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Grand Rounds-Pushing the Boundaries of Endovascular Treatment: The Decision Making Process

Elad Levy

February 12, 2013

Transcript

- Hello, ladies and gentlemen, and thank you for joining us. Today, we have Dr. Elad Levy, is a professor at university of Buffalo, and also the director of neurovascular and endovascular surgery there. He's going to be talking to us about controversial and cutting edge applications of endovascular techniques in management of aneurysms, ischemic disease, and arteriovenous malformations. Elad, I wanna thank you for being with us, and we're very interested in your expert comments.

- Aaron, thank you so much for this opportunity. In the next hour or so, we're gonna review various types of cerebral vascular cases that we've treated with an endovascular approach. What we try to do, is present cases that have an interesting twist that may not be treated with standard and accepted techniques, and really show you areas where we may be pushing the envelope of endovascular treatment for a multitude of cerebral vascular diseases. So, we'll just get right into it and we'll start with the first case. And the first case is of a giant, dissecting/fusiform aneurysm. This was in a 55 year old lady with a medical history of hypertension, who had no family history of subarachnoid hemorrhage but presented to our facility intubated after a subarachnoid hemorrhage. She was a Hunt/Hess 3, Fisher 4, and here you can see her CAT scan showing the blood pattern as well here on the CT angiogram, which we routinely get once we see a subarachnoid hemorrhage pattern demonstrating what appears to be a carotid type of blowout or a fusiform enlargement of this aneurysm. Once we see this, we wanna understand more and we begin our treatment strategies, treatment paradigm. We would entertain clip ligation. However, in such a fusiform dissecting type aneurysm, we feel that that is not optimal and really not feasible. And then we also discuss stent coiling or endovascular techniques. However, in the setting of a ruptured aneurysm and subarachnoid hemorrhage, where the patient will likely require ventriculostomy, extensive ICU care with invasive lines, we tend to avoid or try to avoid the use of stents or flow divers due to the need for Plavix. In the setting of Plavix, there's an increased risk of hemorrhage from a ventricular drain or the lines that need to be placed. But sometimes again, we have no alternatives. And in these situations we place the EVD first. We try to place all invasive type of monitoring first and only then give Plavix to try to minimize hemorrhagic complications. So, prior to stenting, we gave effient, and aspirin, and then heparin. Again at this point and in most situations, all invasive monitoring would be in. So here you can see the angiogram showing again, the large carotid fusiform aneurysm. And here you can see we placed a flow diverting stent, and one coil in the sack. We sometimes place one coil to dampen the inflow into the aneurysm and to augment the thrombosis that the aneurysm will experience once we place a flow diverter. And if you look very closely, you can see that there's an irregular pattern of blood coming through the flow diverter. So you have a jet of blood into the aneurysm, and . You have a jet of blood here coming into the aneurysm and an irregularity of blood flow here indicating thrombus. And if you wait a little longer, the jet is gone, but now you see a feathering pattern, very typical thrombus in a stent. So at this point, a couple of options, we can let the vessel occlude and hope that there's enough collateral. But because this patient was intubated, we could not do a balloon test occlusion. We can't risk the fact that we can take the vessel down and that's why we tried to spare the vessel with a stent and a flow diverter. So we gave a 2B, 3A inhibitor integrilin. Just the bolus. And you can see after the bolus the blood flow appears to be improved. So now we have complete occlusion of the aneurysm with one coil and one flow diverter, and that jet that we're seeing here is no longer present. Here, we are in a followup angiogram at the end of the case, showing again, excellent reconstruction of the vessel, complete occlusion of the aneurysm. And again, this was in a subarachnoid hemorrhage situation which is off-label and controversial, but sometimes certain disease states necessitate that we think outside the box and try to maximize the outcome. So, she had rapid clearing of her mental status issues. And after a prolonged hospitalization due to spasm, she was actually discharged back to home.

- This is a great case. Obviously uses the application of coiling and flow diverter at the same time. Can you tell me more about that, Elad? What other situations do you feel like you need coils on top of the diverters in order to augment aneurysmal occlusion?

