or an old PCA. ASPECT score is actually an 8 here.
The CTA of the neck, this was the dictation that came with patient. It's important for you to review your own studies, and I've just highlighted this one. Severe stenosis near occlusion of the proximal right internal carotid artery.
Secondary to a ruptured plaque versus dissection. The remainder of the right internal carotid artery is occluded. So anytime- >> [INAUDIBLE] >> Absolutely, Dr. Satti was informed, and appeared disinterested. Yeah, they put that there.
>> [LAUGH] >> The bifurcation, like whenever you see these carotid occlusions in the entire vessel, it looks occluded, just keep your mind open for these, cuz sometimes it's just a stagnant column of blood.
So don't get pessimistic right away with these, but I didn't see any good flow at the skull base. Minimal opacification, right supraclinoid ICA proximal right M1 segment. M1 and M2 were occluded. And this is something I included in here,
which is probably why the patient's NIH was so high. The patient's right A1 segment is severely hypoplastic. So this patient has four in essence an isolated right MCA, so there's not really good collaterals. That also makes me very nervous about revascularization of this
patient, because even though the ASPECTS didn't look terrible, ICA, MCA, no ACOM, that's in an 84 year old. So this is the first injection and there is some flow. And this is the AP view through the cervical ICA all the way up to the proximal
internal carotid artery. So there isn't complete occlusion of the ICA. And then on the lateral you can see severe stenosis of the right internal carotid artery. This is not my case, this is my partner's case. But for me the way I approached this carotid lesions is,
number one, what I think about is, is this stenosis in the neck the cause of the patient's stroke? Or does the patient just have some stenosis? If the patient just has some stenosis I'll just get by it and deal with the intracranial. If I'm concerned this is the source,
so it's a large artery to artery embolis? I'll be much much more aggressive about stenting this upfront. I don't like crossing these lesions. You can anything to go by it, you just have to push hard enough. It's just, you're making a mess,
and this can re-embolize. So that's a consideration number one. And then intracranially, you can see this is kind of some spotty flow through the ICA, and you see a trickle of throat/g through the MCA,
and maybe a tiny bit into this hypoplastic ACA. And I'm just showing this morphology of the carotid artery, and this is something to really keep in mind. When you do your first angiogram, I would highly recommend you save those images. So you know what the vessel looks like from the beginning to the
end of the case, and if there's a change. Look at the little bit of this plastic appearance of the intracranial internal carotid artery. It's a little bit [UNKNOWN] So this patient had a trev-umbra. And the way it was described to me for some reason it felt really, really hard to pull it out. Like unusually hard. So I was like oh, okay, I'm feel anxious just hearing that.
This is after one pull. The trev-umbra basically set [INAUDIBLE]. Intermediate catheter is brought up to the face of the clot like the last case I showed you. Attach aspiration to the intermediate catheter and you're pulling it
all out. And so generally I don't feel a lot of resistance with those kinds of pulls, so that makes me nervous. This doesn't look terrible. You have like revascularization with antegrade flow through the
right M1, M2. And this is why I don't like leaving carotid lesions. If you look down on the neck there's a lot of clot sitting there. I don't know if it's propagated, or it's just starting to form. And again, look at how dysplastic and kind of irregular the supraclinoid ICA is.
So then, I'm always looking at my pre-run versus my post-run, and I have a pre-run meaning the first angiogram on the right side. And then so, does anything kind of looks different? This than this. It's very subtle but this looks a little different to me. I'll come back to that in a second.
So here's the AP view and on the lateral view there's pretty large areas of hyperperfusion this posterior division is missing, and so let me just blow that up again. This is the pre, the original angiogram. And this is the repeat, there's like a little
linear filling defect here. You can see it there. So now, the next pass to get that posterior division open, where's Chris? He was upset about that ceracnoid/g I'll show you ceracnoid/g, Chris.
>> [LAUGH] >> So the next pass now, and this is why Allen, I don't know how many times he said this, you never wanna bring a stent trevo up into the head until you've done a micro catheter injection, cuz
you have no idea where you are. So now the catheter is getting up into this area that's dysplastic, where there was a linear filling defect/a pseudo aneurysm from a dissection flap, and now this thing has gone through that pseudo aneurysm. And this is just all,
as you guys know, extravasation subarachnoid hemorrhage. And this is a massive hemorrhage. If you had a balloon, there's no balloon here, you could've at least tried it.
This is like- >> [INAUDIBLE] >> No, I didn't even want my history being that I opened this study. But, anyway put a balloon up if you have a balloon. I mean, this is pretty much
serious. Drop the pressure, or you could do [INAUDIBLE] suppression, mannitol, hypertonic saline, call everybody and anybody you know. And you can see already here is contrast pooling. This was a hand injection, just an oh crap kind of hand injection. And it's really seedy anatomy here. This is basically
the vessels completely unroofed. So ultimately this patient ended up having sacrificed MCA, ICA, with coils and Onyx. This is the last thing. We all have problems with cases and things
go badly, once you have a problem you have to stick it out. Can't just stick your head in the sand, you gotta finish it. So this thing gets occluded, get control of the bleeding.
Shoot the contralateral side. Nobody wants to keep working on this patient, but you gotta shoot the contralateral side. Make sure that there's no bleeding from left to right, and just get it done properly.
This is the initial head CT which just makes me cringe. This is a combination of blood and contrast. This is immediately post, this is post-op day number two. You can see that the entire right MCA is gone,
basal ganglia, everything's out. This is an old PCA stroke. And you can see how poor the cerebral perfusion was, which at two days later you still have contrast sitting there.
This patient never recovered. His comma, withdrawal of care two days later.
58 year old man presenting to outside hospital previous evening with leg weakness, slurred speech, difficulty walking. His initial head CT was described as negative.
One thing that's been really helpful for us, we have like a hub and spoke model. We have two primary hospitals and seven hospitals that refer to us. It's taken about five years, but we've now been able to get access to all of their paxes.
