to address one question that just popped up in the question box before we get started. I'm gonna ask all of the other panelists to go ahead and turn on your cameras. And I am going to address the last question with Dr. Swar if you are on. I wanna clarify one other question that was the first one when we're talking about the TTM and there was a question about contraindications to TTM. And that was specifically septic shock, pregnancy or overdose if there are contraindications. And the response back was that there's no contraindications but it might change the temperature you choose. I was wondering if you could expand on that just a little bit. Sure, so I guess my thought in answering that question was if there's a concern for hemorrhagic shock or DIC as a part of the shock picture, then cooling to 33 or 32 would probably be contraindicated. Okay, great. And then the last one that just came through is when they were talking about the neurological exam and the question was about the target temperature. And it was specifically that they use a group of 36 degrees or normal thermia. Do you have any recommendations on the target temperature for that neurological exam for the prognosis? Oh, I took that question to mean for the actual board exam. So I started answering it like that. I think for the exam, they'll probably want you to know the guideline temperature targets of either 33, 36. Or when it comes to cooling, and then to throw you off, they might ask you like, there'll be an option for like 32 or 31 or 30. So I think just knowing what the guidelines recommend, what those numbers are probably sufficient for the exam. Yes, exactly. If there's anything that's just a little undecided at this point or a little controversial or people use different terms, at this point or a little controversial or people use different varying temperatures, that's not going to be a question on the board exam. If it's a general question on what do you use, then that's a good discussion for this as well, just because there are people here that aren't taking the board exam. But specifically for the board exam, you're not gonna get any of those controversial answers. Okay, I am gonna see if there's any more questions on here. And then I have a few questions to ask the panelists. There is one more about the TTM based on the TTM-2 and asking if our centers, a lot of our centers have moved to the 37.5 for post-cardiac arrest patients. And I will let really anybody speak to that. I will say we are going more normalthermia after cardiac arrest. But Dr. Musavi, what are you guys using there? We do normalthermia as well. Great. We're different in that case, then we are still thinking it's cool to be cool. The reason why we're thinking that fever in our minds is a surrogate marker of a lot of other things that we cannot measure as part of that secondary neurological injury that we're trying to protect our patients from. And then not all TTM is created the same. There's high fidelity TTM and there's low fidelity TTM. And what do I mean by that? Fabio Tassioni wrote a good paper describing this concept of using continuous temperature monitoring, using specific protocols for achieving those anti-shivering protocols. So that attention to detail, not letting your patient become febrile and whatever you need to do to look for the underlying cause. We did not want to move away from that practice. That was one piece. And our interpretation of literature was for in-hospital cardiac arrest, except Hyperion in the recent trials that are looking at these temperature targets, both TTM1 and TTM2 are very much focused on out-of-hospital cardiac arrest for in-hospital cardiac arrest patients. We know that the overall outcomes for these patients tend to be poorer as compared to our outside hospital cardiac arrest patients. And what's amazing is in TTM2, almost 80% of their patients had bystander CPR. How many of our patients actually get bystander CPR when they're coming for out-of-hospital cardiac arrest? So with all of that in mind and the variabilities and the difficulty in extrapolating information from a care setting and health systems, which are very different as compared to our health systems, is it then okay for us to move away from 33 or 36? More than anything else, irrespective of what the target temperature is, whether it's normothermia 33, 36, whatever we choose, re-evaluating why we have chosen that, what are we doing to translate that practice at the bedside so that we know that our nurses, our frontline team members can implement the consensus decision in a high fidelity manner? So that's one of the reasons why we have still chosen to continue with 33. And of course, for the in-hospital cardiac arrest patients and the cohort study from UPMC, from Clifton Calloway that looks at our anticipated burden of injury. They published this in JAMA looking at the anticipated burden of injury. If you anticipate that somebody is going to have mild HIB-E, hypoxic ischemic brain injury, or HIE, hypoxic ischemic encephalopathy, perhaps those patients who are not as sick and in whom you anticipate that they're going to have mild HIB-E, perhaps choosing a target such as 36 or even normothermia may be beneficial, as opposed to those patients in whom we anticipate are going to have moderate to severe HIB-E or who are sicker, they probably will benefit from lower target temperatures. So just something for us to consider, not all TTM is created the