- So, flow diverters are very promising technology. One of the problems with flow diverters is the incidence of rupture of an aneurysm within the acute post-op period. So we're converting an unruptured state into a ruptured state, and we don't really understand why. Some theorize or postulate that it's a ball valve effect. During systole blood comes into the aneurysm, during a diastole blood doesn't come out and eventually the aneurysm ruptures. We have a fairly small experience with ruptured aneurysms after flow diversion. Overall, our experience with flow diverters are well into the hundreds now. We have occasionally placed a coil to dampen the flow. So when you saw that jet stream, the thought is, place a coil that would dampen that jet into the aneurysm and hopefully negate or lower the risk of aneurysm rupture after flow diverter. You don't do it routinely, but we do do it in special situations when we see a jet like that.

- Okay, so, you use your judgment in terms of what you see after you put the flow diverter there. My other question for you is that what's been your experience with flow diverters? We have had a number of ruptures afterwards, just like you mentioned. And the rate for us has been up to 10% and we no longer use flow diverters off-label. What has been your experience in terms of immediate ruptures of aneurysms among unruptured aneurysms who underwent treatment with, for diabetes?

- That's an excellent question. So we've recently published two papers, one looking at our posterior circulation experience for fusiform, hollow basilar-type aneurysms. And I think treatment of these aneurysms actually worsens a natural history. We've had almost a 75% mortality. We really do not recommend treatment of hollow basilar fusiform aneurysms. We've been very successful, however, in the anterior circulation, specifically, ophthalmics, cavernous, proximal, carotid aneurysms. In our series of approximately 100, we've had a very low incidence of rupture and the total complication rate was around 8%. So, we think it's a very favorable technology for the right type of the aneurysm.

- So is it correct that it is very good for a proximal carotid as side wall aneurysms? Would you say that's the best indication of flow diversion?

- Absolutely. Proximal carotid, really pro-- Before the PCOM side wall, you can't use it for fusiforms, but ideally wide neck, large or giant aneurysms and the proximal carotid, all right, are probably best suited for flow that version.

- You probably have the most experience or one of the most experiences in the country with flow diversion.

- Any other pearls you would give others in terms of how else to handle this new technology?

- I think like anything, this technology is gonna require experience. It doesn't function like a standard stent. It's good to get used to it. And in vitro type model, spend time just as you would micro suture technique. Using these stents in Silicon or plastic labs on a bench top, familiarize yourself with them because many companies are going to be coming out with flow diverters, and this technology is here to stay.

- Thank you.

- Okay. So the next case, we're gonna switch gears and go from what was a very large, almost giant aneurysm, to a blister-like aneurysm. This is a 48 year old lady who came in with a ruptured aneurysm with significant risk factors of hypertension and smoking. Again, no family history, but the CT scan demonstrates a subarachnoid hemorrhage pattern seen predominantly on the left side, and 3-D angiogram shows what appears to be a blister-like aneurism off of the carotid. So this is very challenging. This is a proximal carotid, blister aneurysm in the setting of subarachnoid hemorrhage. As you know, from surgery, Aaron, these blister aneurysms can be tissue paper, often very hard to reconstruct, often surgically challenging. We still would argue that for most of these blister aneurysms around the Circle of Willis, that surgery is the main state treatment. However, this is fairly proximal or very proximal, and we think would have been surgically a challenge. The point I do want to get across again, for Circle or Willis- type blister aneurysms, surgery should, and is the first line of treatment. But this was a unique case. It was very proximal. It would have been a part of the carotid wall. That again, is surgically difficult to access, and getting into trouble here can often be fraught with complication and may necessitate sacrificing the artery. So again, trying to think outside the box and moving off label, we decided to use a flow diversion and reconstruct this artery, reconstruct this vessel, and hopefully negate the blister from the circulation. So we loaded in this patient with anti-platelet medication as we always do. Here are the whole list of devices, which is not necessarily important for today. And here's our access. So we have a very navigable guide in the petrous carotid. We have a microcatheter all the way up by the carotid bifurcation, I see a terminus. Here, you can see the flow diverter opening the lead wire. Flow diverter opening. And we're basically gonna paint this flow diverter across the cavernous segment. Here you can see it's opening more, conforming very nicely to the parent vessel, despite the serpiginous nature of this parent vessel. And basically, one pipeline done in a very routine fashion. She remained intact throughout her hospitalization, and she has a follow-up angiogram pending. Blister aneurysms have an unclear natural history. Clearly for coiling, they're very challenging and are often fraught with intraop rupture when you're putting coils in. Surgery therefore, should be considered the first-line treatment in most blister aneurysms. We have a very limited experience in flow diversion, but so far it's been a very positive experience. And this patient like the few others were fortunate and did well.

