Good afternoon, and thank you so much for this opportunity. And there have been some fantastic talks all day long, so let's keep moving right along. I do have a few disclosures, none of them relate directly to the content I'm going to present today. I did serve as a writing group member for the Subarachnoid Hemorrhage Guidelines for the American Heart Association, so I'll show you some of that. So there's going to be a lot of exciting things I want to share with you, because in the last few years, neurocritical care has accelerated at the pace of perhaps one of the fastest growing subspecialties in medicine. So I'm going to show you a lot of literature, but before we look at that literature, I'll try to do a quick recap of some of those core concepts that you already know. So we have a lot of ground to cover, so let's dive right in. So first, a key principle of how we deliver neurocritical care. Very often, as intensivists, we're meeting these patients when that primary neurological injury has already occurred. Whether it's that acute ischemic stroke, intracerebral hemorrhage, traumatic brain injury. And what we do in our ICUs is monitor our patients for development of that secondary neurological injury, whether it's cerebral edema, ventriculitis, status epilepticus, and systemic injuries, whether DVTs, PEs, pneumonias, all of those different things. The very purpose of our monitoring is rapidly recognizing, treating that primary neurological injury, preventing secondary neurological injury, preventing systemic injuries, treating them rapidly. And that's what's going to help us overall prognosticate what is going to happen to our patients, prepare them for that new state of normal. It's imperative that we uphold the principles of providing patient and family-centered care. And I do want to emphasize that although we use a lot of different monitoring strategies in our ICUs, it's not monitoring that saves lives. It's what we as multidisciplinary teams do that saves lives. And delivery of patient and family-centered care needs to be intentional right from triage to recovery well before the patients hit our ICUs and beyond. So we've got to remember, ICUs can be very dehumanizing. We've got to remember the person behind the patient. So with that, let's do a quick recap of neuromonitoring. As intensivists, we use a lot of different strategies to monitor the body. Similarly, when we want to monitor the brain, there are lots of different strategies we can use to monitor the brain, whether it's intracranial pressure, whether it's brain tissue oximetry, brain temperature, microdialysis, cerebral metabolism, electrophysiology. But integrating all of that data, body and brain together, visualizing that to both diagnose problems, treat them, and look at the impact of our treatments is how we can really leverage the power of neuromonitoring. This concept described over 200 years ago still holds true, and you're all familiar with the Kelly-Monroe Doctrine, essentially means that brain, blood, CSF are all sitting in a tight skull. And if something increases, something else has got to give way, right? So in a compensated state, your patient is not going to demonstrate signs and symptoms of raised intracranial pressure. The brain is able to accommodate some of those increases by either increasing the resorption of CSF or by increasing venous return. But when the brain's compensatory mechanisms are overcome, your patients are going to demonstrate signs and symptoms of clinical herniation. The most important principle as we're managing these patients with raised intracranial pressure cerebral edema is, how do we maintain perfusion? We know pressure is not equal to perfusion for the rest of the body. The same holds true for the brain. CPP is equal to MAP, mean arterial pressure, minus intracranial pressure. And no matter what kind of ladder you use for treating patients with ICP crisis, the goal is, of course, we're going to try to lower that intracranial pressure by way of osmotic diuresis. You're going to provide some supportive treatment, but you've got to take care of that definitive management. What is it? What is source control going to look like? The same thing that we do for patients with shock from any etiology. What is the source control going to look like? Two other concepts, intracranial compliance, delta P upon delta P. How much is your pressure going to change for that change in intracranial volume over time? And then we've all seen these Z-shaped curves. We know the brain is able to autoregulate and accommodate for changes in our mean arterial pressure. But in a disrupted autoregulatory state, as your blood pressure goes up or down, intracranial pressure is also going to go up or down. ICP ladders, here's just one example. I'm sure you all have different examples at your institutions. But at every step of the ladder, of course, ABC is always going to come