Thank you to all of you for those excellent presentations. For those of you in the audience, if you have any more questions, please feel free to write them in the questions box in your control panel. I would like to start by addressing just a couple of questions that were in the question box. Number one, when Dr. Al-Basiri was talking about brain death, there was a typo in one of the slides and said that the prerequisite was a temperature greater than 32 degrees. The guidelines are greater than 36 degrees, so normothermia or mild hypothermia is necessary in order to rule out any confounders that would mimic brain death in patients with hypothermia. There was another question about TCDs and whether they could be used to confirm brain death. Basically, all of the ancillary tests, none of the ancillary tests can be used in isolation to diagnose brain death, but they can be used to supplement the physical exam if there's parts of it that cannot be done or if the apnea test cannot be done. Now, TCDs can be done, that you can see high ICPs or lack of flow that might prompt somebody to have a consideration for brain death, but we do not use TCDs in order, we do not use them as an ancillary test in order to confirm brain death, just due to the variability on the tests. And if somebody has never had a TCD done before, you can't necessarily say if you aren't able to get flow that they had the flow before. I am going to go to the questions and see if there's anything else that is on there now. Can you all hear me okay? There was something that said you could not hear me. Okay. So, I would like to, I see Nicole that is on right now, I'd like to start by talking to her for a second. First of all, I just want to mention to all of you whether or not you're just taking this review course because you want to learn more about neurocritical care, or whether you are taking the boards, I want to stress that you should be aware of, say, common doses used in acute settings. There's a lot of doses of lots of medications that you don't necessarily have to memorize, but if there's something, say, for example, mannitol dose in acute herniation, or you have somebody in status epilepticus, knowing the doses for those, or IV alteplase in acute stroke. So, those kind of things, you should be aware of those doses, as well as some common interactions and adverse reactions in the medications that we used. Nicole's talk listed a lot of those common interactions, adverse reactions, dosages, and as a very excellent resource in order to use for those. So, Nicole, I just wanted to ask you a question. You did have a case in your talk, and it was discussing an agitated patient that had a history of atrial fibrillation and was on a PIXIVAN, and that patient then needed an anti-epileptic drug. So, there were three different choices that were there, and if you could kind of walk us through what the considerations are and what you might consider as the answer for that question. Yeah. Thanks. So, you really could make the argument to use any of the three medications I had listed. Obviously, there's a lot more than just the three I had listed, but thinking about, like, the ESSA trial and what the most common ASMs are, those are our big three, right? So, the first one that we're going to avoid is going to be phenytoin. Just because that patient's on a stable dose of a PIXIVAN, phenytoin will induce a PIXIVAN and make it less effective, thereby increasing the patient's risk of having a stroke. So, if you really wanted to use phenytoin or phosphenytoin, you would have to consider switching over to warfarin, because even with the warfarin, like, you do have to monitor INR, and there is a drug interaction still, but you can monitor both the INR and the phenytoin levels. So, it is doable, but unfortunately, you can't combine it with a PIXIVAN. The patient is agitated. So, being in an ICU, you know, we all know that there's a million reasons why our patients get agitated. It's probably never due to just one thing, right? So, with the patient already being agitated, levotracetam is not contraindicated by any means, but you do need to consider the risk that patients could become more agitated because of the levotracetam. So, we see this a lot, especially when we're using levotracetam as seizure prophylaxis. So, we always are asking ourselves the question, is it the levotracetam? Is it the room they're in? Is it just their disease stay or their disease progression? You know, it's a million things. So, while not contraindicated, that is something to consider because sometimes it can make, especially elderly patients, very agitated. But one other key thing I want to drive home is the most common adverse effect from levotracetam is actually sedation, not agitation. So, just something to consider so you could use levotracetam in that patient. I think the best option for this patient would actually be valproic acid. So, the valproic acid could be helpful for his agitation and helping to calm him down. Right now, he does have an infection being treated with cefepime. So, the one thing you want to think about is if this enterobacteriaceae does become more resistant, the next step will be a carpepenem, which at that point, you will have to switch his ASM as he's having active