Hi, everybody, I want to welcome to you to our last session of the day with Q&A and discussion in some cases with Dr. Armanda and Dr. Liebman. Before we get started, I did want to just take care of a couple of housekeeping things. For the people that are registered for the practical for tomorrow, you already have your login and your links to get in for tomorrow morning. So we'll be doing that from eight to noon Central Time. So definitely be ready for a great session there. And then there were questions about the SNAP program that's available on WNS. That again is the sessions in neurosurgery for advanced practitioners. Right now we have it just for the purpose of onboarding or for new people to neurosurgery. There are lots of different topics, lots of great talks. So please feel free to check that out. And as we move forward, we're going to add some more advanced content as well and have a different track. So I did want to just kind of shout that out real quick. And I wanted to thank you all for being here for the last several days. We've had a great course and this far exceeded our expectations with the virtual session this year. So we're really, really happy that you all have enjoyed this. And I hope you enjoy our last session here today. Thank you so much. Thank you. Get started, Dr. Armando with your case. Okay, great. So we're going to pick up with a couple case examples. And we have a interesting situation with a young lady who comes in who has the worst headache of her life. And she then comes back to the hospital after having been sent out for sinus medications. But this time she comes in with a seizure. She's confused, obtunded, and has evidence of a subarachnoid hemorrhage that's quite large here, undergoes placement of a ventriculostomy, and then undergoes an angiogram. So this demonstrates this ruptured posterior communicating artery aneurysm that you see here and a ventricular catheter now in place. So the question comes up, what's the best way to treat this particular aneurysm? And what would be your next stage? Just to sort of poll people what they would do next. So the options are here, microsurgical clipping with hemicraniectomy or microsurgical clipping without hemicraniectomy or endovascular coiling of this aneurysm. So... I don't have anybody piping in yet, but sometimes there's a little bit of a delay. So a couple considerations here in terms of who we clip versus who we coil. Considering patients that you might consider coiling would be patients whose aneurysms have a narrow neck where you're able to create a coil mass that doesn't permeate into the perineurotomy. Patients who you're able to control their ICP versus let's say you put in a ventriculostomy here in this patient, but she has a blown pupil, you might proceed directly to the OR for a decompressive craniotomy and clipping. Rocco, do you mind if I interrupt for just a second? Yeah, go right ahead, sure. There's a couple interesting features here with this angiogram and then this diagram. A couple things that you need to understand with the angiogram, this looks like a very large PCOM and does the patient have a fetal PCA? Do we know that based on this angiogram? Yeah, so this is actually a standard PCOM artery and this patient fills the posterior circulation, fills the PCA out from the vertebral injection. So this is a PCOM that you could sacrifice if need be. I don't know if anybody was on my talk yesterday or two days ago, but that's something that you do with the PCOM. You need to identify whether or not this is a fetal PCA, which means either the PCOM itself is much larger than the PCA coming off the posterior circulation or the PCA comes off directly off the ICA because if you take this vessel and it is a fetal PCA, you have a large occipital infarct. So I'm sorry, I apologize. I just wanted to get that in there, Rocco. That's okay. So we'll go ahead and this is another beautiful artist drawing from Nick Hopkins on this particular case, very useful. So we're able to successfully coil occlude this aneurysm. There's a small residual filling at the neck here. There is still persistent filling of the PCOM, but no filling of the aneurysm fundus nor dome. If you look at the rest of the angiogram, you see that the aneurysm has been obliterated. And I just want to show another picture here. This is her, so what we use as a baseline comparison of her vessels at day zero. And what stands out here that should draw your attention is the significant distention of her periclosal arteries. And the reason why the periclosal is distended so much is really because of her underlying hydrocephalus from her re-rupture. So this is also a good shot of the PCOM, both pre and post correlating. And you can see the PCOM still fills and fills the posterior cerebral artery, which also fills from the vertebral basilar system as well. But she still has issues with hydrocephalus. So typically as a standard protocol, we don't drain the ventriculostomy for ICP. We drain the ICP if it's greater than 20 before the coiling, and then after the coiling, we'll drain it anywhere from 10 to 15. But we try not to aggressively drain the ventriculostomy before the aneurysm is coiled, and that's to prevent re-rupture of the aneurysm and increase in the transmural pressure. So just an aside there. So she wakes up. She actually does very, very well. And for the first five to seven days, she's actually awake, alert, conversant. She's very bored in the ICU with her ventriculostomy in place and is typing on her computer, emailing her colleagues from her work, putting makeup on, checking out her hair. And we're getting some baseline TCDs on her. So baseline TCDs are being done. The baseline TCDs are looking pretty good. Velocities are all under 120 and appear to be normal. Despite this, we go ahead and we do start some volume therapy. We don't drive her blood pressure. She seems to be driving her blood pressure on her own, however. At this point, she's not on any pressers, though, does not require any intervention at that point. We become a little bit more concerned because as the week goes on, this is now day five. And at day five, she's still totally neurologically intact. We see a jump in her velocities by over 50 points. Now her mean velocities are 185. The question becomes, what should we do next? So just a question to the group and to Dr. Leibman, what would you do next? There's always a little bit of a delay, so hold on for a few seconds here, and then I'm sure they'll start saying things. So the options would be, do you take the patient for an angiogram and possible intervention? Do you treat the patient with hypervolemic therapy, hypertension? She's actually driving her blood pressures up on her own, so her maps actually are already up 110 to 120. Do you drain the ventricle more aggressively? It's at a height of 15 right now. So there's a couple different options there. Somebody's voting for imaging with CTA. A few people saying that. Just before we go into treatment, a question I have is, what's the patient's clinical status at this point? Yeah, so she's totally awake, totally alert. She's oriented. She has no drift. She's really at a neurologic baseline post coiling when she improved. Again, she's still without any focal deficits. She gets a little sleep deprived with neuro checks to one hour and gets a little agitated at night, but things seem to clear in the morning and following commands appropriately. Have a vote for doing nothing considering she's neuro intact and make sure she's optimized from a hemodynamic standpoint. Some people say angio. Others say also no treatment unless clinical vasospasm. Keep an eye on her. Those kinds of things are coming up. I like the spirit of the people that say go to an angio. Of course you do. I've never met a neuro interventional doc who doesn't like that. Right, right. Because of her exam being so pristine and because she's following commands, we did get a CT scan. Ventricles were a little plump. We ended up draining the ventriculostomy a little bit more aggressively to a height of 10 at this point from previously 15, but we