This was before that. Now, if somebody calls me about a case, we can just tell them to push that patient's images to our pax. If you can get that kind of arrangement, it's been very, very helpful for these kind of cases. The family declined
IV TPA. I'm always very suspicious when I see stuff like this, because this is half of it. It's the consenting process that the neurologists frequently dissuade people to get IV TPA but this really annoys me to no end. Next morning 08:10 hrs, patient found unresponsive by the nurse. Repeat head CT/CTA was performed at outside hospital.
So this was the initial head CT which was negative, and the patient has a hyperdense basilar artery. This is the repeat head CT the next morning, that hyperdense basilar is still there, and now there is a anterior [INAUDIBLE] and lateral pontine infarct
and a left cerebellar infarct as well. CTA was performed at an outside hospital, and again we were able to review these films, and there's a top of the basilar occlusion. At this point we get called. [COUGH] I'm just showing this.
The other thing we have is an EMR at our hospital. I used to find that pretty painful, but it's actually nice because actually you can read what people are writing now. And one thing that's built into the EMR is an NIH Stroke Scale. Every nurse in the ED, resident and attending in the ED, all
of the nurses on our stroke units like the neural ICU, and our stroke treatment and recovery unit, is trained to do NIH stroke scales. And so there's no longer as much guess work. There could be errors with this, but they do full NIH stroke scale and it's documented. It's documented when it was performed, when it was entered,
by whom and NIH stroke skills. This NIH stroke scale and admission from the ED was 31. We always repeat head CTs when we get transferred patients just to make sure that they haven't had significant progression of their infarct. CT showed no significant change in my opinion, anterolateral pons and cerebellum.
Now the patient is intubated, so we have no exams by the time they got there, and by the time downstairs. Maybe my approach is too simplistic, I don't see a huge utility for MRI in these situations. If you have basilar occlusion your chance of survival is about 20%. You're gonna die from this thing.
You could die, and the only time I get concerned if you're less than eight hours, or are we gonna leave people locked in. I have two patients I have left locked in. Once you're beyond a certain time I think the MRI is useful, but waiting to get an MRI at our institution at least, is like a two
hour delay to be honest. So I just proceed from here. I don't have the CTA imaging but the patient but had very, very severe tortuosity of the innominate artery and the right sublavian with a hypoplastic left vertebral artery. There's no access from
the left vertebral, I'm gonna go in the right vertebral and I have tons of tortuosities. I'm a big fan or radial access, so I just do primarily radial access for these kinda cases. I'm just showing my basic setup here, this wasn't this patient. The patient was African-American
but this was just another patient. I usually use ultrasound guided single wall micro puncture technique, put a micro puncture, you can see how clean and neat this is. I don't do anything different, this is a femoral drape,
I just move the femoral drape over the wrist, and the other side of the femoral drape is over their groin, but I don't even prep the groins anymore. Here's the micro puncture, here's the 6 French sheath, I don't hub the sheath. You don't need all of the sheath
in the patient, the sheath gets bigger as you get further so I basically just tape it down, put two or three centimeters in. First thing I generally do will do an angiogram, renal artery angiogram, make sure there's no tortuosity and loops. And if it's pretty straight
forward I'll just go up with a glide. If there is tortuosity and loops then I'll go try axial with a microcatheter, and it usually straightens up pretty quickly. In this case we just had this sheath and then we went up with a penumbra 4 max catheter. I usually will use a fathom wire which is basically a syncro wire
and an .O16" platform. Here's the initial, right vertibral artery injection. You can see a mid to distal basilar complete occlusion. Here's the pike on the lateral, and there's no real reflux of contrast into the left verterbral artery. I did three passes with the penumbra 4 max,
TICI 3 revascularization. Radial puncture to penumbra deployment was six minutes. From first micropuncture stick to deploying, 6 minutes, and then three passes, took a total of 22 minutes. And everybody else showed some amazing cases and I feel embarrassed to say, most of the patients I see for basilar occlusions,
by the time they get to me they're intubated or comatose, they do extremely poorly. The my consent for these patients and families is, your loved one, I'm sorry to say,
the natural history of this diseases to die. They're very unlikely to make a meaningful recovery, I would say like 30% chance of a recovery at all. So I think setting these expectations is extremely important.
All of the data that we've presented over today and the last couple of days is based on ICA-MCA. Post your circulation. So these are good discussions to to have with families, to really under promise and over deliver.
And the other thing I do discuss here is are end of life issues, that if this patient doesn't make a meaningful recovery in two or three days, it would be reasonable to consider supportive care. Because your loved one could potentially be locked in, and we briefly discuss that.
I think it's a disservice to just open up basal arteries without having that discussion ahead of time. Anyways, it's a little bit of aside. [COUGH] Immediately after procedure, next day here's the NIH stroke scale that the nurse put in. NIH stroke scale was 18. We have two
nurse practitioners that are just on our service and they enter these for us as well. So unfortunately for us, this patient NIH stroke scale, despite revascularization went from 31 to 21. She was 17, two weeks post-procedure, discharged at SNF. Unfortunately his modified rankin at four and a half months
is still a four. Unfortunately most of the patients I see for for basilar occlusions by the time we revasculadrize them they tend to not do well. Any questions on that case?
do have a strokes. They didn't come to you in proper time. Is there something that we can do to prevent their strokes? That's called medicines. That what we normally do. But there's some patients where you see
that the carotid arteries are still pretty narrow. It may have contributed to their stroke maybe they're outside the time window for you to be able to treat them with these. But now you know you have an
opportunity to treat the carotid disease it doesn't cause another stroke. That was the case that you have in front of you. A 72 year old man who came in with weakness in the left side couldn't see had slurred speech. He
unfortunately came a day after. So we couldn't offer him anything other than medical management. But a month later he came back so that he could have the carotid artery addressed. You can see on that picture that's a reconstructed
picture that shows the narrowing of the blood vessel with the arrow. There's hardly any flow across that narrowing. And the 2D reconstruction here with the coronal picture show that there is a huge atherosclerotic buildup to the point
where there is no flow. And the key to treat this is no small undertaking. Because if you go ahead and you angioplasty that atherosclerotic lesion you can actually send all the debris upstairs.