same, not everything that we study in trials can be extrapolated to our practice. And it takes a really long time for us to change practice and translate what a trial has shown to the bedside. So just from a pragmatic perspective, that's how we came up with, we're still cooling down to 33 versus 36, and we'll rearrange the, we'll shift the target based upon whether a patient is able to tolerate that particular target that we chose or not, say very, very hard to control shivering or their shock is worsening and you're adding your third inotrope or pressor, they're going on mechanical circulatory support, whatever the situation, just reevaluating that target then. Wonderful, TTM is a very, I guess, highly debated subject at this point, and it's a very interesting topic and we could spend a lot of time on it because we all really love that topic. Again, I will remind everybody who's taking the boards that it will be based on the guidelines, not from current kind of discussions that are going on related to the latest information and discussions going on. This is, that was great. I am gonna kind of go back to the beginning from about three hours ago or so when we first started talking about ICP management and the cerebral hemodynamic monitoring. I'm gonna ask a couple of questions and I'm gonna start just with Dr. Musavi just because she started from the beginning and just to kind of clarify a couple of things and one is that as a neurointensivist, I get a lot of questions on the best hyperosmolar therapy to use in the management of ICP. And it's another discussion on hypertonic versus mannitol. And I wanted to ask you, is there any benefit to using one over the other? And is there something, say on the boards, they would say, absolutely, you must always use mannitol or always use hypertonic. So the data is, it shows that people have better outcomes with hypertonic and that people, there was a higher mortality with mannitol and it caused increased kidney injury. But it's always different with data and exactly what we're talking about in practice is if you have a patient, a lot of times the patient comes in the trauma bay, you have evidence of herniation and you don't have a central line. And so a lot of times in my own practice, I'll use mannitol first to try to treat the increased ICP until we're able to get central access. You can use 3% peripherally, it's safe to use peripherally. However, it's not, in my opinion, it's not as effective in terms of if they use it continuously. So they did some studies and looked at that bolus dosing was probably better, but it's whatever we have access to at the time. But what I have heard from the data and they did a meta-analysis is that there was a higher mortality with mannitol and higher side effects. Great, and as far as the treatment of ICP, if you were to use either one, is there one more beneficial for the treatment of ICP over the other? You know what, I'm not exactly sure to be honest with you. In my opinion, I thought it was hypertonic from the data. I don't know if anybody else has an opinion on that. I thought that the ICP, they had better management with hypertonic. Just make a quick comment here about hypertonics. The 2018 Neurocritical Society Guidelines on hypertonics and different percentages and of sodium chloride as well as mannitol. They do a nice job of summarizing and what you do notice, just like Dr. Musavi was saying, literature is not super, super high quality. There are very few RCTs, which is completely fine because from a practical implementation perspective, you could go with either, whichever one is available. But what the guidelines do mention, yes, hypertonic saline in patients with different kinds of severe acute brain injuries is going to potentially give you faster decrease in ICP and perhaps a more sustained response in that decrease in ICP. And you may be able to get by without getting some of those adverse effects that you may end up seeing with mannitol, including sometimes a rebound. But can you alternate these two, mannitol versus hypertonic? Of course, guided by your BMP, your osmolarity, et cetera. So of course, choose what you have available, the faster, the better, but hypertonic saline in different solutions. The 2018 guidelines did a nice job and they have some nice accompanying infographics with the guideline too. I wanted to add one more thing. So we have a lot of patients, especially in TBI that have really refractory ICPs. And so in my practice is once your sodium's goal is where you want it to be, you kind of have to start using mannitol. So we kind of do both. So again, it depends on the patient. Yes, perfect. Those were excellent discussions on those as well. So hypertonic would be preferred, although either one of them will lower the ICPs. You need to understand the risks of using either one. When you're looking at it clinically at the bedside, a lot of people do a lot of different things. Sometimes it's continuous, sometimes it's bolus, sometimes they schedule hypertonic or mannitol. Those kinds of things are just kind of style that you manage at the bedside. We don't have a lot of data to suggest any of those are better than the others. And so those won't be the typical questions you'll see on the boards if you're doing it strictly for the boards, okay? I just want to make a comment. So when it comes to the hyperosmolar therapy, one thing has been consistent. For the boards, we don't increase the sodium for