didn't see a role for angio because we didn't see a role for any prophylactic intervention and that's really based on studies that have been done that show no benefit for prophylactic angioplasty or vasodilators intraarterially in patients who have a normal exam. And that's exactly what I would have done. I think one of the people said I would have maximized. I would maximize hemodynamically. Obviously she's pushing her own blood pressure, checking hemoglobin. If we give her some blood products, great. And then I would have done exactly the same thing. I would have dropped her EVD and been a little bit more aggressive with her EVD drainage. That's exactly what I would have done. So things get a little bit more interesting. This is the next day's TCDs and at this point she's still normal, but I was very, very concerned with the velocities being higher. Now she's normal in terms of neurologically, no drift, but something's different about her and it's very hard to characterize. And she's just not, from a behavioral standpoint, her usual self. She starts pulling things out. In fact, she pulls out her ventriculostomy and the ventriculostomy goes back in. But still she has no aphasia, no motor drift, no focal deficits, just seems a little bit more agitated. So question is, what do you want to do now? So again, she went from means about 185 and left MCA to means of 347. And I'm sure the ratios are really high as well. Yeah, her ratios now are close to like seven. Yeah. Waiting for the responses to come on in here. Okay. Again, the variety of things are medical treatment, repeat CT imaging, CTA imaging, or angiography and intervention. Some people are saying repeat CT or CTA. I like this one. Somebody says, squirrely and TCDs are worse equals time to go for angio and IA. Yeah, so that's what we chose to do. We said that, you know, this is not who she normally is. In fact, I'll never forget what she said. She said, I can't remember what it was that I have already forgotten. And it's a real quotable. I can't remember what it is that I have already forgotten. It means that she has some conscious awareness that she's losing her cognitive ability, but she can't quite characterize it. So under general anesthesia, we take her to the IR suite, make sure that we maintain her blood pressures and ventricular drainage. And this is what we see. This is a left ICA injection. This is the ICA from a frontal plane, some narrowing spasm of supraclinic carotid, but marked spasm of the A1 segment and marked spasm of the MCA, and then spasm of the distal branches, particularly this sort of inferior division, the MCA and very slow circulation times. So the question then becomes. Can I interrupt just real quickly? Are you getting things out on the angiogram? Because I can't see a cursor at the moment. I'm sorry, I'm on the wrong side here. I'm sorry. So here's the supraclinic carotid artery. And there's some narrowing here that you see better on the lateral, but marked narrowing of the A1 segment and long segment narrowing the entire M1 segment, narrowing of your M2s and your inferior division. And so this is filling up the PCA from the PCOM, no filling of the aneurysm of any significance. That's right. I think we ought to, before we go on to treatment, I think we ought to really emphasize a point that you're making. And that is spasm can be manifested with not necessarily a focal finding. It can be worsening headaches with elevated TCDs. It can be increased urinary output. It can be, as you just described, especially with the ACA spasm, a change in behavior. And that's a really important point. Because if, although the patient doesn't necessarily have a true focal finding in terms of weakness, expressive or speech issues, but they did have findings. And I think that's a really important point. Sorry. Yeah. And concomitant with this, we also saw a drop in the sodium. She started going into more cerebral salt wasting, which we've seen very characteristically. We started 3%. And she started raising her temperature. So the temperature shot up to 38.5, almost to 39. And we got very active and very aggressive with cooling her as well as treating. So the question becomes, how do you want to treat this? There's a couple of different options on the table. One is just vasodilators like IA verapamil. Another is with angioplasty alone. Another is a combination therapy of both IA dilators and angioplasty. And then the question sometimes at some institutions become, how do you do that? Do you do the vasodilators first or the angioplasty first? And do you bring a micro catheter into this A1 or not? So what we opt to do and what we typically do in our protocol is first we give the intra-arterial vasodilator. And that allows us to navigate the micro balloon into better position. And we tend to under inflate. So we do very, very small inflations to avoid a rupture of the MCA. And we make sure that the balloon is prepped with 60% of contrast and 40% of saline so we can see it very well. We make sure that the balloon does not have any air in it. We purge the balloons. A couple of different balloons we use. We use the Scepter C balloon. There's a three millimeter balloon that's very small that actually is useful for these very spastic MCA vessels like this. There's a four millimeter balloon that we use as well. And then there's also a transform balloon which we've used as well. The advantage of the Scepter C balloon is that you can perfuse through the balloon as well as doing your angioplasty. Can you guys speak to how long generally do you expect results after giving like IA, verapamil, or angioplasty? Or is it all just kind of following the patient afterwards and seeing how they're doing and their TCDs and all that kind of stuff? Yeah, so in our experience, we've had patients that we've had to take back multiple times. We have a subgroup of patients that we've taken back three, four, five, even six times. And these are patients that we've treated with both angioplasty and intra-arterial vasodilators. The vasodilators tend to have a much more transient effect. If patients have what we call diffuse vasospasm or distal vasospasm involving the distal MCA or distal ACA, usually you're going to have to take those patients back more frequently. If patients have persistent fevers, younger patients, you have to take them back more frequently as well. So we usually plan, you know, for a younger patient to be prepared to take that patient back, you know, at least two, maybe three times. We wait for the patient to show us not that they don't need it rather than that they need it. We use, I personally, I'm not a big fan of the chemical dilators, as Dr. Armando was mentioning, because everything he just described, it's very transient. And you can often make an angiogram look better initially, but I don't, I have not personally had great results with chemical vasodilators. Obviously, if it's distal spasm, and when I say distal beyond the second order vessels, I will balloon angioplasty all the way up to the second order vessels because theoretically, the concept of a balloon angioplasty is you're causing damage to the muscular layer in the arteries. So theoretically, they can't spasm further. So it has a much more durable treatment. Now, that being said, if the patient after angioplasty, if indeed they have recurrence of their symptoms, or if their transcranial Doppler's start to go up again, then I often will get a CTA and do a CT perfusion. I think a CT perfusion is very valuable, it helps just that, it helps assess the perfusion to the brain. But I tend to go more with a balloon because I feel it's a much more durable treatment. And so this is what we ended up doing. So we did a combination of therapies, we did, this is our initial, we treated this initially with intra-arterial vasodilators, and then we followed those vasodilators with sequential balloon angioplasty. So this was post-dilation, post-verapamil, and then we followed with sequential dilation. And we even brought up eventually a microcatheter into the A1, not for angioplasty of the A1, but for verapamil