first. Whether you're thinking about sedation, analgesia, how you secure their airway, or osmotic therapies, you're reaching out to your neurosurgical colleagues and friends and asking them, is there anything that you can decompress? And when do you decompress? You need to come up with those triggers in a multidisciplinary fashion. I wanted to highlight this because as intensivists, we must know how to read our own images. And making sure, because you have the luxury of having the patient in front of you correlating what you see on that image, is there an imaging and clinical exam disconnect or not? And do I need additional imaging to figure out whether there is that kind of disconnect? For example, your patient who's in a coma with a normal CT head, do they have a basilar clot? I'm just showing you from left to right different signs. In a patient with traumatic brain injury, you're seeing a large acute subdural hematoma, big midline shift. Here's a patient who could very well be a fulminant hepatic failure patient who initially came in with a normal head CT and then develops global cerebral edema. Here's an aneurysmal subarycnoid hemorrhage hydrocephalus. Here's a traumatic brain injury patient with right frontal contusion. So just thinking about how you review your own images, compare your read, your assessment with your radiologist's read, because you have the luxury of seeing the patient in front of you. And whether you need vessel imaging or not, before you stick that critically ill patient in the scanner, make that decision before you send them down with your nursing team and with your respiratory therapist. So where are we now when it comes to multimodal monitoring? So in 2014, the Neurocritical Care Society published this guideline statement synthesizing literature from 1980 up to 2013. When we think multimodal monitoring, we're thinking about ICP, brain tissue oximetry, brain temperature, microdialysis, EEG, all of those different things. I'm just showing you a little, it's a synopsis to highlight that the level of evidence for a lot of these different modalities continues to remain low to moderate. And when you look at the class of recommendation, the class of recommendation does not need to be concordant with your level of evidence. If something makes sense, but you don't have data for it, a lot of guideline statements will give you a higher class of recommendation. But the most important thing for this was mostly, all of this was based on observational studies, small studies. Most of our understanding about multimodal monitoring comes from traumatic brain injury patients. And then some studies come from subaryknoid hemorrhage patients, very few from acute ischemic stroke patients. So then where are we now? So these authors looked at papers that were published after the publication of that guideline statement. So from 2015 to 2022, a little over 100 studies were published. But again, the same kind of trend. Most of these studies are in TBI patients, some studies in subaryknoid hemorrhage patients. Very few studies actually reported that interventions based upon the results of this multimodal monitoring changed outcomes. Very few studies reported that. And on the right-hand side, you can see a lot of those different modalities, including surface EEG and depth EEG and ECOG strips. So there's a lot of different modalities. One of the biggest challenges, we've heard so much about systems of care, right? Multimodal monitoring has remained limited to very, very few academic centers, because it's very hard to implement, very hard to keep up with your competencies. So how do we democratize some of that is a challenge before us. We heard a lot about invasive ICP monitoring versus non-invasive ICP monitoring, right from our TBI talk to our fulminant hepatic failure talk, pupillometry. So there are lots of different non-invasive strategies. You should be aware of pupillometry. Pupillometry is an objective assessment, looking at the pupils with a device, handheld device like this, called a pupillometer, gives you a lot of different parameters in addition to the size of your pupil, how quickly the pupil is constricting. And there's lots of papers that have looked at the association of changes when you give patients hyperosmotic therapies, the diagnostic yield of using pupillometry. What I want you to recollect or remember, this Neurological Pupillary Index is a proprietary index, so we don't know what all goes into the NPI, but there are enough papers in different kinds of brain injuries that say the cutoff of three correlates with an ICP of 20 or higher. So if somebody has an NPI of three or less, the higher the likelihood that they're going to have a high ICP and a poor outcome. I'm going to show you the largest observational cohort study, including 4,000 patients or so from North America and Europe, called the ORANGE trial. And this trial looks at pupillometry