- May I ask Elad, do you see post flow diversion and plantation that the blister aneurism actually improves on angiogram or is it just still there and you're assuming the flow within it has decreased?

- We assume it's there, that's an excellent question, but we don't see it on angiogram, which tells us that once we use a flow diverter, hopefully we've diverted enough flow that we don't see the dye flowing into the blister. And at that point there'll be neointimal growth, neointimalization of the stent. So, excluding the blister from the parent circulation.

- I want to echo your very eloquent statement that, these are very difficult lesions. I think we should give credit to a new treatment options because surgically, these are very high morbidity. Intraoperative rupture is very high, even at the best hands. And so, if there is other options such as flow diversion, I understand the experience is small. It is definitely worth trying. This is not a saccular aneurysm, that doing an operation you have a good chance of taking care of it. The ones that I have personally done, my complications have been over 20%. Either have intraoperative rupture or-- And I had to sack some of the perforators to reconstruct the vessel with a dead chronograph, or patient unfortunately had embolic phenomenon because of temporary occlusion post-operatively. So, these are very difficult cases, and I think that's a beautiful job you guys have done with using flow diversion there.

- Thank you. So now we're gonna switch gears completely from aneurysms and look at AVMS, and maybe talk about some of our philosophical approaches to AVMs. As most people would agree, AVMs really require multimodal treatment ranging from surgery, to endovascular, to radiosurgery, to a cocktail of all three. So, at least in Buffalo, clearly we have a bend towards endovascular, and we're gonna show a few cases that hopefully demonstrate some of our philosophical approaches to AVMs. The first case is a young male, 23 years old, who comes in with new headaches and new seizures. No significant past medical history, and overall he's neurologically intact. He had some imaging as part of his workup and it was found to have an AVM in the right frontal lobe. Here we can see on the MRI, the standard MRI appearance of an AVM, and then here on the CT angiogram in 3-D, we can see the nidus, the arterial theaters from the MCA and the venous drainage. That would always be part of our typical workup. At this point, we often get an angiogram to understand the transit time, the flow into the AVM and the flow out of the AVM. And we can see this is in the peri motor region, fed from the right carotid artery and the right middle cerebral artery mostly. There's also some collateralization coming from the ACA, but again, this is predominantly fed from the right middle cerebral artery. Looking at a Spetzler-Martin grade, which is really more appropriate for surgical planning, however, still most people understand Spetzler-Martin grade gives us a good idea about what kind of AVM this is and what surgical risks they are. This is the law of Spetzler-Martin grade. And something that in general would be amenable to surgery. However, this is Perry motor, and this is a young man who basically other than seizures isn't currently intact. So options include resection, which again, given the motor strip area, we are more reluctant to consider. Radiosurgery, which is a fine option and embolization. At this point, given the fact that he's relatively young, and we thought had very accessible vessels, we wanted to embolize as much as we can and that's part of our philosophy here. We will embolize the AVM in a staged fashion. And if we can't cure it, that we thought we could, if we can't cure it, we would then consider either surgical resection when appropriate or embolization of a much smaller nidus. So one feeding pedicle was successfully embolized, and because we do these awake, we do Wada testing. So we give Amatol injection before every embolization and upon Amatol injection of the second pedicle, he developed a left facial droop and dysarthria, which only lasted about five minutes until the drug was out of the system. That is a key reason why we do these awake. Even under general anesthesia with neuromonitoring, the subtleties of dysarthria or facial droop may not be picked up. We have very rarely the false positives or negatives. And when using the awake technique, we rarely have an unknown deficit. So in light of that deficit, from the Wada test, we aborted the procedure, brought him back a few days later, access to different pedicle, he passed the Wada, and now you can see embolization of a new pedicle. Here again is a residual portion of the nidus. You can see the draining vein draining into the superior sagittal sinus. And you can see predominantly, nearly 90% of this AVM has been embolized. There's a little bit of filling here. This is venous, already venous drainage, late capillary phase. So at this point, there is a very small residual, which will be highly amenable to radiosurgery. And this patient went on to have a radiosurgery for a very small core residual of the nidus.