injection as well. And it was interesting, unfortunately neurologically she actually got worse. We did a head CT, and we saw low densities, and she had problems with seizures. So we put her down for her seizures, the TCDs were definitely better over the next couple days, but all of a sudden she started developing more low densities. So we ended up bringing her back again, we brought her back again, and she had some recurrent spasm, and here you can see angioplasty of the supraclinoid carotid improvement from there. And then we brought her back a third time because she had, again, some fluctuation in her exam, and to our surprise, and you see this not infrequently, we saw evidence of some significant posterior circulation vasospasm. And again, we treated this with a sequence of vasodilators and angioplasty as well. So it was a total of four treatments for this particular patient. Unfortunately, though, it was really her seizures that really were the biggest problem in her particular case. And, you know, in retrospect, what may have helped is continuous EEG. So I didn't talk a lot about continuous EEG in our particular talk today, but I think continuous EEG really plays a big role for the management of these patients, especially the patients who are at higher risk. And if I could have done something differently, I think in the management of this patient, I think continuous EEG after the first treatment to make sure that she wasn't still seizing, and then the role for, you know, continued intervention as we did, but help, you know, manage that with the use of better EEG monitoring. So this is another lady that was referred to us. This patient was referred to us as a trauma. She was in a fight with her boyfriend, and after being beaten up, she had hit her head on a glass table and came in with this scan. So it was initially billed as a traumatic subarachnoid, but it didn't look to me like a typical trauma. It looked like a subarachnoid with blood concentrated mainly in the sylvian fissure and the ambient cisterns here. She also had what looked like a very, very tight-looking brain where you see sort of a reversal of the low density of the white matter versus the cortical mantle, and she was severely compromised. She was hemiparetic on her right side. She was aphasic and really very, very somnolent. So she was intubated, ventriculostomy was placed, an angiogram was done, and what we found, in fact, were two aneurysms almost side to side, PCOM and anterior coroidal. And so the question comes down to which aneurysm would you treat? How would you treat that aneurysm, or would you treat both aneurysms and by which method? So here's a little bit better view. Both of these tended to be narrow-neck aneurysms. For the subarachnoid hemorrhage patients, our approach is endovascular first, unless for some reason they're an acute extremus with a blown dilated pupil and she did not have that. So we ended up using endovascular means, and we actually ended up coiling both of the aneurysms. So we coiled the more distal aneurysm first, and then we coiled the more proximal aneurysm. There's still some residual filling of this aneurysm and filling of her PCOM and some residual filling here, but we felt that at least this offered some immediate protection of the aneurysm dome and fundus. So because this patient was so compromised and we did not have a very good exam to follow, we ended up placing a rheumatic monitor, which is a brain oxygen and brain ICP all in one bolt and followed her along. And it looks something like this. So she has her ventriculostomy in place behind the bolt, and here's the actual bolt, and it does brain oxygen and brain temperature. And that combined with her TCDs, we were able to follow her because we didn't have much of an exam to follow. And then this is the trend for her TCDs. So this sort of gives you an idea of what's going on with her TCDs. So if you look at her TCDs, you see the TCDs are on the lower side, and then she has a little bit of a bump on the 25th, and then all of a sudden there's this dramatic drop. And the day the TCDs dropped that dramatically, we saw that her brain oxygen dropped. And because the brain oxygen dropped so much, despite adequate ventilation and oxygenation, we ended up taking her to angio, and this is what we found on her angiogram. So this is a frontal plane injection, left internal carotid artery, and if you follow my arrow, you can see marked spasm of the supraclinear carotid artery, and then of the A1, but most markedly of the M1, and dilation of all of her lenticular striates, but that's that tiny little spastic, almost submillimeter size of her M1 now, and she also had spasm distally as well. We ended up treating her with combination therapy again, so she got treated with a vasodilator, which was verapamil, as well as angioplasty, and she underwent, again, about two different sequences, excuse me, two different separate additional days for three total treatments for her vasospasm. So if you compare the two, you can also see that there's a big difference in terms of the circulation time. Her circulation time was much slower. She even had some stagnation of vessels here, and you can see it better on the lateral image. On the lateral image, she had some very slow flow in her rolandic artery pre-treatment, and it almost looked like there was thromboemboli there. In fact, when we did a capillary phase, you can see what looks like a punched out area there, and I thought it was thromboemboli from our angiogram, but it actually reversed after the verapamil. So what happened is that this vessel that goes out towards the rolandic artery was actually in such a state of spasm that there was such poor filling of her capillary distribution out there. So we found that the verapamil here was fairly effective. It literally took about a half hour, though, to see this change. So one of the other things that we do that's been helpful, one of my other partners has brought this with his previous practice, is for vasospasm treatment patients, we put verapamil in the perfusion bags. So they're heparinized bags with verapamil that's also perfusing our guide catheters, and I think that helps decrease some of the spasm in addition to the verapamil that we give this patient as well. So again, this is pre-, this is post-treatment, but I think what was happening from a TCD standpoint is that the reason why her TCDs dropped so much is because these vessels became almost pre-occlusive. Yeah. So if you see a pattern of TCDs getting better, getting lower, that's not always a good thing, especially if they become pre-occlusive like that. So Ken, I don't know if you have anything to add. No, I can't agree more with everything you're saying. One of the things is just that with TCDs, you're exactly right, it can, it's worrisome if you see this continual rise and then a rather profound drop. That is, to me, that's a concern, it is pre-occlusive, and I do take those patients to the suite. A couple of things that you commented on, the first patient and this patient. I would very, very unlikely take these patients ever to the OR. They have angry brains. It's the dominant hemisphere. You're going to cause significant neurologic, I don't care, in the best surgeon's hands, there's going to be a greater chance for protraction, dissection of injury to the dominant hemisphere. So I would always, even if that first patient, it was a dominant PCA, it was a fetal PCA, I would then coil the dome and then get the patient out of the acute phase, and then if I need to, bring her back in a more controlled fashion. And then one of the other things you mentioned is if the patient's an extremist. What we found and actually published, you can often with EBDs and with appropriate osmotic therapy, you can kind of get them out of extremis in a transient way, do the angio, do the coiling, and then do a decompressive hemicraniectomy, and again, avoiding injury to the dominant hemisphere. So that's another thought. Yeah, we definitely have done that, even to the point where we've coiled the aneurysm and then take them to the operating room