You could say that you could use a distal protection device but you would have to get through that narrowing. And when you do that you're going to dislodge all the debris upstairs. So in this case we wound up using a proximal flow arrest
device so that when you go ahead and do the angioplasty and lay the stent there is no forward flow to shower all that emboli. And that's exactly what we did. So here is the before and with that degree of stenosis the very next picture
shows you how much blood flow is going to the brain. (Thank you so much) So this is the narrowing. With that narrowing this is all the brain that this blood vessel is able to supply. The brain is starving for oxygen. Once we did the
procedure and you can see the outline of the stent here that looks like a very nice result. What does the brain look like. This branch wasn't even seen before. These branches were not even seen before. Now they're all open. So again there are
things that we might be able to do provided that the patient comes to us in a reasonably timely fashion to treat them from very their ischemic stroke and prevent the future risk of a stroke. So I'm going to
another example you can see the arrow is pointing to the blockage and after doing...in this case we just did suction thrombectomy. You can see that the configuration of
the clot mirrors the bifurcation. And that's what we pulled out with suction thrombectomy and this patient also did very well. The unique thing about this patient is that four days ago the patient had
CABG for symptomatic coronary artery disease. So when the patient was discovered in the morning 15 minutes prior to discovery with stroke symptoms she was fine. Talking moving everything. 15 minutes later somebody
walked in she was doing nothing. Couldn't move couldn't talk. So we couldn't give her tPA because she post surgical. The risk would be unacceptable. So we brought her in and this is what we found and we did aspiration thrombectomy and that's
what we pulled out. And she went from a stroke score of 22 which is very severe for a stroke score of 1 the next day. So again examples that show that we now have a very effective way to treat ischemic strokes. The key here is that it
needs to be timely identified. And that's that's what you know it's still a work-in-progress nationwide but now we have technologies to treat these people that improves outcome and decreases mortality.
treated. 77-year old guy comes in with slurred
speech. Left side of the face left side of the arm they're both weak. Patient was last known well sometime at night and has hypertension cholesterol. Has had a history of heart attack and heart failure takes Plavix.
There is a standardized way of assessing these patients symptom severity and that's called the NIH Storke Scale. It goes from 0 to 42 points and this patient's number of points is 12. And it's an under-representation of the severity of
the patient's symptoms because the way you measure this is weighted for right sided symptoms rather than left sided symptoms. Anyway the patient gets IV tPA to thrombolyze because if the patient came in
within a three to four and a half hour window. He was eligible and he got tPA. The tPA reduces the disability score from 12 to 9. It did not decrease any further. Why is that. Well it's like saying that the kitchen fire extinguisher should be
able to be as equally effective as a fire truck that comes to put out a very massive fire. Small fire in your kitchen can be handled by the kitchen fire extinguisher. But if you have a building on fire that kitchen fire extinguisher isn't
going to do anything. So in this case the way to think about this is the clot is big for what tPA can be expected to handle. So the pointer is not working and I don't think you can see the arrow. But the circle on the picture that shows
the CT scan of that patient's brain is dusky within the circle compared to other areas. Dusky brain is brain that is ischemic. It is on its way to die unless you do something. The scan on the other side with the arrow
pointing to is the blockage of a blood vessel that supplies that area of the brain. So if you can open up the blockage in a timely fashion you can prevent that dusky brain turning into completely dark brain which means it's dead brain.
Ok so people have looked at this and said okay tPA is a good medicine its FDA approved for patients who come in with stroke symptoms of who don't have bleeding in the head who could be having ischemic strokes. It works. But just like
the example that I used it can't be expected to be effective for every clot size. And that's that that's what the figure shows. ICA MCA Stem MCA division and MCA branch are all different distances from where the carotid bifurcates. Ok.
The farther out you go in the blood vessels branch the smaller it gets. Which means a small clot will cause a small branch to be occluded but not a large branch to be occluded. So therefore if you have a small clot in a small branch
tPA has a better chance of breaking that clot up than a large clot which is stuck in a more proximal branch. And that's intuitive. But somebody actually looked at those numbers and they said well you know what what we thought
turns out to be true. If you give tPA to all comers with ischemic stroke it has a less than one in three chance of being effective and opening that blood vessels. And if you look at the location of the blood clot to where
the branches as you go farther out into smaller branches and block that blood vessel and then give tPA the more effective tPA is for the smaller clot than it is for the larger clot. So that's intuitive and that's what this study shows. So this
explains why maybe the gentleman who came to our ED...77-year old man...didn't fully respond to tPA. So if this were about 12 years ago we would have used the device that's on the left called MERCI device. It's like a cork screw on a
catheter end of a wire end which is fed through the catheter to the area the blockage and you engage the clot and you pull it out. As you move along the timeline more and more devices started to become available for thrombectomies.
So the next device is Penumbra. You've heard that device in the previous talk. And it has that little separator wire that's got a little bulb which distrupts the clot mechanically as the other catheter goes up and down which is
connected to a suction device. They were effective but by the time they actually open the blood vessel that didn't seem to make a whole lot of difference. Not as effective. Patients didn't do all that well despite having spent the time. So the
field continue to work towards something that was more effective in opening up blood vessels. Then came 2011 there abouts when 2012 two devices came out that are both called stent retriever both Solitaire and Trevo and the picture is
what you see. It's a collapsible stent that you cannot leave. It's not a detachable stent that you advance against the clot beyond the clot and unsheath. And engage the clot so that you can retrieve the whole stent back.