- Elad, you brought up the issue of awake for monitoring. How about a patient was right-handed, had a, let's say, right premotor area arch venous malformation? Are you willing to put them to sleep and to evoke potential monitoring and embolize AVM?

- I think we've become so comfortable and reassured by having the patient awake, that it would almost be taking us out of the comfort zone. Is it safe to do what you suggested? Absolutely. But in addition to the Wada feedback, when we're manipulating the devices, the patient gives us feedback and the patient shouldn't feel uncomfortable when we're moving wires and catheters. And often if the patient starts feeling a little bit of pain or discomfort, or maybe they start feeling that an arm is heavy, that's because ischemia is developing because we may have to move our catheter 'cause we're restricting blood flow. It's these subtleties and these nuances that we get from the patient feedback when they're awake, that I think really enhances the safety margin of our procedures. And again, this is cutting edge. Most people would not do AVM embolization awake. This is how I learned from my mentor, Nick Hopkins, who's been doing this for decades, and we've gotten very comfortable with the awake technique. And truly our philosophy is, that we think it enhances patient safety because of the dynamic feedback throughout the procedure.

- I totally agree with you. I think this is a very nice way to do it. You can never argue with an awake patient monitoring. You know, it's just the safest ways to do. I mean, you have tremendous experience a lot, but for peoples who don't have as much experience in this difficult area of AVM embolization, do you recommend them to do awake embolization? What is important in terms of doing embolization awake?

- Well, for us, the importance is the Wada test. And by having them awake during the Wada test, we have a lot of reassurance that when we embolize a pedicle, we're not gonna be causing a neurodeficit. So, if there is a lack of comfort, one can become comfortable with carotid stenting and other more, or potentially less challenging endovascular procedures. If something is in a fairly non-eloquent region and they don't feel comfortable doing it awake, I think that's very reasonable. But when you're dealing with eloquent cortex, high rent area, it's important to either have excellent monitoring or to understand the potential of sacrificing a pedicle.

- I'm sorry, I may have confused you. What I meant is technically, what's important to symbolize the AVM if the patient is awake. You said a lot of people don't feel comfortable doing AVM embolization in the close areas of eloquent areas awake. Can you tell us why that is? Because to me it makes more sense to embolize these AVMs for the very good reasons you mentioned.

- When a patient's awake, there is a little bit of motion artifact. So I think the operator has to be a little bit more patient because motion will distort the anatomy. And as we get into the distal cerebral vascular, so, the M3, M4, and these vessels become smaller and more tangled, one has to understand how to transition the image in one's own mind with movement artifact. Often, if you're not used to having the patient awake, and speaking, and conversing, it may unsettle the operator. And for this reason, for better image quality, meaning patient asleep has better image quality. And so the ability to keep a patient comfortable for a long time, that's why people prefer general anesthesia. If you're gonna do this awake, you have to work relatively expeditiously and have to be comfortable with a little bit of degradation of the image due to patient motion.

- Okay, yeah, this is a great case. I guess you can argue radio surgery versus surgical resection, but after such a nice job with embolization there, a lot of radiation is very minimal. My last question is this, how many percent of your AVMS in your group, you guys are curing with embolization these days?

- That really depends. So for these smaller ones, for the Spetzler two and three, we're probably carrying close to 70, 75% with embolization, without any adjuvant therapy. When we get beyond that, very rare that we're going to achieve a cure with only embolization. And that's why AVMs, we believe, still remain a multimodal disease state.

- So you guys have a very high success ensuring most of the type one and twos through solely embolization?