for a hemicraniectomy. Yeah, exactly. Rare. You don't have to do the arachnoid dissection. If you leave some residual aneurysm, you wait several months until it's time for the cranioplasty, and then you can clip the residual aneurysm and do the cranioplasty. Right. And it's just sort of basically doing a damage control type of operation, where you take care of the most important priority. You're not fixing an x-ray, as Robert used to say. You're basically fixing a human being, and you're trying to tailor your approach such that you limit the amount of secondary injury from your therapy. Exactly. You know, that can be a real issue. Also, the anesthetic is really important in these cases, and I really have to emphasize that. Communicating with your anesthesiologist so the patient doesn't get hypovolemic, hypotensive, you don't let their temperature spike to, you know, 39 degrees while you're doing your interventional approach, that you don't let their sodium drop to the, you know, 130s during the approach. If they're on a 3% for a reason, you continue the 3%. You continue your ICU care into the IR suite. You don't just all of a sudden stop all of their ICU care that you're doing when you're in the IR suite, because you don't want them to have this sort of drop in loss of continuity of their therapy. In these cases where they get this loss of continuity, where their 3% is turned off, for example, and they're diuresing because of cerebral salt wasting, they get hypotensive, and they get hypovolemic at the same time, that you really see some bad strokes as a result, regardless of what you do angiographically with the pictures. And that goes for any time, as you said, you go into the angio suite. If you're doing a treatment for a mechanical thrombolysis for an ischemic stroke, it's imperative to have direct communication with the anesthesiologist, preferably actually have a screen that you're viewing to look at the vitals to make sure, as Dr. Armando said, to make sure that the patient during intubation doesn't get hypotensive. And then irrespective of what you do thereafter, the cat's out of the bag, because the patient was hypotensive the whole time, or hypoxic, or whatever. I have several questions here. I'm not sure, was that the end of that particular case, or are you still going with this? This just sort of shows the treatment with the angioplasty in her particular case. And then just a little dynamic video here of the sequence of inflation. And that's it. That's all we have for now. Okay. I'm going to take a break in then, because there are lots of questions that you guys have both had from both your sessions, and now we're kind of racking some up here too. So I want to get in and have you guys kind of talk about some of these things. So a few people have been asking about basically the concept of cerebral salt wasting, what that means, and what's the mechanism, why does it happen? It's a great question. So we don't know exactly why it happens. It seems to be part of that systemic response to the stress of the subarachnoid hemorrhage that then affects the kidney's ability to secrete appropriate mineral corticoid. And so the kidney becomes deficient in its ability to secrete the appropriate mineral corticoid. And so the body starts dumping high volumes with these high sodiums into the urine. And one of the ways we try to combat that is with a combination of therapy. Part of it is to give the mineral corticoid, like fluconazone, and then also is to give 3%. But to titrate it so that you don't put the patient into pulmonary edema. And what's important to note is because salt wasting versus SIEDH, the inappropriate secretion of antidiuretic hormone, the treatments are a little different. And sometimes it's difficult when you're working people up because you're giving them certain medicines so that when you're doing the workup, it gets a little confusing. But it's a very important point that someone who is salt wasting also is volume depleted. So you can do daily weights to help with the diagnosis. Salt wasting when it gets, cerebral salt wasting when it gets significant, you can get hyperkalemia. There's not a lot of disease processes where it causes an elevated potassium. So those are some lab values or ways to indicate whether it's SIEDH versus salt wasting. And the other thing that, and Rocco said it, is fluorine for fluconazone. The point being is that that works on the distal tubules of the kidneys. And it works directly on the sodium potassium pump, specifically for salt wasting. So people give that fluorine up a little too liberally, and you don't do it for SIEDH, you do it for salt wasting. Again, it works in the distal tubules. And if you do give fluorine up, you just got to keep an eye on the sodium, but also the potassium. Yeah, so I'm just trying to show this slide here for a second. So I don't know if you guys can see this. I think what he's saying is it's just a little bit smaller. If you put it on presenter view, I'll be able to figure it out. Oh, sure. If you can see that. Yeah, that's perfect. So this is a characteristic trend that you see, and sometimes people talk about this being the fish curve. So what happens is that as your sodium drops down, your ICP shoots up. And so you sort of make this sort of fish pattern here. And then as the sodium goes back up, the ICP comes back down. But one of the problems that you get into is these big fluctuations in sodium. So that can be quite lethal, especially as you see a patient with a sodium that's in the 140s. And then all of a sudden, within a period of it could be 24, 36 hours, they have a sodium as low as in the 120s, as in this particular case. And then bring that patient's sodium rapidly correcting it can cause a central pontine myelinolysis. So you really want to avoid that big fluctuations in sodium from the get-go and prioritize what your sodium target is with your ICU team and the rest of your team. So people know that you don't want to go through this period of big drop. And you can see part of the reason why this was dropped is because it's not checked. Like everything else that we emphasize in medicine is that things will be addressed and things will be taken care of are those things that are checked. If those things go unchecked, there's a sense of complacency that comes in, and that's where complications happen. So no sodium is being checked from this point here to this point here, and that's really unacceptable. So that's where we get into these problems. So you really have to be vigilant with these patients, and they're usually patients who have an exam that's clinically better than what they should. So they have an exam that looks very, very good, and so they get parked off into a corner or a step-down unit or onto the floor, and that's when they really deteriorate in terms of their metabolic problems because they're not being watched as closely as in the ICU. Great. Thank you. Another question for both of you guys here. When is baloney angioplasty contraindicated? Yeah. Great question. Rocky, do you want to—it's spaz—I mean, I'll—do you want to—I'll add, or— Yeah. I think that it's contraindicated in a patient who has intractable ICP, for example, a patient who has a ICP crisis that needs to be addressed because they may need a decompressive craniectomy, a patient who, for example, has ICP spikes, but you can't lay that patient flat. So you can't lay that patient flat because their ICP becomes, you know, basically super, super high, and you might have concomitant drop in their brain tissue oxygen. A patient who is prone for their lungs, and they can't be supine, you're not going to take somebody who's supine for ARDS for an angioplasty. So if their lungs or heart are so metabolically affected because of pulmonary edema, neurogenic pulmonary edema, or Takotsubo's that we talked about, they're not going to be a very good candidate for a balloon angioplasty. Who else might you not do a balloon angioplasty for? Those are the major cases. I think people with distal spasm, as Dr. Rehman mentioned. So the way I break it down, and it was the