the osmolarity prophylactically. So if that's a choice, that's not the answer. Yes. So I would like to move on to Dr. Sarwal and ask a question about the CPP thresholds. And you had mentioned CPP thresholds based on whether or not auto-regulation is intact. And you had mentioned that if it's intact, you can press a CPP goal at a 70 to 90, and otherwise you just want to prevent a low CPP of less than 50. And you mentioned the PRX, which is the pressure reactivity index, so that you can use that to determine whether or not auto-regulation was intact. And I was wondering if you could just describe a little bit at the bedside on how you would evaluate that PRX to determine the auto-regulation. Dr. Sarwal may be having some difficulty. Would anyone else would like to have this, to take this question? So basically what we're looking at with the pressure reactivity index is that as the pressure goes up, do the ICPs go up? So the loss of auto-regulation is when the pressure rises and the ICPs rise as well. Whereas if you had an intact auto-regulation as the map went up, the ICP should stay relatively the same. So if you are at the bedside and you have the patient on a presser and you increase the map and you see the ICPs have a relative rise that goes up with the map, then that is the indication that the auto-regulation is not intact in that patient. And so that's what she was referring to as the pressure reactivity index. Another question for Dr. Noblesa. I wanted to talk about the kind of the treatment algorithm for the neuromuscular conditions you talked about. You talked about some neuromuscular conditions that have these classic findings on examination. And you look at those and you say, oh yes, this is GBS, this is myasthenia. And so the question kind of based on standard of care as well as the boards is when you see a patient with these classic findings, do you treat or do you get the lab studies in order to verify the diagnosis and then treat? So we don't wait for the labs because that will take time. And we follow, just like what I mentioned, we always go back to our ABCs. And if the patient is deteriorating from an airway standpoint, regardless of the lab, actually regardless of what diagnosis we're thinking of, we have to protect ABCs first. And then if we're leaning on a neuromuscular condition, it can take a while for the labs to come back. So based on the clinical presentation and what our highest differential diagnosis is, we can proceed to treat. Great, thank you. Dr. Chirula, I'm gonna ask you a question. I'm gonna take this off of the question list though. What they're asking is the upper goals for hypertensive brain bleeds. That can actually be another discussion in itself on what we use for the top. Basically, the question would be, which agent should we use? And is there a preference or basically guidelines that would direct which agent we would use for hypertensive bleeds? And you can venture the top systolic blood pressure goal for the brain bleeds if you'd like to talk about that as well. Nihat, did you wanna talk about that? That was, I think, on your section. Sure, happy to. So the ICH guidelines that were just released a couple of months ago. Again, I happen to be a fan of guidelines, so I'll say, yes, overall, they did a good job. They chose a target that most of us were not using before, 130 to 150 for spontaneous ICHs. However, the guidelines do acknowledge, and this was based off of ATAC2, mostly ATAC2 and Interact2, as well as some secondary analyses that were published from both of these trials. The goal is, of course, you don't want hematoma expansion. At the same time, you don't want to cause perihematomal ischemia. So how do you cut the difference and at the same time translate that evidence for the bedside nurse? Of course, one question that comes to mind, so if it's 130 to 150, does it mean that if a patient's blood pressure goal is less than 130, do I start a presser? Simple answer is no, you're not going to be starting a presser. But maintaining 130 to 150 to ensure that your patient's getting adequate perfusion, no perihematomal ischemia and no hematoma expansion. However, the guidelines acknowledge that based on current data, for patients who have a large low-bar ICH, lowering their blood pressure rapidly to this particular goal, is that safe or not? There are cohort studies, as well as MRI-based analysis of the patients who were included in ATAC2 that show increase in diffusion restricted. You end up seeing some infarcts in areas that are also away from your hematoma. So these are obviously patients who come in very, if they're coming in at very high blood pressures, they have a large low-bar ICH, then you have two competing priorities. Of course, these are also patients who are used to living at higher blood pressure. So if you rapidly lower their blood pressure, other areas of the brain will also potentially become vulnerable. However, the CPP where MAP is equal to, where CPP is equal to MAP minus ICP, you're not always going to have an intracranial pressure monitor in place for you to guide what your CPP target should be. So you don't want to go too low in these patients. Is it okay to then target less than 160 in those kinds of patients? It may be okay, but that's an area that the guidelines acknowledge. We don't know enough, but the current recommendation is for this 130 to 150. But again, very controversial topic that we can talk a lot about. Great, thank