- We do, for the small ones through a stage wide approach, we rarely try to cure them in one stage and I'll show you the next case. We take a stage approach and that often helps us segment out different parts of the nidus for the smaller AVMs. They give us a high rate of cure. But again, beyond Spetzler three, we rarely cure these with embolization alone.

- Thank you.

- So, this next case is a case actually in progress, we haven't finished treating this case. It's a pediatric case, but again, to show that even in younger patients, we still choose to do these awake. It's a 15 year old female who was hit in the head with a Lacrosse ball. And during the workup for her headaches after having this mild head trauma, she was found to have an AVM. So again, seeing large midline, a relatively midline AVM. Here again, we can see large venous varix, venous drainage. And as expected, the angiogram will show enlarged pericallosal and colossomarginal feeders, to what appears to be a relatively compact nidus with a very large draining vein into the superior sagittal sinus. Here is a very standard AP view. This is a little too big for radiosurgery upfront. It exceeds the three centimeter window. So at this point we're considering some type of adjuvant treatment. So, our philosophy here is if we can, she's a young woman, she doesn't want a surgery then we can shrink the nidus to make this more amenable to radiosurgery, that would be the goal. Potentially cure with embolization or at least shrink to make this amenable to radiosurgery. So again, if you look at this picture closely, we can see the microcatheter, is positioned here approximately. And the distal tip is just at the edge of the nidus here. Here, we can see a very large Onyx cast, taking the anterior portion of the nidus. So the anterior portion of the nidus has been embolized, and here you can see the pericallosal, high perch or the enlarged pericallosal vessel filling the posterior part of the nidus. Now, one would argue or at least inquire why we would not go up with a new microcatheter and just finish the job. And again, this is a philosophical approach. At least at our institution here, we try to embolize not more than 30%, approximately 30% of the nidus in any one sitting to try to avoid reprofusion hemorrhage. By doing 30%, that allows the brain to accommodate the newly displaced blood that was feeding the AVM, that's now being redistributed with good blood pressure control, and only taking 30% of the nidus, hopefully we'll reduce the risk of reprofusion hemorrhage. We will come back in four to six weeks and then try to attack the posterior portion of the nidus, hopefully get a cure. If we can't get a cure, at this point we would consider radiosurgery because the nidus will be a much smaller than it was when it started.

- That's a very good point. I think getting too greedy in AVMs in one stage can be a very high risk for hemorrhagic conversion. I really like your pearl, Elad, I think it's really important.

- Thank you. So, just some few discussion points, the natural history still remains unclear. We like to quote data of approximately a 3% hemorrhage risk per year. However, that is still undebatable. We talked about staged embolization of a goal of approximately one-third of the nidus for every sitting. And then the role of stereotactic radiosurgery for AVMs larger than three centimeters that are amenable to embolization using radiosurgery or surgery as agiment treatment.

- When you guys do the embolization and whatever is left, obviously you just radiate that part. You don't radio part of the AVM that is embolized to decrease their risk of recanalization or any of that sort. Has there been any question for you guys in that part?

- So now that we use predominantly Onyx, with use of liquid embolic we have not seen significant recanalization in nidi that we only radiated the residual component and did not incorporate areas of embolization into the radiosurgery field. So we have not seen a significant recanalization.

- Thanks.