way Dr. Armando said, was very good and systematic. So the first thing you do is you determine whether or not the patient's stable to go to the angiosuite, because balloon angioplasty is an invasive procedure done in an angiosuite. So the first thing you want to do is, is the patient stable from their airway, their breathing, and their circulation? Or is the patient, as Dr. Martin said, if you lie them flat, do they have ICP issues? So you're not going to do really anything with that patient in terms of the next escalate to the next step. Once you get the patient in the angiosuite, to me, the only true contraindication, and it's also somewhat to the discretion of the endovascular doctor, but the only true contraindication is distal spasm, because vessels are serially, they're just not robust enough to accept or accommodate a balloon. The types of balloons we use, I tend to use, there are three basic balloons that we can use, and it defines the compliance of the balloon. So we have a compliant balloon, a semi-compliant balloon, and those are primarily we use intracranially. And the only true contraindication is a more distal spasm. And what I also mentioned two days ago is know the vessel, what the vessel looks like on the initial angio, because an also contraindication is ballooning either a hypoplastic baseline A1 or an absent A1 was never there. So that's a contraindication if the vessel at baseline is hypoplastic. Okay, great. Thank you guys. So someone else is asking about kind of specifics regarding I's and O's. Is there something that you look for specifically as far as, do you want them neutral, euvolemic, you know, or negative net balances, negative positive? How do you normally run patients? I guess, and probably in the setting of, you know, vasospasm. We usually keep the patient, the one thing that you'll notice is, especially in someone who's a young person who's got normal kidneys, the more you give them, the more they're going to dump. So to chase it, we do keep them more, we try to keep them euvolemic. We don't, we don't really go into this hypovolemic mode unless the patient is starting to have clinic symptomatic spasm. But even so, it's very difficult to get hypovolemic, especially if the patient has normal kidneys, the more you give them, the more they're going to dump out. But what we also try to avoid is diuresing them. So if the patient starts to, if they're start to have pulmonary issues, respiratory problems, we're very careful. And if we do give a diuretic, we're removing the crystalloid, we give back colloid. So we, because colloid will tends to stay in the intravascular compartment a little bit better. So we keep them essentially euvolemic. Okay. Dr. Armando, you have anything? Absolutely. One thing we do is we look at weights, you know. So it's, it's hard to match your Is and Os in the unit because they might get more fluid in the IR suite or in the OR and elsewhere. So we look at baseline weights and we look at how many, you know, kilos are they up or pounds are they up from their admission weight and make sure that, you know, we're keeping an even balance there. And what's been very helpful here is some of the newer technology that's been used in the cardiac care units and elsewhere, where we try to assess, you know, what is their cardiac performance? You know, in the old days we used to put in a swan. We're not putting swans in these days. Most of the time we're actually using these other modalities and, you know, transthoracic echoes to correlate what is their filling volumes, you know, is their intravascular space depleted and, you know, this is all third spacing, do they need more intravascular volume? And in that case, you know, the 3% and some of the colloid actually is a better agent. Got it. All right. Here's something that I find, at least in my professional world, to be kind of controversial. Patients who either have large, so large bleeds and aneurysmal cell backbone hemorrhage and the use of prophylactic, anti-epileptic drugs. Yeah, I mean, we tend to use Keppra in a patient from the baseline if they have a large subarachnoid hemorrhage. We use it in all patients prophylactically. Most of the time, yeah. So we use Keppra most of the time. And then if they have a seizure beyond that, we usually add Dilantin and we do an EEG. There have been a group of patients who have not tolerated Dilantin very well, but, you know, if they're seizing, Keppra doesn't usually seem to stop the seizure as well, so we tend to go to other agents. And that's where we get our neurology specialists, epileptologists involved in terms of helping us with other agents like Lamictal and so forth. It depends on the bleed, the distribution of the blood, but we primarily, from a prophylactic standpoint, keep Keppra only on for one week. And then after the week, and from the trauma literature, then we wean it off. So we do not keep people on Keppra or any type of anticoagulants indefinitely. The only time we keep them on for an extended period of time is if we're concerned if the bleed is in the temporal region, a very high epileptogenic area, or if the patient indeed has a seizure. And then we'll add, we'll continue with the Keppra if they need another agent, we'll add another agent, Venpat, whatever it is. And then, as Dr. Marda said, if they continue, our threshold to put them on continuous EEG is very low. Okay, great. Thank you. All right, I'm going to grab from actually some of the earlier sessions here. We have a lot of questions for you guys. So let me get into some of these. And again, I did a screenshot on my cell phone, so excuse me for one second here. One of the questions was about vasospasm and what your thoughts are about the use of intraarterial milrinone. So we don't use intraarterial milrinone, we'll use IV milrinone, but we have to be careful with how we dose our milrinone if the patient's hypotensive. If you have a patient who has a cardiac systolic ejection fracture problems, the milrinone will actually exacerbate that. So in those patients, they do better with dobutamine. But in patients who can tolerate milrinone, we will go ahead and start according to the Canadian protocol. And we have that written out. Okay. But not intraarterial. So intraarterial, done, IV. Got it. Second part of this question, in a patient who already needed intraarterial therapy, and you have no exam and no windows, basically, on TCDs, how often do you get surveillance CTAs? Do you just surveil patients daily, or do you just take them automatically for a diagnostic angio? A patient who's not having any symptoms? Correct. Yeah. No, I would follow their exam. I think their exam, again, irrespective of TCDs, if their exam is stable, then I don't get imaging unless there is a concern I have. And I want to pipe in and say that it was actually no exam, like maybe they're sedated or something. Yeah. Sorry about that. Then I would lean, if there was a concern, and kind of all the other things we talked about. If the patient starts having increased urinary output, hyponatremia, rise in their ICPs, if they don't have an exam, they're likely going to have an EVD. I'll be aggressive in terms of lowering my EVD and drain more aggressively. And then maybe peak hemorrhage day, I'll do a CTA, CTP. I think a CTP, as we keep talking about angios and CTAs, I think a CTP is extremely helpful in terms of just that, assessing the perfusion to the brain. Okay. Yeah. So, I mean, we tend to do this similar thing, except we're not as facile with our CTP for subarachnoid hemorrhage patients. So what we tend to do is, again, use a brain tissue oxygen monitoring with a hermetic monitor, and then we'll combine that with a continuous EEG. We've done some pupillometry measurements as well to try to use that. But another protocol that we typically employ is that if the patient has a very poor exam from the get-go, let's say a grade four patient, you don't have a lot to follow, you don't have windows, is to do a surveillance angiogram at day seven. Or if it's going to be a long holiday, like Labor Day, then, in fact, your Friday becomes busy