And when you retrieve it back you find that the clot has also been retrieved. Ok so there are two devices they're both FDA approved. And there is now overwhelming data that mechanical thrombectomy is very successful and
effective in opening up these large vessel occlusions. There's one more device that has since undergone a iteration in development and that's the Penumbra 5MAX ACE and there are few additional devices. They're nothing
more than if you think about it like a Dyson vacuum cleaners. it's a large-bore aspiration catheter that you go ahead and park in the face of the clot turn on the suction canister which is connected to this
aspiration catheter and you engage the clot with this vacuum and the aspiration catheter. Wait a few minutes and then retrieve the clot back. So with these new technologies we have actually seen great improvement in how
we can benefit our patient. So what we did in the 77-year old gentleman is you can see there is that arrow showing on this side of the screen where there is blockage. You see that the central blood vessels fill but the ones going
towards the side of the screen the MCA branches don't. On the other side where there's the circle that's the lateral view showing that the branch is going to the top of the head fill but the ones going towards the side of the head
right over here they don't fill. So in this case we went ahead and deploy a stent retriever. I can't remember whether it was Solitaire or Trevo it was one of the two. And the red line on that image outlines where the stent is spanning
between from the distal end to the proximal end where the clot is. After five minutes we removed the stent retriever and what you see is fragments of clot that are brought back. And now that blood vessel that was included is
fully open as you can see where the arrow shows. And the circle outlines what was missing its now fully filled in. So this gentleman comes back to see me in clinics a month later. Walking in no deficits. How representative is this
of the results that we saw in the trials. There were five major trials. Now there are more that have all shown that somebody who comes in has a large blood vessel occlusion like this gentleman did if you treat them in this fashion
there is a roughly sixty to seventy percent chance that they will be independent after such treatment. Previously the independent score was at best high thirties. So this is a big revolution in the way we treat the
ischemic stroke patients. Now there are other this is not just a one-off there may be such examples that we see daily. You have a blood vessel here that's the carotid artery and it stops at the skull base.
Beyond that there is no blood flow. So we use not just a stent retriever but a combination of stent retriever and aspiration catheters and after using these devices in multiple passes were completely able to open up that blood
vessel. Ok. What this patient was left with was that area that's demarcated in a circle that's all the stroke that he has. And he actually walked out of the hospital. And what we pulled out is laid out on
the bottom and those are the different clot fragments each time we did this procedure we recovered. And it measures several centimeters actually. So again this patient also went some from very high disabling numbers to actually no
deficit at the time of discharge. Here is
world problem. And stroke is very much a problem in the US. And this is us...and the more purple we are the higher the risk
of death stroke. And though these numbers are from census data from 2007-2009 this purple color and intensity of this purple color has not changed. This map has really not changed. So this tells us how serious this problem is. And we need to
do everything we can to identify patients quickly and get them to the right place so that they can get the right treatment. So this is a cartoon that lays out what we're dealing with when we talk about different types of stroke. This is a
blood vessel cartoon which is blocked up. And when either it's blocked here or the blockage breaks off and occludes an artery in the brain you have a ischemia and infarct. And you have an ischemic stroke. Hemorrhagic stroke in this
cartoon there's an aneurysm that ruptures and blood leaks out in the brain and now we have a hemorrhagic stroke. But they're not fifty-fifty in disease prevalence. We have way more four times more ischemic disease than
hemorrhagic disease that contributes to stroke. But they're both equally important for obvious reasons. If you suffer a stroke the number...the amount of disability that you have is very severe. It is the leading cause of
disability in the U.S. We spend about 80 billion dollars...80 million dollars...every year paying for various aspects of stroke care. So it's it's a problem that's very important to all of us. So talking about ischemic stroke one of the key things
in our minds we are dealing with this is where did the clot comes from. Did it come from the heart did it come from the aortic arch did it come from a plaque that's sitting in the carotid bifurcation or is the
intracranial vasculature already at atherosclerotic and becoming norrow and forming an in-situ thrombus. These are just some examples and the prevalence of this is in this chart. The vast majority of them...more than a third of
them...we still don't know where the clot comes and that requires a lot of investigation on the back end when the patient is admitted. One-in-six are because of carotid disease. One-in-five because of a clot that forms in the
heart or somehow gets to the heart. And one-quarter of them are because of very small blood vessels that are getting smaller and smaller due to long-standing issues like high blood pressure diabetes cholesterol and smoking. And there is still
a fair segment where you don't really know why they had the stroke. So ischemic stroke is not one disease. Its causes are varied. And based on symptoms timing how they present that all goes into your thought process as to how you're going to treat
them. Ultimately regardless of where the clot came from the problem that you're dealing with that time is ticking away when the brain is suffocating for oxygen and energy. This is an example of a brain that is
got ischaemia and infarct. The dark areas are areas of the brain that are dead. So when this patient comes to the emergency room and can't speak and can't move part of the brain is already dead. What we're trying to save by attending
to the patient in a timely fashion is the areas and various shades of blue from turning into dark. So we're trying to penumbra. Okay. The most striking way to think about it is if there is something that's on fire
there's already damaged that's happened. What you're trying to prevent is the damage from spreading further and becoming irreversible. Same idea applies here and each minute that passes where the brain does not have
oxygen is a problem because you're losing two million neurons each minute that you don't have blood flow. And the brain ages for every hour that it's not reperfused about four years. So this is a very
important concept because time is brain. And that's what we're trying to do to save when you're trying to reperfuse these patients with various technologies. So here's the case. Somebody that we
last few minutes i'm going to talk about intracerebral hemorrhage. The other kind of
of hemorrhage that I showed you where the hemorrhage is in the soft tissue of the brain. Very high mortality rate. Very important to pick them up. Very important to look for an underlying blood vessel abnormality because if you do maybe you can treat it from happening again. If you don't these
patient's can re-bleed and that contributes to a very high degree of mortality. So take a look in any manner that's represented here. You have a lobar hemorrhage a basal ganglia hemorrhage temporal lobe hemorrhage a convexity parenchymal
hemorrhage. And the location of the hemorrhage doesn't tell you the underlying cause even though people used to think that it did. And up to one out of every two patients has an underlying vascular abnormalities
and this was not felt to be this high previously. That's because people were not looking for anything underneath. They thought it was due to hypertension or amyloid. So there are certain things that you can look for on the CT scan that
clues you in to there being something else underneath. Like a spot of calcium or dilated blood vessels on a CTA or a blood vessel coursing through where the hematomas is or an aneurysm that doesn't look like a star pattern bleeder or a subarachnoid bleed
but this huge pool of blood eccentric in one part of the brain. So these are just various examples that you might see that can clue you in as to there being something structurally abnormal in these scans. So here's a
patient that came to us. 76 year old man still working still very active. He presented with a seizure and when he got a CT scan you see this big left frontal lobe hemorrhage with a lot of swelling around it. We did the
angiogram we found this AVM. AVM you know is an abnormal connection between arteries and veins in an organ with a nidus that is at the crux of the vascular malformation. So this is a lateral view where you
can see branches from this artery both supply normal brain and also the AVM. So this patient came back from the hemorrhage and is now going to be treated with radiation treatment given that parts of these blood vessels supply normal brain.