you. Okay, Dr. Tirula, you had mentioned that there are some neurological conditions that cause sinus bradycardia. And so my question is how long do they typically last in these acute neurological conditions? And when would you pull the trigger on a pacemaker? Typically, they would last for a variety of these conditions in the days regions. Occasionally, they can go into the weeks, and I've certainly had people who had bradycardic issues up until like day 12, 14, that type of thing. So it's usually not until after that time do I consider the use of a more permanent pacemaker. So I try not to jump ahead of myself in those cases. I have one more question for you. One more question for you as well is that you discussed the sympathetic activation in the microvascular spasm in stress-induced cardiomyopathy and the EKG, which looks very similar to an MI, and the troponins are elevated in those patients as well. So do you treat them similarly, such as do those patients need an aspirin if they don't have contraindications? The question is do they need an aspirin. I think if they don't have a contraindication, the aspirin use, at least in the short-term period, could be argued for. Now, there was a recent meta-analysis that was published last year, actually, showing that at least the long-term use of aspirin may be actually detrimental depending on which patient population. And in the short-term, it didn't demonstrate any change in the outcome, really. So I think a lot of people will choose to use an antithrombotic in these patients. The actual evidence doesn't suggest that it's useful. Again, as with most of neurocritical care, look at your individual patient. Great, I wanna go back to Dr. Musavi and ask one question before we're gonna be heading out. I know we're right at the end of time, but I want to reiterate that the board exam is largely based on clinical scenarios. And just like all board exams, if this, then this. Here's this patient scenario. Now, what do you do? And I would like to direct to all of the flow charts that you see on the presentations throughout this course. But Dr. Musavi had an excellent flow sheet where she talked about the treatment flow diagram for somebody who had presumed herniation. And so could you just summarize that flow sheet? You have somebody that you're at the bedside and say they blow a pupil and they have presumed herniation. What would be the, if this, then this, this, this, that somebody would wanna take away home? So a lot of, it's the same thing with resources. So a lot of times, if your hospital has resources, the first thing, if there's a neurological change in the exam, we do a stat CT head if we're able to. There are some, when I was in fellowship, we had the CT scan right down the hall and was able to look, get one easily. And sometimes it's not possible. So if we have a blown pupil, you think that they have an increase in their ICP, they're herniating and you can't get a CT head to confirm at that time. I usually treat, if they have a central line, we'll give the 23%. If they don't, we can try mannitol. But usually, we'd go to CT as quickly as we can, see what the cause of that herniation is. A lot of times a patient will bleed. I've had a patient who had a brainstem bleed and started to herniate and blew a pupil. And then we started to be more aggressive in terms of medical management, or we had a patient that had a subdural, and then we called neurosurgery for an evacuation immediately. So I think it depends on why the ICP went up and if we can get imaging. And if you can't, unfortunately, you wanna try to prevent them from herniating. So usually I will, if I have to, I'll treat. Yeah. So treating what you see on the clinical exam finding, treat first, and many times diagnosis is secondary to that, absolutely. Yeah, because sometimes there's a surgical intervention. We had a patient that he had a huge subdural and blew a pupil and then immediately went to the OR. So if those are possible, and some hospitals are not, but if you are not able to get imaging, I would just treat. Okay. I don't see any more questions in the question box, and I'm gonna ask the panelists if there is anything else they would like to add. Good luck on the boards. Everybody's gonna do really well. These are going to, the boards are written well. They're very clinically relevant questions. These are scenarios that you have seen. There's going to be a lot of fundamental critical care for patients with different kinds of acute brain injuries, spinal cord injuries, neuromuscular problems. You'll see a combination of all of those. You'll see a combination of those kinds of questions. So as long as you stick to the basics, they're not going to ask controversial things on the board. So I think everybody, particularly if you're taking this course, you're absolutely going to do well. So good luck on the boards. Yeah, I took it last year and I felt the questions were very fair. And I took this course as well last year, and I felt that all of the topics were covered. So I felt like the, I took the ABPN and I felt like the questions were very clear. Wonderful. Well, thank you all so much for taking this week's session and please be sure to complete the evaluations for today's sessions. And again, I want to thank all of our speakers and this concludes the session. Thank you.

neurocritical care

targeted temperature management

contraindications

hypertonic saline

mannitol

autoregulation