- Excellent question. So again, now we're gonna switch from hemorrhagic disease states to ischemic or atherosclerotic disease states. And I think this fifth case is an important case in light of the New England journal of medicine SAMMPRIS paper that was presented. Buffalo was one of the lead enrolling sites. So, not only are we quite familiar with that paper and the patient population, but we were a significant contributor to that study. And in spite of that, we believe there still is a significant role for surgeons to treat this disease state in certain patient cohorts. So, we'll use a case and then we'll further discuss which cohorts may benefit from intervention. So, this is a 45 year old male who presents with left hand and arm numbness. He has high cholesterol, he has diabetes, he's already on aspirin Plavix and anti-lipid medication. He was found to have a narrowing of his MCA in the M1 region. This is a CT perfusion which we do routinely, which again, here shows an area of increased time to peak. So this is ischemic penumbra. Again, we see changes in blood flow and volumes. So this is area that has decreased volume and flow, increased time to peak, suggesting there's a type that's is in an occlusion or a stenosis there. So the CTA is a little poor quality, but the angiogram here demonstrates a critical stenosis in the M1, with a positive filling of the MCA candelabra. You can see the MCA barely fills out compared to the robust nature of the anterior cerebral artery. So, this is the cause of the symptomology. We do not think this is embolic when it's so severe. And that as a cohort, we think will benefit from intervention. When it's truly ischemic due to flow restriction, not embolic. When someone is symptomatic from emboli, we feel that anti-platelet medication or best medical therapy as a first-line treatment. However, when the stenosis is so severe that it's restricting flow, at this point, we feel that there's ischemic symptomology and not embolic symptomology. And therefore, in the setting of ischemia, we need to augment the vessel lumen. And flow, as you know, is proportional to the radius, to the fourth power. So a little bit more radius in the vessel goes a long way, . So here you can see a very small balloon in the area of a very focal stenosis. We have a wire very distal. And you can see after the angioplasty, how robust the MCA candelabra is compared to where it was before. We can see xxx, vessels are also hypertrophied. But this is a patient who is symptomatic from flow restriction. And most cases, this needs vessel augmentation, lumen augmentation to treat flow restriction. And this is a patient that if they fail medical therapy as in this case, despite the SAMMPRIS data, is somebody we would consider using angioplasty and/or stenting.

- You know, Elad, I think you answered most of my questions. What's the role of this kind of intervention after this SAMMPRIS study in this form of ischemic disease. And it seems like you guys main criteria for intervention is, severe critical stenosis of the vessel in an individual who has failed maximal medical therapy. Is that correct?

- Very well said, exactly right. Failed maximum medical therapy with a high grade, basically greater than 75% stenosis, that's a patient that I think is an excellent candidate for intervention.

- So, what do you quote as the risk of intervention of balloon angioplasty and stenting in this case?

- Well, I think in the US wingspan registry that we were part of, it was as high as a 10%, but that also included stenting. And angioplasty alone, it's gonna be a little bit lower, but I think it's fair to say that it's gonna be around eight to 10%.

- Thank you.

- So, one thing we don't talk about often, are vertebral artery disease. So, before we talk about carotid disease, which we know well, I wanted to shift gears and talk about vertebral artery stenosis. Vertebral artery origin disease, is something as neurosurgeons we don't see that often, as relatively challenging surgery, just because it's not in our everyday comfort zone. So this is a 56 year old male, who comes in with a stroke. He has some sensory loss and dysarthria. He's a smoker and a drinker. He started on medical therapy, and his imaging demonstrated AI diffusion weighted image hit, as you can see there. And his left vertebral artery appears to be fine, but he has a critical stenosis, just distal to the origin on the right side. Again, surgically, that's something that's not in our comfort zone and we don't do that often. We can talk about a vertebral carotid transposition, potentially we can talk about occluding this vertebral artery because it's likely giving emboli, since he has a healthy vertebral on the other side. But again, we don't want to take down vessels. As neurosurgeons we're in the business of saving vessels, not taking them down. So this is a very straightforward fix with intervention. This is a 20 minute procedure that's gonna change the quality of this gentleman's life. So, you can see here, he's symptomatic 'cause he had a PCA occlusion, likely from that vertebral emboli. That we're not gonna chase. So at this point, we can keep him on medical therapy, but I do believe again, as we mentioned in ICAT, he has a critical stenosis. And in this setting, we can treat him with vertebral artery stenting or medical management, is dealer's choice, because he has another xxx. We would elect normally to stent this individual.

- And Elad, may I ask, how do you know that this is embolic versus ischemic?

- Great question, and because we don't know that, because this isn't a 50% stenosis where you'd say it's not ischemic or 60%. Because it's a high grade stenosis, we believe there's an ischemic component. But he had the PCA occlusion, which tells us there's also embolic. So you feel it's a combination of two. And for that reason, philosophically, we would lean towards stenting. If this was a 50% stenosis with the PCA occlusion, we would use best medical management. Excellent question.