Otherwise we would take it out endo- vascularly. This example is such an example where we did take it out endo- vascularly. So this is a 61 year-old gu he was a school school security guard came in with this hemorrhage. Very odd looking
hemorrhage. Had headache and some memory loss. So we did do the angiogram. We didn't find anything when he first came so we went back and look again at three months. When we did that you can see that this artery here supplies branches
and here it's actually filling early an arterialized vein which drains into one of the sinuses. You really shouldn't be seeing any of this in an arterial phase which is what the rest of the scan shows.
So we went ahead and took progressively smaller catheters and ultimately this microcatheter that we parked as close to the fistula point of this vascular malformation and from here injective a substance that would fill that connection
so you would not be able to continue... you would prevent the shunting from happening anymore thereby decreasing the risk of re-rupture again. So here is the video that should show that and here's the microcatheter and
at the end of it is glue or NBCA. And I'll play that again because it goes pretty quickly and it is that quick. In fact I've slowed this down for the purposes of the video. Here it come. And there's the glue cast which looks like what you see before we actually
embolized. And after the embolization the final rung looks like this. Where previously you had this fistula right here you no longer see it and the cast formed by the NBCA is in the location where
the patient initially had the bleed. Untreated this has a rupture...re-rupture risk anywhere upwards of fifty percent. So if you didn't look for this you wouldn't be able to identify it and treat this. And this guy who was
independent would loose his independent or his life if this were to happen again. So he's actually back in school doing his job and doing very well actually. Here's a 33-year old guy with another hemorrhage
and came in headache and weakness in the right side and some confusion. He had some funny looking features on a CT scan so we undertook an angiogram. This angiogram shows a blood vessel going to an AVM right here with pseudoaneurysms
within this AVM. These pseudoaneurysms is what ruptured. That area is difficult to get surgically so we went ahead and put in a microcatheter and did something very similar to what I showed you. So what you're seeing here is the glue
cast that's pretty much what the blood vessel looks like. And here's the 3D of the same. Here's the AVM with pseudoaneurysms. The glue cast shows you the same appearance of the blood vessel because that's what we took down. And again this video
ok the video is not going to play but effectively it shows the glue going from here to the pseudoaneurysm and filling back to this point right about here. How did that patient do. Well there is
the...you saw the rupture in the previous scan right here. Not all of it is the malformation. Only part of it is because of blood just ruptured everywhere from the AVM. So the glue cast itself is within the
crux of the AVM itself. And this is the post-treatment injection where you don't...you see very little of this AVM left at this point and we expect it might actually thrombose in due time. Here's another pattern of blood.
This is actually multi-compartment hemorrhage in the 62 year-old lady who presented with headache nausea and dizziness. She actually had an AVM with some flow related aneurysms and this was sitting right in the hematoma bed. So we went ahead
put in microcatheters...catheter through which microcatheters were advanced and coiled off the aneurysm. She also had two additional flow related aneurysms. These aneurysms are actually very malignant. They don't tolerate all
that excess flow through the vascular bed. And they are at very high risk of bleeding especially in a patient whose already had rupture. So here is the other artery that's supplying feeders to this AVM with
very dysplastic segment and aneurysms here. So we went ahead and injected Onyx...this is the cast that's left behind by that... which is within these magnified views of the aneurysm and dysplastic segment and the pseudoaneurysm. And she'd done well
after surviving the hemorrhage and the treatment and she has come back to clinic and she's contemplating getting the AVM treated. So in conclusion
of debated concepts within the world of flow diversion so all patients that receive flow diversion like most stents get dual antiplatelet therapy. There's a pretty...the majority of physicians that do this type of procedure test their
antiplatelets to make sure they work. So all you guys probably know that thirty percent of people don't...are sub-responders or non-responders to Plavix. Maybe five just ten percent of aspirin users are sub-therapeutic or
non-therapeutic responders. So we want to make sure that our patients are adequately antiplateletized. But there's a lot of discussion about how long you keep those patients on antiplatelets how aggressively test you for it. There's no
consensus on that right now. A big discussion about whether or not to use coils with this technology. As I've laid out earlier on this is a competitive technology to coil technology. Some people coiled it and if you're going to coil
them how much you coil them. Do you go ahead and coil the whole aneurysm. Do you just put a couple coils in for stasis. Do you not coil aneurysms because they're competitive technologies and you're adding potential complications of coil
technology and flow diversion technology together without a really strong understanding that you help out with the rupture risk. A big discussion about the number of devices that we use. So if you look at the worldwide literature
they're using one device. So if you can put 1 device in and treat an aneurysm people are putting in one device. If you look at the PUFs study which was done as our approval device they put in on average 3.1 devices. And there are a
couple reasons probably why they put in 3.1 devices. One is the one of their main points was complete aneurysm obliteration at six months. And I think they felt that they would get that more reliably with multiple devices. Second
the person that invented a device was one of the major primary investigators so maybe some secondary financial interest in having multiple devices used. But if you look at all the literature there is a pretty strong movement towards using
less devices it in the majority of cases. So more people using a single device rather multiple devices. And then a lot of discussion about all the catheters that we use to access. I use a tri-axial system which means I put my
sheath...my 6Fr sheath into the carotid artery and then I put an intermediate catheter into the intracranial internal carotid artery and then use a microcatheter deploy it. Many people use that technology although
certain people certainly use micro...or use guiding catheters don't you sheaths don't you tri-axial techniques. So there's a lot... a lot of wiggle room in how we use these devices. So this is an example that represents
this these clinical conundrums that we have. You can see here a giant cavernous... or a giant posterior communicating artery aneurysm you can see the posterior communicating artery coming out here. There's your aneurysm on a lateral view.