doing a surveillance angiogram. You just plan for it so that you have that in the books, you have anesthesia, you're prepared for that, so that you have some idea of what the vasculature looks like going into a period where they may not necessarily get monitored as closely, so you don't want to lose that. So, Rob, if you do an angio as a surveillance and you indeed see spasm, you obviously proceed with treatment. That's right. So, this isn't a poor grade patient who we're saying, you know, we got a CT scan, we don't see evidence of a new hemorrhage or a new stroke. We make sure that it's not an issue that's irreversible and somebody that we're going to be, you know, very aggressive with, a younger person with a better prognosis, perhaps. And so, in that patient, we will treat higher grade patients based on angiographic information, especially if we don't have much of an exam to follow. And that's not necessarily something that you can find a large randomized study out there to support. It's basically empirical. And so, it's an empirical, you know, intervention based on our experience that patients do better if in fact you can treat their vasospasm and poor grades before they develop the infarcts. Now, this goes back many, many years. We've seen cases where you see low densities, you think it's an infarct, but it's actually reversible. And you have to be careful whether you call it a true infarct or not, because some of that may in fact be reversible. And that's where I mentioned the CTP is valuable, because you're exactly right, vasospasm, you're treating it like a stroke, right? So the concept is, because they have all these papers and quoting about doing treatment within six hours. I mean, that's silly. I mean, you treat a stroke ASAP to try to reverse a reversible penumbra. It's the same concept with spasm. Yeah, the sooner the better. It really becomes down to the fact that we just don't have an ideal monitor. We don't have, in a poor grade patient, you don't have one single monitor. I think he kind of froze here for a second. Other than taking them down for axial imaging, like a perfusion study. So it doesn't really sound like either of you do kind of surveillance CTAs, it's kind of looking at all the other pieces of information you have that are probably a little bit less invasive, per se, and obviously including the exam. I mean, it's not an unreasonable thing to do with a poor grade patient and opposed to subjecting them to an angiogram. No, no, that's what I'm saying. I do. I would go more of the CTA, CTP route first. That's so often, though. I think that's what they were trying to get at more. Do you do it on a certain schedule? Say you have a grade four patient who's really sick, sedated, paralyzed, and you don't have any exam to go on, and you don't really have any other information that you're able to provide. I would probably do it in the peak period. Again, there's really no data to say this is how you should do that. It gets back to the, also, are you going to start moving a patient who is sick? I mean, those patients who you don't have an exam on are also sick as hell. Moving them actually carries with it a greater morbidity than keeping them at bay in the unit because they're so sick. Sure. That makes total sense. Okay. Question about the use of microdialysis. Do you guys use that to help detect vasospasm or mostly rely on the TCBs and exam pieces? We don't have microdialysis. I think it's a great research tool. I'm not quite sure in the majority of places that it really has come down to a practical application because it is so manpower intensive. It requires a great deal of support from a laboratory and nursing standpoint, and it's very focal. It's great for that small region of brain that it's in, but unless you have bilateral microdialysis catheters, you may miss something. Same thing. We don't have that capability, and we use the transcranial dopplers with an exam with, again, CTA, CTP if we need to escalate. Okay. Fair enough. Someone's asking about the risk. Since there's a risk of DVT, PE in these sick subarachnoid hemorrhage patients, what do you guys do for screening? Do you screen your patients? How do you closely monitor your patients for these complications? Are there any recommendations on screening guidelines and protocols for this? We are very aggressive with our DVT prophylaxis. It really upsets me when I hear people holding DVT prophylaxis. The neurosurgical literature is rich with, you can indeed start sub-Q heparin irrespective of the emitting CAT scan. So we put them on sub-Q heparin TID, and the trauma patient, we'll put them on Lobinox if a 24-hour scan shows stability or no intention of taking the OR. So we start with chemical prophylaxis quite quickly, as well as sequential TEDS. Then we screen our patients twice a week. We screen them every Mondays and Thursday. We screen them twice a week. So we are aggressive. Ultrasound of all four extremities? We do ultrasound of the lower extremities. If they have, obviously, symptoms such as a swollen upper extremity, or if they have fevers of unknown origin, we'll get four extremity DVTs. But we primarily, twice a week, lower extremity. Okay. Yeah, we've had a pretty significant shift over the past five years from our previous approach of basically intermittent heparin use to much more aggressive scheduled heparin or Lobinox use and screening. And the other thing we worry about that we've seen also is heparin-induced thrombosis and thrombocytopenia, which can be a real issue in these patients because they get exposed to heparin during their initial angiogram. They get exposed to heparin again when you do subsequent angiograms, and that can lead to HIT. So really, in addition to this, being very vigilant about looking for HIT, looking for a drop in platelets and screening for the potential for DVTs and thromboemboli. It's quite serious in our population of patients when you look at neuroendovascular in general, the incidence of HIT. It actually is occurring a lot more than probably what's been reported out there. And then to just answer the piece about, I don't think there are any guidelines that are specifically for this population. As far as screening or treatment, there's a lot of variation from what I've seen as far as both screening and treatment because some people like to take heparin, some do Lovenox. I mean, AHA has recommendations for prophylaxis. So the 2012 guidelines does include the role for prophylaxis for a DVT and the stroke guidelines do. But Jared, there's no guidelines really for screening, for the screening. And the trauma guidelines strongly, they recommend Lovenox, not sub-Q heparin. In fact, they would sprinkle pixie dust. They feel that's comparable to sub-Q heparin. So they're really aggressive. Yeah, they're very strong in Lovenox. Okay. All right. Let's see. Somebody wanted to know why younger patients were at higher risk for vasospasm. I'd have to venture to guess that they have more vasoreactive vessels. When you look at how their vasculature responds in general, that they have the neurovascular coupling is basically much more responsive. There's less atherosclerotic disease perhaps that may add to it. And so their vessels tend to respond more. Smokers is another population of patients that we see a lot of vasoreactivity, drug abusers as well, patients who, you know, cocaine or crack or things like that, that they also seem to have a system that's attuned and a little bit more sensitive to vasoconstriction, so it probably has to do with the fact that they have younger vessels that tend to be much more vasoreactive. In general, younger patients with a bad subarachnoid tend to be much more sympathomimetic, more adrenergically driven, you know, where they go into a crisis quicker, pulmonary edema quicker, things like that quicker. That's always been my summation of why younger people have, they have more reactive vessels, exactly right, less intracranial atherosclerotic disease that's going to sort of prevent or prohibit the actual spasming, the muscular spasming of the vessel. And as Rocco said, I mean, the