data and correlates this with outcomes. So patients who had an NPI of less than three, higher the likelihood of having a worse outcome. And most of the distribution, when you look at it, it's serial measurements every four hours for a week of a patient's admission after any kind of severe acute brain injury. That's what was included in this trial protocol. Optic nerve sheet diameter, we heard a little bit about this. This is also very promising. So one caveat here is just learning how to do it does not take a lot if you know how to use your point of care ultrasound. But getting an average of two to three readings, a single value is not as important as trends. And this is true about everything in critical care, right? A single value is not as important as trends. So make sure you get a single value, and then you keep trending it, and you come up with whether you're going to do it Q4, Q6 hours, depending upon the underlying brain injury. Manitol versus hypertonic saline, not a lot of new data here, but I do want to highlight the Neurocritical Care Society 2020 Guideline Statement. And for all practical purposes, if you used hypertonic saline for different kinds of severe acute brain injuries, preferentially over manitol, you should be OK. However, it's more important to use what you have at the right dose at the right time rather than waiting for hypertonic saline if manitol is all that's available on your unit. Osmotherapy typical doses, not a lot has changed here either, but just remember that no matter what you choose, choose the right dose. And these are equi-osmolar doses for different kinds of concentrations. This is available in the book chapter as well. Adverse effects both with hypertonic solutions, no matter what the concentration, as well as manitol. Of course, it's going to impact your volume status. Of course, it's going to impact your kidneys. And you've got to know whether your patient has underlying cardiopulmonary problems already, any kind of heart failure. Are they in worsening shock? Choosing what therapies to use, and these are all going to be used as a bridge to something definitive. So is the patient going to need a decompression? Do they need an EBD? And then there is a cohort of patients who will just need max medical therapy. So as you're choosing between these different osmotherapies, and you're continuing to give this repeatedly, make sure that you at least get your BMP, your Osm's Q6 hours so you can at least monitor for adverse effects from these different therapies. So from monitoring to hypertonics to acute ischemic stroke now. And we saw in Dr. Murli's slide that patient had a massive midline shift and an evolving subacute right MCA territory stroke. This is what a hyperdense MCA sign would look like. This is not a CT with contrast. It's a hyperacute thrombus, and it appears hyperdense. And on the left-hand side, just for reference, it's a normal head CT. How are you going to meet these patients with acute ischemic strokes? So you're going to meet them in your ICUs. They can be right under your nose. That sedated, paralyzed ARDS patient you're proning, at least check their pupils. Often your patients on ECMO, on different kinds of mechanical circulatory support are going to be on heparin, at least check their pupils. They're going to be at a higher risk of developing acute ischemic as well as hemorrhagic strokes. Or you may end up, depending upon your ICU patient population, you may end up meeting them post-thrombosis, post-thrombectomy, or maybe the kind of patient that Dr. Murli showed us where there's all the cerebral edema. Are you going to send them for decompression? Are you going to do a thrombectomy in that patient or not? Mechanical circulatory support, lots of these patients are going to suffer from different kinds of stroke. So let me just put a reference there to give you a sense of what is the burden of strokes. In non-neurologically critically ill patients, the percentage of these patients who can suffer from strokes will vary from 1% up to 10%, maybe 15%, depending upon your patient population. Cardiothoracic ICUs and CICUs much more as compared to in a medical ICU. Here's just a figure we included on neuro MCRIT, which I also write for. These are all DWI images just to show you a recap of if somebody is going to infarct a particular vascular territory, what is it going to look like on your DWI imaging on MRI, and what is that clinical syndrome going to look like for large vessel occlusion? So let's talk a little bit about thrombosis, what's new in this world. Quick recap, NINDS, the trial from the 1990s that gave us the FDA approval in the United States for the TPA dose of 0.9 milligrams per kg, 10% as a bolus, 90 milligrams is your maximum dose. The FDA approved TPA on the basis of NINDS. And then fast forward to ECAS3, which comes from Europe. It helped us expand the window from three hours to four