Here's device deployment you can see the distal wire here this is the device being unsheath. And here's tip of the microcatheter as it unsheathes it. Here's the intermediate catheter in the cavernous segment of the internal carotid artery.
Here's the device deployed or almost completely deployed you can see it opening very well. Here's the device...the post run after the device has been deployed...you can see it's very well opposed throughout the vessel. There's a
microcatheter that was jailed here...you can see this distribution of the jet of flow into the aneurysm sac. So a lot of stasis already. And then two coils were placed to promote...quote-unquote promote stasis in the aneurysm...on this
unruptured aneurysm. Patient woke up great. Did great. Went upstairs. Precipitously declined. Became comatose. Brought down emergency for a head CT and you can see the head CT here for any they're familiar with looking at
head CTs. All these areas that are filled with bright stuff should be filled with dark stuff which is CSF. All this bright stuff is blood so you can see this big round object here is the aneurysm. This is an external ventricular drain that has
been placed.... I'm sorry this is I think some of the stent...and then you can see diffuse subarachnoid hemorrhage. So the important thing here you can see here is your stent. Here's the aneurysm.
And that coil that was filling the aneurysm has now been squished and pushed back outside the aneurysm. So the whole coil mass was extruded. So the back wall of the aneurysm ripped open. Adam Arthur who's the endovascular
neurosurgeon in Memphis calls it the "fat man pants syndrome". So the aneurysm just split all the way along the back wall the entire coil mass was extruded from the aneurysm. This is not a survivable subarachnoid
hemorrhage. So you can see here...here's the immediate post-procedure image with coils filling that aneurysm sac. And here's a CT image with the device here with this space here and coils squished back through the aneurysm into the
subarachnoid space. So to summarize
complications. So you can see there are a lot of things that you can get into
trouble with and having an understanding of what those complications are and how to potentially get out of them is very important. There are some complications that come to the theory of the device and the theory of the disease that we're working
on that are very vexing. And the two basic ones are delayed aneurysm rupture. So we see about one percent of patients.... you put a Pipeline in them you sent them home and their aneurysm ruptures. One day three days one week two weeks three
weeks later. We don't know why that happens and we don't know how to select which patients we think that's going to happen to. And the other one is that these patients...there is a percentage of patients that have a remote parenchymal
hemorrhage which means that they have a brain bleed usually on the same side of the brain but remote from where the aneurysm is. And we don't know what causes that and that happens as much as three or four percent of the time.
There's no clear etiology. There are many theories and again these two complications add up to a significant portion of the complication rate that we see with these patients. And a very demoralizing complication for a
physician to have is treated the patient that's done while has gone home. And how are we trying to figure out how to minimize these complications. Well we're trying to understand the devices better. We're trying to understand...
we're trying to understand and improve the devices and we're trying to understand and improve our understanding of the anatomy of the aneurysm as it relates to the devices. So if you ever pick up the AJNR one of our...or
that JNIS one of our big neurointerventional journals there's always an article about the flow dynamics of aneurysms that are undergoing flow diversion. And so there's a lot of research looking into that. A lot
So let's look at some images related to trouble with access. So for many people
their first cases is their first exposure to flow diversion are going to be their toughest cases. And these giant cavernous aneurysms are routinely and reliably our toughest cases. We have an inflow here
this big sack where coils and wires and catheters just flopping around. And then somewhere in this nebulous region is the outflow. So you have to fish your wires around to find an outflow which is oftentimes stenotic. So it can be an
incredibly labor-some task. Can take hours. I've had several cases that the operator was unable to get the outflow and had to abandon or abort the case because of this. So this access can be an enormous issue. Here we'd spent several
hours trying to get a wire across this sac into that outflow. We were unable to do so...could never get it to engage. So we took a large compliant balloon inflated the balloon in one catheter in the aneurysm sac to help kind of pin and
deflect the wire and then we're able to deflect the wire around the catheter get it into the outflow and then track microcatheter over it. There we are with the microcatheter out of the MCA branch so internal carotid
anterior cerebral middle cerebral artery. We have a catheter tip out here. So here's another example of a giant cavernous aneurysm with a very technically challenging access. We were able to get the wire out but we were
never able to get the catheter to track over the wire into the outflow tract of the aneruysm. So in here we actually took a balloon over the wire inflated the balloon in the distal outflow and then use that the pin the wire so
that we could then track the catheter over it. Once we've got the catheter in place then we can pull back to reduce the redundancy of the catheter in the aneurysm sac to give us that straight shot.
So obviously some concern about inflating the balloon and the vessel and using that as an anchor. Obviously opportunities for parallel there. So here's another giant cavernous aneurysm. Here lateral view cavernous aneurysm
middle cerebral artery branches. So here we are after we've deployed the device we've removed the device construct. So the microcatheter...so when you deploy this device you deploy...you unsheath it over a wire and then you track the
microcatheter over the wire through the stent over the wire to recapture that distal wire. And that's how you keep your microcatheter access. The microcatheter is 0.27 so a pretty big microcatheter. The wire that stent
deploys over is 0.08. So much much much smaller than the catheter. So it is very technically difficult sometimes to get that catheter to track over that wire. If you don't...if you can't get that catheter to track of that wire you
lose access. Which can be a big deal and this is an example why that's a big deal. I don't...can you guys see that. So there's a device here that goes from here to here. There's a device that goes from here to here. Unfortunately what it
looked like in the beginning was a device that went from here to here. So this portion was the inflow of the aneurysm when we removed this distal wire in the catheter this proximal portion herniated into the aneurysm sac.