smokers, you actually see catheter spasm. When we put our catheters into the internal carotid artery, the vessels are so reactive, the vessel will spasm down. And the spasm patient, the vessels are so spasmic, they're so reactive. When you advance a microcatheter in the vessel, that actually sometimes causes a pre-occlusive to a completely occluded vessel. Okay, so how about patients, basically sounds like low-grade subarachnoid hemorrhage, good clinical grade. How long do you monitor them in the ICU and hospital before discharge? We usually, I mean, we historically used to keep people in the hospital for 21 days, 21 days checking transcranial dopplers, many times keeping these patients in the intensive care unit. Then we just started, our big jump was, okay, well, they can go out to a step-down unit. Currently what we do now is if a patient's good grade and their transcranial dopplers are, do not show evidence of spasm, clinically they're doing well, we will discharge them post-hemorrhage day 10. We do not discharge them on Keppra, we do not discharge them on nemotipine and on post-hemorrhage day 10. If they're going to have a little bit more of an extended course, we will let them go out of the unit into our step-down unit or less intensive care and monitor transcranial dopplers and keep, so if they're healthy, doing well, post-hemorrhage day 10. Okay. Yeah, so somewhat similar for us, I mean, I think you have to look at what's the distribution of blood. In some of these patients, it's a very thin amount of blood and they're totally awake and alert, they have a good exam, which also means that there's a lot to lose in these patients too, so you want to make sure that they don't have any other problems, that they're not in serotal salt wasting, they're not febrile, some of these other issues. But with a good step-down unit, you can transfer these patients who don't have a ventriculostomy in place that you can then watch. You probably don't want to necessarily move these patients sooner than day five to seven. In fact, it's in that range of seven days that you're going to be most interested to see if they develop spasm. So I'm a little hesitant to discharge a patient, not a perimethocephalic hemorrhage, a very distinct type of subcategory, but in true aneurysmal serotonin. So some of the perimethocephalics are different. Those patients, we usually have a different protocol in terms of transferring them out of the unit. They typically are not as clinically sick, and most of those patients, most, do not develop the same kind of basal spasm, symptomatic basal spasm that we see. Okay. Somebody has a question about kind of what your thoughts are with a neurointerventional requesting a pre-procedural EVD to all patients who are coming in for ruptured aneurysm, like before they go and have their aneurysm coiled, I'm guessing is what they're getting at. I bet you that question is coming from a person where the radiologist is the one doing the treatment. Right. I was just going to say that. Yeah. Because I think that's, I would say, fire the neuroradiologist and hire a neurosurgeon to do the procedures. Here we go. Well, I mean, so basically, if you have somebody who's totally awake and alert, and has basically some mild hydrocephalus, but is in a situation where they have a normal exam, we rarely, almost, I hate to say never, but almost never put in a ventriculostomy in that patient. That's exactly right. And in terms of, I can see some of the logic, because if you put an EVD from the beginning, then if something happens during the procedure, for example, if you coil, and then there's some coil prolapse, and you need to put a rescue stent in, where then you have to put a person on aspirin and platelets, and then afterwards, the patient has problems, where then you need to put a ventriculostomy. But I do not think that's, if the patient, you follow an exam, a person is more important than the actual imaging. What I mean by that is, if the patient is completely awake and alert, has no deficits, if they have an altered mental status, meaning their HUN has grade three or higher, that's different. But if they're completely, if their mental status is completely intact, and there's no focal findings, I would not put an EVD in that person, trophallactic. Okay, that makes total sense. All right, how about patient who's hemodiluted in the setting of, we don't call it triple H therapy anymore, but triple H therapy, do you adjust your threshold for hemoglobin and hematocrit? Yeah, you got to be very conscious of, what was the patient's baseline hemoglobin? And if the patient's a smoker, and their hemoglobin is normally very, very high, let's say their hemoglobin is something like 15, for example, a smoker, and now their hemoglobin is like eight. Well, that's a huge change for that individual patient, and it's a different situation than if you have a young person whose hemoglobin is, let's say, around 11, 12, and it drops down to nine or 10. So you have to sort of individualize it based on, does the patient have a baseline history of elevated hemoglobin, and polycythemia, for example? Or does the patient, normal, general, healthy, has good cardiac reserve, doesn't have atherosclerotic disease as well? Because in the atherosclerotic patient population, those patients, they don't tolerate the lower hemoglobins. Older patients, they don't tolerate the lower hemoglobins. And a lot of the ICU team is like, oh, it's okay if their hemoglobin is eight. Well, if you're in your 70s, and you've got atherosclerotic disease, and your hemoglobin went from 12 to eight, that's a huge insult to the brain. So the older patients, we try to keep their hemoglobin closer to 10 or 11. Okay. Yeah. We do as well. We keep it around 10 or 11. And the concept is, you want to, obviously, your oxygen carrying capacities depend on the hemoglobin. So you don't want it too low. But you also don't want the blood too viscous, right? So I mean, that's where that hemodilutional concept came. But we keep it around 10 or 11 as well. Okay. How about, this is a good one, too. This is, we have nine more minutes left here. So I'll try to get through a few more of these. We still have lots of questions. Everybody really loves this content. So I'm happy about that. So can you guys tell us what kinds of sedation you prefer to use? And how long do you typically hold it before you have a good neuro exam? Yeah, be very careful with the use of propofol. You know, propofol infusion syndrome, it's real, it's a significant issue, especially younger patients. Propofol also tends to basically cause a drop in their blood pressure. A lot of other side effects you can lead to, you know, significant acidosis over time. So it depends what the patient responds best to. Some of the younger patients, it turns out that they do very well with Versed and fentanyl. And the Versed, the benzodiazepine seems to help this irritated brain, especially for those who may have some subclinical seizures. So patients with Versed and fentanyl. Other patients who are very agitated patients might do better with Presidex. So Presidex has gained a lot of attention in our units now and seems to be, you know, something that works well for some patients. I'm sorry, Rocco, I didn't mean to interrupt you. You just have to be careful that people, not that people don't know, but Presidex also has a fair bit of triglycerides. So you got to keep an eye on that, like the propofol, you got to keep an eye on the triglycerides with Presidex as well. And how, like, do you guys have, you know, nursing staff turn off, you know, sedation at a specific time before you come in and around, or do you do that? Depends on the sedative, right? Because for Presidex, you can turn it off within 10 to 15 minutes and then you should get an exam. You don't want to turn off. So the Versed or the fentanyl drips take, fentanyl's not so bad either, but the answer is we do. We do sedationalities every hour, obviously, if they're being sedated, we stop the sedation so the nurse can do a neuroassessment. And then roughly 20 minutes prior to