and a half hours. This is not an all exhaustive list of all the thrombosis trials, but these are just representative of where we get a bulk of our evidence for using this particular dose and the expanded window of four and a half hours. So the new kid on the block is tinecteplase. I'm calling it a new kid, but it's been around for a little bit. What is tinecteplase? Tinecteplase is a modified version of alteplase. And essentially it's a larger molecule, easier to give, that's the biggest advantage. It's easier to give you just give it as a bolus, 25 milligrams is your maximum dose as compared to alteplase that you need to give or your recombinant TPA that you need to give 10% as a bolus, then you give an infusion. A lot of these patients do need to get transferred to thrombectomy capable centers or comprehensive stroke centers if you don't have thrombectomy on site. So it's much easier to give tinecteplase. However, when they go head to head, I want to just remind you when you look at this meta-analysis, it doesn't include the results of TRACE-2, which was published in Lancet in Feb of 2023. But all of these trials were non-inferiority trials. They were not superiority trials. So from a non-inferiority perspective, smack in the middle, better to use just because it's easier to give. So a lot of health systems in the US have moved towards tinecteplase. In Europe, an advisory was released that preferentially, you can use tinecteplase as compared to alteplase, although there are no superiority trials. We'll see some publications in the next few years. How did thrombectomy become the gold standard for emergent large vessel occlusion in the anterior circulation. December 2015, the first RCT followed by four other RCTs at Hermes, which is the systematic review meta-analysis, showed us that the number needed to treat to improve outcomes for a patient with a large vessel occlusion in the anterior circulation up to six hours is only 2.6. Then fast forward, how did we get that window up to 24 hours in the anterior circulation? Thanks to DAWN and Diffuse 3. The number needed to treat to improve outcomes in patients with anterior circulation strokes all the way up to 24 hours is only two. When you innovate and there are new therapies, it's extremely imperative for all health systems to change to increase access to care to these kinds of therapies. Otherwise, what is the point of showing that in trial settings, there's an improvement in outcomes? So I'll show you some innovations in systems of care for acute ischemic stroke. The hub-and-spoke model we're all super familiar with, multi-hub, multi-spoke, thrombectomy-capable or thrombectomy-ready sites. Then you have this mobile stroke unit. Does every health system really need a mobile stroke unit? Not one size is going to fit all. This trial comes from Germany, flying interventional teams. Yes, you're going to give access to thrombectomy faster but doesn't translate into improvement in outcomes. NYC MIST, which comes from our health system, it's the mobile interventional stroke team model. Again, faster thrombectomy, maybe some signal to improve outcomes. Bypassing primary stroke centers, this has already happened in a lot of our states. Bypassing primary stroke centers to take patients to thrombectomy. But should you bypass thrombolytics because thrombectomy is so good? The simple answer is no. Lots of trials which answer that question. This mobile stroke unit trial published in the NEJM a couple of years ago. This is not a randomized controlled clinical trial. It's a smart clinical trial design, very pragmatic. Most of the patients come from Houston but there were six centers essentially looking at standard of care versus mobile stroke unit with a stroke neurologist or telestroke capability going out to the community, delivering care thrombolysis to a patient and then bringing the patient over for thrombectomy. It obviously improves time to TPA but it also led to improvement in outcomes. What's new from last year? Large core. Understanding what is large core. So in all those trials that I showed you right up to this point, the aspects or looking at that non-contrast CT head and how much of the area on that CT head in the MCA territory is already infarcted. That's what the aspect score which is your Alberta stroke early CT score. In all of those trials, we thought, you know, if the aspects, 10 is the best and every single hypodensity, you know, takes a point away but an aspects of less than six, we would not send those patients to thrombectomy usually. And there were a bunch of RCTs last year including angel aspect from Rescue Japan, select two, which came from North America. Defining large core is varied in all these different trials. Some use CT perfusion, some use CT. The bottom line, looking at the meta-analysis, those patients who have a low aspects or a large core, even those patients can benefit from thrombectomy