So now we have a stent that goes from here to somewhere in here in the middle of this giant aneurysm with no connection to the inflow and no ability for us to access that stent from the inflow. So this is an example of how
we're talking about needing to go from somewhere else. This patient had an intact anterior communicating artery. We went from a...we put another puncture in the left leg went up with another catheter into the right internal carotid artery.
Put a microcatheter in the internal carotid artery anterior cerebral artery across the anterior communicating artery in this anterior cerebral artery down this internal carotid artery. Put a wire into
the aneurysm sac through that stent so now you have a wire through that stent into the aneurysm sac coiled up. And then we went with a loop snare. So now we have a microcatheter with the loop snare we've snared that wire so we have a catheter
with the snare attached to a wire that comes out this. And we call this the flossing technique. So by combining a pull push technique we're able to jimmy that catheter over that wire... whoops...into so now we've
straightened the system out and then now we have that wire. We removed... we've taken out the snare. We removed this wire and we placed a wire out this MCA. Now you'll notice one of the other things techniques that we use is that
this 0.27 catheter can house two microwires. So we have a 0.14 and 0.10 wire out for extra support so this catheter will track out. We get into the MCA and then now our device is being deployed. And that's what it looks
like again. So now we have one device two devices much more redundancy here much better coverage of the inflow and that's what the aneurysm looks like at the end of the case. So deployment...this is a self-expanding
stent it's very supple. It's is very soft it takes turns very well and opposed walls very well. But the downside of that is that it doesn't have a strong impetus to open. So we see flattening we see narrowing of the stent. So it is entirely
possible to have a device like this that goes from here to here where the midsection is severely narrowed. Now when you do an angiogram at the end of this procedure the vessel is going to look fine. But what we know is that when you
bring that patient back in six months the vessel is going to look like the stent. So we have to do something to make this stent more open or the patient's going to have a severe stenosis when we follow them up. So in this case we've
gone back through that device with a balloon...a compliant balloon...and you can see the compliant balloon opens up. We still...after this inflation...you can see still significant residual stenosis. So another example of issues related
to deployment. This is a middle cerebral artery bifurcation aneurysm here. You can see on the CAT scan image a enormous calcified largely thrombosed aneurysm. So that the lumen of the aneurysm is actually a very small part of the actual aneurysm
itself. What we know about this is with coiling...when we coil aneurysms like this they very commonly recur. Almost all of them recur because the coils just insinuate into the clot it regrows you recoil them and that happens over
and over and over again. So there was...a decision was made it to Pipeline this case. You can see the device being deployed. So here's that distal wire. Here's the device unsheathed and here's the catheter here. When we got to
the end you can see that the device doesn't want to open on the proximal end. And so we have the device open and here we are right here the device is pinched down where the catheter is. So multiple attempts to get that distal....that proximal
end open didn't work. Catheter was...the wire wasn't moving. There was no way to get this device open. It was elected to leave the device like that. This is what the initial run after removal of the wire looked like. You can see
maybe a little bit of clot. We waited over time and you can see over time the inside of that device completely clotted. So it's very important that even if the initial imaging looks ok with these devices if the device doesn't look right
something down the road is going to happen. And this is a prime example of that. So the vessel thrombosed. Over time you can see complete thrombosis of the MCA trunk related to the vessel. This is what the MCA look like. So this is the anterior
cerebral artery which continues to fill. This is the middle cerebral artery where you can see a large portion of the exception of this branch here is absent. That patient obviously did not do well. And then this is what we're talking about with
recapture. So when we take our microcatheter which is right here through our device we take that over an O.08 wire. So there is a a big step off between the catheter and the wire. So when you push you can scrape the vessel wall
and if you push too hard you can puncture the vessel wall. So this... this case in an attempted to pass the catheter into the device there was a significant amount of resistance met at the proximal margin of the stent. The
vessel ruptured and this patient being treated for cavernous aneurysm ended up with a CC fistula. So this is a basilar artery here.... basilar artery apex aneurysm. Previous coil material in here recurrence of the
aneurysm. The decision was made to flow divert this. Again an off-label use of the device. You can see deployment of the device across the neck of the aneurysm. But when we removed the wire the distal end of the wire was not with it. So the
distal end of this wire had broken off. This was more common with the first generation we don't see it as much anymore. But you can see here...here's a native image flow diverter in place we now have a microcatheter with a loop
snare. Here's a lateral view you can see the loop snare engaging the wire tip and removing it. This is a patient who wasn't as fortunate. So here the catheter engages this wire...
so here's your catheter tip here's the wire they were never able to get the wire quilted into the catheter....it got kind of stuck or lodged at the tip of the catheter so they decided just to remove the whole thing in total.
And as they pulled the wire back through the stent...so here's your stent here in the cavernous internal carotid artery...as they pull the stent through here the wire broke off...as they pull the wire the wire broke off. The
wire was stuck in the stent. Here they are trying to remove the device...the distal wire with a alligator snare. You can see they've engaged it with the alligator but the alligator was too flimsy to pull it and it kept breaking off.
So they elected just to leave it. And you can see the immediate post-procedure run with the wire remaining in along the wall of the stent. And when they brought the patient back in six months the aneurysm was gone and the wire was still there. So
there was no clinical sequelae of this despite the fact they had to leave the wire. So and then finally touch up. Once
flow diverting is planning. When you're looking at images there are a lot of things that can happen during a Pipeline procedure and understanding what those are understanding what
your potential bailouts are very important. So does the patient have an anterior communicating already do they have a posterior communicating artery that you can access the aneurysm from another vessel in case you bugger up
the access that you have from the vessel that you're going through. How aggressive do you want to be. If a patient comes in with a giant cavernous aneurysm and their 85 years old and they have minimal symptoms from it and you can't safely
and easily get through the outflow of that aneurysm do you want to try to go from the other side across the AComm and down into the internal carotid artery in order to access that aneurysm or you want to just leave it
alone. Do you want to consider doing a balloon test occlusion to determine if the patient can just tolerate having that blood vessel sacrificed in case you need to shut it down. And then you want to make
sure that you have all the equipment available to perform your bail out. So we need to be able to pull the device out if we have to. So microsnares alligator retrievers balloons to open up narrowings or
stenoses in the stent. Having all that stuff available are all very important parts of the pre procedural planning. Whenever I go to a facility with a physician to talk through the case with him that's one of the things that we
talk about is...okay what are our planning strategies what are our bailout strategies what equipment do we have available to get us out of trouble.