rounding, they turn off the sedation. But you also have to be careful with these bold statements because you have to know why the patient's on sedation, why they're on Presidex, why they're on propofol, if indeed they're on, because if their person is in status, and the reason I say that is because this has happened. The patient's in status, they're in a propofol drip because of status, the nurse actually stopped the propofol so we do a neuroexam, but we said, so you've got to understand why the sedation's on, so rather than just make this bold statement of, oh, every 15, 20 minutes, et cetera. Yeah, and I would add to what Dr. Wiedemann just said, you get these groups of patients who have, you know, very fragile ICP. And so they're being sedated because their ICP is very tenuous. And so it's okay at times to forego the exam because you're controlling their ICP. So running quiet, running silent, and running deep is a true strategy, a tactic to be used to protect the brain. And if that's what the patient needs at that time, then it may be safer than all these frequent neuroexams. There's also another population of patients that I think might benefit from pausing exams, and that's a good-grade patient, someone who has good exams, but they're in the ICU for a week, and it's like Guantanamo. They're being interrogated every hour on the hour for seven days, and they're terribly sleep-deprived. So in those cases, we've started to try to do a little sleep protocol where they're allowed to basically be uninterrupted except for vital signs, you know, basic blood pressure and oxygen saturation from, let's say, 11 till 5 in the morning. So at least they're getting a block of sleep. Because when you look at patients in an ICU, they're massively sleep-deprived, and it's those better-grade patients that then become confused and agitated, and then you're not sure is this a behavioral change because of ACA spasm or is this just being in the ICU and not sleeping. Right, they're delirious just from being woken up constantly, yeah. We also have been more liberal with that as well, and not so much Q1-hour neuron checks. We do Q2 or doing these sort of neural holidays, we're allowing them to sleep. We're moving in that direction as well. The other thing that is important, and maybe in most of your ICUs, but make sure there's a window. There was one critical care setting where the patient's ICU psychosis or sundowning, gee, surprising enough, was more problematic in two ICU rooms where there are no windows. So we mandated that no neuropatient goes into those. No, any patient should go in, but keep that in mind. Okay, and then here's another one that's kind of a general question, but I think this is a good question for people. When is it best to ship patients to a place with a neurointensivist? Like when do you do that? When would you tell her to pull the trigger? I'm sure probably immediately, but depending on like your kind of patient. I mean, I think that you have to look at the entire picture, and what I mean by that is obviously it depends on why the neuropatient's being admitted. Obviously, if we're talking about what Dr. Amano and I were talking about in terms of subarachnoid hemorrhages or neuroICU, we have neurocritical care. So if the patient requires quaternary care, then I think a neuroICU is appropriate, or an ICU team that maybe not necessarily a dedicated, although I do believe in dedicated, we have dedicated neuroICUs, or at least a ICU where the team is comfortable and familiar with all the different, not just what's going on intraoperatively, but the preoperative setting and the postoperative setting. Dr. Amano made some really important points about EBDs. So EBDs and the pre-aneurysmal treatment, you don't want to drop it too much because you'll affect the transmural pressure induced for subruption. In the postoperative setting, you need to have protocolized ICP treatments, status treatments, subarachnoid hemorrhage treatments. So do they need to necessarily go to a dedicated neuroICU? I would say yes, but that's not really true. I mean, the team needs to be comfortable and confident with all the aspects of the disease process. Yeah. Yeah, I think it's a real issue these days because, you know, I like this, the more subarachnoids your hospital does, the better it gets at doing subarachnoid care in general, right? And the opposite is also true. The fewer subarachnoids your hospital does, the worse it gets. You could get to a potential place where you do way too many subarachnoids, you have way too many patients, and the staff is overwhelmed, under-resourced, and then patients don't get good care. But for the most part, if you look at low-volume hospitals versus high-volume hospitals for subarachnoid, you can see a difference in outcomes in those that treat more subarachnoids. And the number is around 35 that they report. So you know, in general, your patient will benefit if they're at a higher volume center. And the smaller places that are doing subarachnoid patients care, they're going to have more problems with, you know, missing the vasospasm patient who's symptomatic, missing the electrolyte abnormality patient, having the resources to do appropriate cardiac support for some of these sicker patients. They're not going to be able to take care of the sicker patients better. The problem is when a patient comes in the door or a good grade, you don't know if that patient's going to turn out to be one of the sicker patients or not. It can be very deceptive, you know, a younger patient that looks fine, but they go on to really crumple. So I think subarachnoid patients in general should be treated in a neuro-ICU. I don't think a general ICU is ideal. I think that's less than optimal. I think a multi-trauma ICU is, you know, probably not ideal either. I think in the ideal world, the subarachnoid patient should be in a neuro-ICU. Now that patient may not be in an ICU very long. As we've mentioned here, it might be a shorter period of time and they might basically have no additional requirements and then they can be, you know, triaged out. I think that sort of a second part of that point is, and I agree, I mean, in a perfect world, a neuro-ICU is ideal and even if there's not a physical neuro-ICU, a virtual neuro-ICU where there are certain part of the ICU is where there's neuro-nurses, they don't matriculate with the other nurses, the critical care team knows this is the neuro area. But the other part of that is, if you're accepting a certain type of pathology, you have to have all the armamentarium in that hospital to treat that pathology, whether it's tumors, whether it's trauma, whether it's aneurysmal treatments. For example, if the person, obviously you can treat the aneurysm, but you can't treat the spasm that occurs thereafter, the person, I don't think, and it's kind of what Dr. Martin was saying, even if it's a good grade, I don't think the patient should go there because the good grade patient can deteriorate very quickly and it's tough to anticipate. Well, thank you both so much. We are at the end of our session now. I really appreciate you guys handling all these questions and going through cases for us. This has been really great. It's our pleasure. Thank you. Thanks, Robin. Thank you, Rocco. Thank you both for joining us. Take care. Tell her I'll see her. I will. I will. All right. And thank you to our attendees. We really appreciate you guys sticking with us for the whole day and throughout the week this week. So I will see probably a good chunk of you tomorrow morning at the practical part of the conference. And I know that there have been some questions for AANS that are kind of going off over here on the chat. It looked like Shannon had gotten to most of those, but if not, you're welcome to email as well. I will see you guys tomorrow. Thank you. Thank you guys for coming to our course. Our pleasure.

Neurology

Neurointensive Care

Balloon Angioplasty

Fluid Management

Anti-epileptic Drugs

Prophylactic Treatment

Vessel's Appearance

Subarachnoid Hemorrhage

Sedation Preferences

Neuro Exams

Microdialysis