but there is a little caveat. The amount of hemorrhagic transformation, not necessarily symptomatic hemorrhagic transformation but some hemorrhagic transformation was more in these patients but large core should not deter us from thrombectomy. Malignant MCA infarction, nothing new necessarily in this realm but I just wanted to remind everybody, you know this malignant because rapidly evolving swelling. So that timeline, and if you don't do something aggressively, these patients are going to die. That's why it's called malignant MCA syndrome. The AHA guidelines and the NCS guidelines have not been updated here. Just a quick recap, this is a good paper looking at this review paper published by Lin et al in Stroke in 2021. There are eight RCTs, I'm just showing you the major ones. The classic ones are Decimal Destiny Hamlet, less than 100 patients in Decimal Destiny Hamlet combined but they were the first RCTs that showed us that the number needed to treat to save a life from malignant MCA stroke is three to four. So these were the first trials that showed us that but then what about our older patients, Destiny 2 published in 2016, NEJM. Again, remember when you're looking at these trials, a good outcome was defined as a modified Rankin of zero to four. Those thrombectomy trials I showed you, zero to two is a good outcome. In hemorrhagic stroke trials, zero to three is a good outcome. So you just have to be careful when you're reading these trials because older patients will survive more but with more disability. That's what we learned from Destiny 2. Both of these guidelines statements from the AHA and the Neurocritical Care Society address all of these different aspects. The most important takeaway, the optimal trigger, like how do you know which patient needs to go to decompressive hemiclinic? We don't really know. The more important thing is to have a multidisciplinary discussion, the critical care team, your neurosurgery team, your stroke neurology, neurocritical care, just have that discussion on day zero. Take a united front of the family. Are you going to put decompressive hemiclinic as an option on the table or not? And clarify with the family, what is a meaningful quality of life for your loved one? Would they be okay surviving with some level of disability and going to a nursing home depending upon their age? So from a case by case perspective, older than 60 years of age, you're going to have that kind of discussion. But even for younger patients, it's important to preface this with, it's a life-saving surgery. It is not a quality of life adding surgery. So for acute ischemic stroke, direct thrombectomy without thrombolysis is a no-no. The SBIN, which is the Society of Vascular Interventional Neurology did a systematic review of several trials and provided these recommendations. I showed you data for the anterior circulation. The same thing happened last year for the posterior circulation. So basilar artery occlusion, which is a type of stroke that has very high mortality. There's a lot of practice variability. Some centers would do a thrombectomy. Some centers would do heparin and dual antiplatelets. Basilar artery occlusion, at least two trials to remember, and there are several others. Baoqi and attention both come from China. All the way up to 24 hours, basilar artery occlusion thrombectomy is a gold standard. For anterior circulation, I showed you large core infarct data, TNK versus TPA. Although the FDA has not approved TNK, a lot of health systems in the U.S. are moving towards TNK. I did not show you the results of ELAN, but that's an important trial for you to check out. Looking at this question of when do you restart anticoagulation for a patient who has atrial fibrillation and who sustained a stroke. Systems of care, I showed you some innovations there. And decompressive hemicrane, not a lot of new data, but saves lives. In the next 10 minutes or so, I'm gonna go over intracerebral hemorrhage, highlighting some high-level exciting things that are happening here. ICH used to be a disease process where there was a self-fulfilling prophecy, DNR-DNI, and a lot of these patients would die. That is not the case now, and there is caution. The American Heart Association cautions you to institute a DNR-DNI within the first 24 hours of these patients presenting to you. We do not want to get caught in that trap of a self-fulfilling prophecy. You've got to be aggressive, you've got to be fast. There's a lot that's happening in the ICH world. The American Heart Association guidelines from 2022 cover the entire realm, not just about survival, but a lot of emphasis on survivorship. So I'll highlight surgical interventions. Not a lot happening in the open surgical realm. All of those classic indications, you know, cerebellar hematoma, let's do a suboccipital crani in those patients, EVDs for patients with hydrocephalus, ICH with IVH. So things