is a big deal. And one of the things that I do in my free time is a travel around teach other physicians how to use it the device help other physicians understand the properties of this device. It is a
very finicky device it is probably...of all the devices that I use probably the one that you can get into the most trouble in. And it's....some of these pitfalls is I think a very important part of that device. So how can we get into trouble. So
we can get into trouble with technical complications related to the deployment of the device and we're going to show a lot of pictures here on that. And then we have clinical complications that are related to the device itself which we
don't fully understand or the disease process. So like we talked about we treat these aneurysms we don't cure them right away. So some of these patients are going to have a natural history of
an aneurysm that ends up rupturing before the device is done what it is supposed to do. So we see this and we see this. This we try to work on with our technique and our understanding of how to deploy these devices. This there's a
lot of research going on right now to help us try to understand how to help eliminate or reduce these risks and I have some pictures of those at the end of the talk. So how can we stay out of trouble.
Obviously number one don't do the case. Wrong! Always do the case. But that is the first answer so you know as a physician making these decisions you need to be clear with yourself and have I think a strong ethical compass about when you're
deciding to do these cases on aneurysms. Feel like you understand the literature. Know what the risks and benefits truly are. Make sure that you're giving an inappropriate summarization of that to the patient when you're talking
to them about cases. And travelling the countryside you see a very wide range in people's though process. And a lot of that is because there is not an enormous amount of data or literature that drives our decisionss. It's a lot of smaller
studies and anecdotal data which leaves room for a very wide interpretation of how patients should or need to be treated. So I think for every individual operator it's important to come to that point that you feel is the ethically the
right...the right place to be. There are numerous opportunities to mess up this device. Access detachment deployment recapture and touch-up of the device are all things that happen in every case that all carry a set of pitfalls and I'm
gonna show some of those images. So you can remove this device. The first generation device...we're now in the second generation device of Pipeline...the first generation device the only way you can remove it is to cork it. So the
device opens up over a catheter...through a catheter...over a wire. And you could pull this little capture coil back and pin the device against the catheter. It's called corking it. And then you just pull the device out and start
over. You couldn't resheath it you couldn't... you couldn't manipulate it you just pull it out. So anytime historically that we would get into trouble with this device we just pull it out and put another one in.
Well now the second generation device we actually have the ability to resheath it and and reposition it. So if the device starts acting a funny way we don't necessarily have to pull it out. We can resheath it and start over.
So one of the most important parts of
some cases. So this is the idea of the Pipeline device. And so the interesting thing about flow diversion
is that flow diversion now as compared to coil technology you guys have probably heard talks about the pros and cons of coiling vs clipping this sort of an age-old conversation. Coiling seems to be safer than clipping. Patients recover
faster they seemed to recover better there are less seizures less neuro- cognitive dysfunctions obviously none of the complications related to craniotomy. But the downside of coiling is that coiling is not often durable. So we see
somewhere between 25% and 50% of aneurysms have some degree of residual aneurysm with coiling. And there is some number depend on what literature you read ten- percent or so of aneurysms that need to
be retreated because they recur and re- grow with coiling. The idea behind flow diversion is that it is the first opportunity that we've had in a endo- vascularly to actually provide a reliable cure for aneurysms. But it has a
significant side effect profile that is to date riskier than coil technology and so we're going to talk about all that. But it's so here's an ideal case for how we use this. This is a patient that came in with a giant....this is a T2 weighted
MRI sequence in a patient with a giant left cavernous internal carotid aneurysm. This big bright sack here is the aneurysm. Patient came in with ophthalmoplegia. You can see his conjugate gaze here. Ophthalmoplegia on that side. So when we
did an angiogram here...so this is a digital subtraction angiogram lateral view. So eyes here back of the head here. You can see this giant aneurysm coming off the cavernous segment of the left internal
carotid artery. Here we are as we're getting ready to put the flow device you can see already stagnation of flow in this aneurysm sac. Contrast is already subtracted out from the last run in the dependent portion. So you have contrast
and then swirling contra...subtract out contrast swirling contrast and the non opacified blood is the least dense. Here's what it looks like after we've deployed the device on the DSA image. You can't really see the device. You can see the
vessels opened a little bit better with the device in place. But now we have the parfait sign which is my favorite so you have subtracted blood from the last run and then you have ecstatic contrast from the current run and then you have un
opacified blood which is the least dense and so it looks like a parfait. So this is the flow diversion we're starting to stack contrast because there's so much flow diversion. You can see the aneurysm's not gone and you can
see the device is subtracted out. This device spans the neck of the aneurysm. This is what it looks like immediately after. This is what it looks like six months later. So you can see that area where there was an aneurysm sac there's
no longer an aneurysm sac. So the patient's symptoms went away the aneurysm went away and when we do the angiogram here's the native image...you can see this is what the device looks
like it may be hard to see out there it's a fairly radio non-opaque stent. It can be hard to see and it takes the contour of the vessel and when you do the angiogram you can see this is what the vessel looks like. So the
aneurysm has thrombosed because of the flow diversion. The device has re-endothelialized and we've reconstructed this vessel for a cure of this aneurysm. So we've looked at our data ...the PUFs trial which we'll talk about in a minute....of aneurysms that
go away and that's somewhere between 75 and ninety-five percent of aneurysms that we treat with this technology. If an aneurysm goes away with this technology there's never been a reported case of an aneurysm recurring. So we can consider
this a cure which is a pretty neat phenomenon for us to be able to say. So
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