seizures to something different. So, it's kind of, are you going to, you know, think about if he could get resistance and avoid the valproic acid, or are we going to bank on he's not going to become resistant, let's just do the valproic acid, and then we'll address it later if we have to. Great. Thank you. There is a question that I will just ask all of you as well that is asking about chemical DVT prophylaxis in potentially seizing patients. I'm not sure if that question relates to interactions or risks of bleeding, but I personally use chemical DVT prophylaxis in patients who may or may not be seizing or who are at risk for seizing. Any thoughts on that? Anything different, Nicole? No. For our most common agents, we'll be using either inoxaparin or heparin. So, there's no ASM drug interactions that we're that concerned about. The only thing that I would think an interaction could play a part is if you're using a pixaban for your chemical prophylaxis, which is not, from what I've heard, not really common in ICUs at this point in time, but no other contraindication that I can come up with as it relates to bleeding and seizures. Great. Thank you. Dr. Sanussi, there are some excellent questions from our neurosurgical specialty here. I'm going to ask you one question that I have, and then we're going to go to some questions that are in the box right now. You had discussed the DECRA and the RESQ-ICP trial in TBI. We do have some trials as well in decompressive hemicranes in malignant strokes, Hamlet, Destiny, Decimal. My question to you is if you could kind of summarize the results of those studies, and more specifically, if a family member, we're trying to get consent for these procedures, what would we say would be the overall summary of those trials? Can you guys hear me okay? Yes. Okay. I think the bottom line is that when we're talking to families, like highlighting the fact that decompressive cranial improves survival, but not necessarily functional outcome. That's basically the take-home point from it. It becomes even more difficult for, and I've found that families of patients with left-sided severe stroke have a more difficult time dealing with that, because it's important to kind of impress upon them, particularly for a right-handed individual, like this is going to impact their life, language, whether that's global aphasia, whether that's isolated receptive aphasia. So patients after left-sided MCA imparts tend to have a more difficult time, but ultimately the summary from all of those trials is that it helps with survival, but not necessarily functional outcome. Great. Thank you very much. Okay. I'm going to ask you about a couple of questions that are in the box right now. And one of them is, it's an interesting question. The specific question says, what are the pitfalls of using MMA embolization for chronic subdural? In addition to the pitfalls, I will also ask you the benefits. And from what I have seen, it's being used a lot more in the last, say, 12 months than it really had in the past. Yeah. So that's absolutely, that's a good observation. And I think, so when MMA embolization kind of took off, if you will, I would say that's probably maybe about two, three years ago was when it initially took off. And after that, there were a lot of case reports, individual cases, and people that looked at using MMA embolization as a sole treatment for treating chronic subdural hematomas versus as an adjunct, whether that's pre-surgical evaluation or after surgical evaluation. Basically, the idea with chronic subdural hematomas is that patients have septations in the subdural hematoma, and then there's basically increased risk of bleeding from those septations over time, right? Because we all see the patients who they get their hematoma evacuated, whether you do burrow holes, you do a cookie-cutter crani, or a large crani, they do fine, and then two weeks, you know, four weeks later, there's still evidence of recurrence of their subdural, particularly if the brain doesn't re-expand. So essentially, there's randomized trials right now, and actually we have one at our institution that's looking at MMA embolization as an adjunct, so patients would get randomized into surgery alone versus surgery with MMA embolization. Anecdotally, what I have noticed, though, is it does help those patients who do get the MMA embolization have a decreased likelihood of having recurrence of their chronic subdural hematoma. Interesting. At the bedside, I've seen that as well, but it will be nice to have the data to support that. Okay, I'm going to ask you about, let's talk about AVM management. Could you expand on that a little bit? I know we could spend a whole hour talking about AVM management, but just in summary, different variations, you could say there's embolization versus surgery versus radiation, and when would you choose which treatment? Oh my goodness. There's so many things that go into deciding what to do for an AVM. So basically, the first step is, how are they presented? Are they presented incidentally, or are they presented because they had a hemorrhage from the AVM? And then the location of the AVM also matters. But in general, maybe I'll use an example of, say, a patient that presents with seizures, like a small