- Thank you.

- Okay, I think we're gonna end up talking about carotid disease, which again is a disease state that's being treated by neurosurgeons, cardiologists, neurologists, and probably is one of the sources of the greatest turf wars in vascular medicine in most hospitals centers. But it's an important disease state, and one that's affecting about 150, 200,000 people a year. So first, asymptomatic carotid stenosis, we wouldn't treat asymptomatic carotid stenosis with surgery or intervention, unless it's about 80%. Despite ACST or ACAS, philosophically, we use about an 80% cutoff as when we initiate treatment. So this is a patient who we have an incidental finding. They're found to have about 80% stenosis. In this point, it was 62. However, there are caveats. And when there's a significant wind sock ulceration, this portends an increased risk of stroke. So, if we just saw a 62% stenosis like this, without the ulceration, we would consider medical therapy. When we see irregularity or ulceration, or a wind sock ulceration like this, we believe this suggests a higher risk of stroke. And in a cast of all comers, it was about 11% over five years, we would then consider surgery or intervention. So, obviously Dr. Dumont helped me prepare this. Thought this looked like a cactus, hence the cactus on the right side of your screen. So here we can see a very nice stent reconstruction. The wind sock is still present, but it's excluded from the circulation. Over time this will thrombose, but the chance of debris coming out of this wind sock through the stent now, is extremely low. We didn't have to create significant revascularization. We did augment the vessel some as you can see, but most importantly, we shielded the circulation from the atheromatous material, that's gonna be in this wind sock. So, a few discussion points 'cause again, this is a little bit controversial. It's not your standard asymptomatic carotid. High-grade features that suggest a higher risk of stroke in the asymptomatic setting, ulceration, irregular plaque, or plaque hemorrhage which can be seen on MRI, different plaque morphology studies on MRI. Typically different types of carotid lesions, we use different types of stents. And for today, that's not germane to this discussion.

- How do you apply the crest data in your practice these days, Elad? You know, what surgery stenting for symptomatic carotid stenosis?

- So we reserve stenting for what's considered NASCET high-risk. So NASCET high-risk, or a lesion at C2 or below the clavicle, previous radiation, previous neck surgery, a laryngeal nerve palsy with swallowing deficits, contralateral occlusion, or tandem lesion. When they add these NASCET high-risk features, we tend to lean towards stenting. In the absence of these anatomic high-risk features, we will consider surgery unless there's a trial or a study that these patients will randomize or be enrolled into. But again, for non high-risk patients, the current state of affairs is, surgery is considered the first line treatment. For NASCET high-risk, we would consider stenting as a first-line treatment.

- So, is it correct for me to assume that you operate on most of your carotid patient these days?

- Our practice is unique in that we probably stent about two-thirds and operate on one-third. And that's more of the fact that, many of these are enrolled in the trials. And many of the carotids at the neurosurgery services, are not the ones that are in the community. So we tend to see the high-risk carotid lesions, that many of the community surgeons are not interested in revascularizing. So they refer them to us for stenting. So the fact that we stent more than we operate, is not that we believe stenting is the first line treatment. It's a bias of the referral pattern.

- Thank you.

- Great question. All right, so this is a symptomatic carotid stenosis with less than 50% stenosis. Again, typically we treat symptomatic carotid disease with 50% stenosis or greater. What we tried to do today is show you cases which don't fit them all. All the cases you saw today are not the typical cases that we can read about often, but they're diagnostic and treatment challenges because they don't really fall into natural spaces. This is a 72 year old man with left arm and left leg weakness. He has a medical history of high blood pressure and hyperlipidemia. He was found to have a cerebral infarction and he had an extensive medical workup, which was negative for cardiac or cardioembolic disease. So, when we typically don't see a good source of stroke in the carotid or intercranial circulation, we'll turn it over to the cardiac colleagues to look at the aorta and the heart. And this was negative. And if you look at the MRI, is basically unilateral to xxx. When we see carotid sources of emboli or aortic, typically it's a shower in both hemispheres. That's not the case here, this is unilateral. So therefore, one must think it's likely coming from the carotid distribution on the right side. And if you look at this carotid, the stenosis is only 40%, but look how shaggy it is. Look how ulcerated it is. It's a really diseased vessel, but it doesn't fit into that 50% NASCET criteria. And we know from NASCET, 50% symptomatic, you can operate on below. You probably do medical therapy. But I think we've evolved beyond that. We've ruled out cardio embolic sources. We've ruled out aorta. This is a source. The DWI is on this carotid distribution only, it's not bilateral. So even though it doesn't fit into a sort of nice box, I believe that this lesion merit stenting or surgery, or at least treatment. So in this case, we use a very smooth type of stent called a wall stent, that we don't need to plasty, we don't need to augment the lumen because there's only 40% stenosis. We just need to give wallpaper. We need a wallpaper that will certain prevent all that Atheromatous debris from recirculating into the carotid, and causing the emboli that you saw on the MRI. So in this sense, in about 10 minutes, 15 minute procedure, we wallpaper the vessel with a wall stent, and that's the result we see here. We've excluded the ulcer from the circulation with the wall stent, technically very straightforward to do. So high-grade features which suggest a higher risk for stroke, just like in the asymptomatic population, ulcers, irregular plaques, plaque hemorrhage. And this is basically an endoluminal reconstruction for a symptomatic lesion that doesn't fit nicely into our known criteria for treatment.

- Do you agree in this case that it was just as reasonable to do try aggressive medical therapy? And if the patient has another event to proceed with stenting, what are your thoughts there?

- I think that is a very reasonable option. But we know in symptomatic lesions or even on medical therapy from xxx, that the stroke risk in two years is above 20%. And then with revascularization, it drops it to around 11, 10%, basically cuts it in half over two years. From 20 to about 10 and change. So, in one sense, we looked at the symptomatic lesion and thought that because he's symptomatic, surgery or stenting stairs better than medical therapy. If this patient had been asymptomatic, then for sort, he would remain on medical therapy because there's no luminal stenosis. So that was our philosophical approach. Would it be wrong to do medical therapy? Absolutely not. It is also a reasonable approach because the stenosis was less than 50%.

- Thank you, Elad.

- I think we have one final case and more to demonstrate that we don't age discriminate. This is a 95 year old man. And people hearing 95, you know, say you shouldn't touch 95 year olds. And it's very controversial. But as a matter of fact, not in preparation for today, but yesterday, I actually just saw that the oldest man to complete a marathon was a hundred years old. It was in the newspaper yesterday. And he actually beat seven people, but it was a very interesting story. But this is a 95 year old gentlemen with the chronologic age of about a 70 year old. He had a CABG 20 years ago, probably the first guy who had a CABG. But anyway, 20 years ago. And he has a family history of stroke. Here, he has an 80% stenosis, he's 95 years old. These are his actuarial tables. So life expectancy you can see is basically 4.89 years at 87. We say if these patients can live about five years, it's worth treatment. He was 95, but again, chronologically young, very adamant about treatment. Typically we would use medical treatment for patients this age. This is a controversial case, it's outside the box. It's a patient who's healthy and takes care of himself and knows what he wants. So you can see a critical stenosis here. Again, a very straightforward stenting technique, not technically challenging, and basically taking an 80% stenosis and getting a full luminal reconstruction. So, we treated about five patients older than 90 in the last three years. I put this slide up to say this again is not common. In three years of about 350 carotids a year, so that's about 900 carotid cases, we've only treated five over the age of 90. And these fortunately have been very healthy people and I've had no perioperative complications. So, it's a very difficult discussion, but again, in the right physiologic age with the right lesion and careful patient selection, often again, you'll see patients that don't fit nicely into any one box, but who are reasonable to treat.

- Well, Elad, I wanna sincerely thank you. You have been not only a leader in neurovascular surgery and endovascular surgery, you really have proven to take the cutting edge to a new level, to help the patients. You have been really a great role model for many of the younger neurosurgeons. So, I want to really thank you again for joining us, and we look forward to having you with us in the near future.

- Aaron, thanks, this has been an honor and a privilege, and again, I look forward to the opportunity.

- Thank you.

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