hemorrhage from an AVM. The first question is, what's the size of the AVM? So one of the things that we do as neurosurgeons is we grade the AVM based on Spencer-Martin grade, which has to do with the size of the AVM, whether or not there's superficial venous drainage or not, and then whether or not it's an eloquent cortex. For small symptomatic AVMs, where there's ease of accessibility to basically the arterial supply of it, the ideal scenario in that situation would be embolization for cure. Although for the most part, it's very rare that you find the perfect AVM that's the perfect size that embolization alone can carry. So most of the time, what we end up doing in those situations is we embolize to decrease the risk of bleeding intraoperatively, and then still take the patient to surgery after. Versus if you had a patient who, say, shows up with an incidental AVM that has concerning features, even size-wise, then in that situation, you can plan for, say, it's a small AVM, partially eloquent cortex, depending on how you define eloquence, and you can do radiation as well. And then there's been so many things that have been looked at into embolization plus radiation. And years ago, we used to think that embolization decreases the efficacy of radiation in these AVMs. But then more recently, people have looked at gametite and have essentially said that in some situations, you can do embolization for radiation. But it's important that when you do radiation, you have to remember that it's a delete effect. So yes, it's a good 70%, but that's over five years in terms of obliterating that AVM. So there's a lot that goes into it. You also have to look at, is there a prenatal aneurysm if a patient comes in with a rupture? And then sometimes you can treat the aneurysm alone without treating the AVM and addressing that later. So there's a lot that goes into it. So a lot of the patients that we see in the neuro ICU that already have a hemorrhage might not be a candidate for radiation at that time. Because over those next five years, they're at a higher risk for re-bleed, basically, while that AVM is being obliterated by that radiation. Correct. But then there are some situations, the only caveat to that is if the bleed was caused by prenatal aneurysm to the AVM, you could treat the aneurysm by coiling it and say the AVM is not in a surgically easily accessible region. Then once you treat the, you know, the reason for the bleed, then you could potentially deal with the AVM down the road, whether that's with radiation, obviously talking about the risks that's associated with that with the patient and the family. Great. Thank you. I'm going to ask you another question that's in the box. It says, do you use half normal saline to re-expand the brain after a subdural? I'm assuming that's after a subdural evacuation. Yeah, we don't. I mean, as neurosurgeons, we shy away from icosmolar solutions. I'm sure many of you with your interactions with, you know, neurosurgeons and versus, you know, like neuropolitical care folks and things like that. So the answer is no. It's very rare where we would be comfortable with that. Typically, in terms of helping with brain re-expansion, like we would just give normal saline, but just more aggressive uvulemic goal, right? Versus typically in these patients when they come in with concerns for brain shift and things like that, we're more likely to be judicial in the fluid management. Great. And one last question for you is, what are your thoughts on the efficacy of subdural treatment with SEP strain versus EVD catheter uses a subdural drain versus an EVD catheter with active irrigation? Yeah, so I posted a response to this. Hopefully it was helpful. But essentially, you know, SEPs, there's been studies, mostly case reports and maybe some case studies that look at it. One advantage to it, though, is the fact that you can do it bedside. So you don't necessarily have to do it in the OR. So, like, if you're in a situation where you don't have OR time or whatever, it's on the weekend, you can easily do that bedside. But then you think about the risk of infection, right? As well, too, which also goes to the question about the, I think, irrigating through the EVD catheter. That would make me nervous. And I think that would make most of us nervous just in terms of risk of infection, right? Because you don't want to replace one problem with another. In terms of the type of subdural drain catheter that's used, there's really no study that's compared them that's compared with it. You know, as neurosurgeons, when we evacuate the subdural, do you put an EVD catheter as the subdural drain? Some neurosurgeons use red rubber catheters. Personally, I use a JP drain with active drainage. But there's no studies that directly compare them. I think it's really just surgeon preference. But active drainage is better than passive drainage for subdural anatomists. Great. Thank you very much. We are out of time. And again, I thank you all for your excellent talks and for the audience participation. And I would like to ask you to be sure to complete the evaluation for today's session. And this concludes today's session. Thank you very much.

neurological topics

brain death diagnosis

seizures

AVM management

subdural hematomas