haven't changed there. But in the minimally invasive surgical world, a lot is happening. Lots of different strategies are being studied. I'll highlight MISTI-3, which was not a positive trial because it did not meet its primary outcome. When you look at the shift analysis, the outcomes were the same in the MISTI group versus the standard medical arm. Here, it essentially looked at the intervention arm, essentially looked at taking a catheter, putting it in the body of a hematoma and dripping TPA. Can you lyse the clot? And in those patients, in a subgroup analysis, in patients who had less than 15 cc's of that clot left, they did have a signal of a good outcome. So what this trial essentially told people who believe that this therapy could work, including myself, was if we had a technique or technology that helps us evacuate clots better, maybe this therapy can do what the thrombectomy has done to the acute ischemic stroke world. 2022's guideline statement does provide recommendations on MIS because of various studies, including MISTI-3, that you can offer it to improve mortality. You may offer it to improve functional outcomes. What about blood pressure? So some odd targets here for primary ICH, SVP goal of 130 to 150 because you don't want to cause perihematomal ischemia. You don't want that hematoma to expand either. So how do you strike the right balance? A lot of that recommendation is based on the results of Interact-2 from Europe and ATAC-2 from North America. Interact-3, which was a step wedge randomized controlled clinical trial published last year, very nicely conducted study, 17 centers, looking at this bundle, blood pressure control, coagulopathy reversal, glycemic control, and fever prevention. Improvement in outcomes if you use a bundle of care for ICH. Seizure prophylaxis, the PEACH trial, small study did not finish enrollment because they ran out of funding. But if you put appropriately selected patients like low-bar ICH patients on seizure prophylaxis, it may be appropriate. It may reduce the burden of seizures in those patients, but this is controversial. So bundled care works. MIS does improve mortality. This is an exciting arena. Look for more papers in the next few years there. And short-term seizure prophylaxis, case-by-case, yes. SAH, worst headache of someone's life. I'm gonna show you a couple of things here. The SAH guideline statements was published last year. Again, lots of emphasis on survivorship, multi-domain screening. These survivors can suffer from a lot of multi-domain problems, but be aggressive early. The guidelines do a really nice job of synthesizing multimodal monitoring for delayed cerebral ischemia, one of the most dreaded complications of aneurysmal SAH. And they provide you with some recommendations on how to do this. Early drain. Early drain after the 1980s nemodipine studies. This is perhaps the first positive RCT in the aneurysmal SAH world. Looking at standard of care, which is an EVD, external ventricular drain, EVD plus lumbar drain in the intervention group. And they showed an improvement looking at that shift analysis improvement in outcomes in the patients who got lumbar drains. And I'll just highlight perhaps why. This is the collection chamber of the EVD, collection chamber of the lumbar drain. You're seeing much better clearance of blood admixed with CSF with a lumbar drain, perhaps because of gravity too. So moving forward, survivorship, big emphasis. So these patients do need to be screened for multi-domain problems in the physical cognitive mental health domain. Multi-modal monitoring for DCI with TCDs, exam your multi-modal monitoring invasive bundles. EEG, there are strong recommendations for that. And then lumbar drain versus EVD case by case. Trauma TBI, we heard a lot of amazing things about trauma and TBI systems of care. I'll highlight a couple of things for you. Tiered management. Tiered management for ICP. I showed you that ladder. The CIVIC group, looking at severe traumatic brain injury, this international consensus does a really nice job of looking at what each tier should look like for patients with severe traumatic brain injury. We included this table, but very intuitive. ABC always comes first. You want to target a good CPP, seizure prophylaxis. To do, not to do. If somebody has seizures, of course you're going to treat it. When do you go to the OR for decompression? What should your systemic injury management look like in these patients? So they provide recommendations. These are consensus-based recommendations. Two trials I'll highlight, DECRA and RESQ-ICP. So this question, decompressive hemicrania in traumatic brain injury patients. DECRA published years and years ago now. Did not really show an improvement outcome. In fact, those patients who underwent early decompression may also have some more complications. RESQ-ICP, like the name suggests, let's rescue it as the last tier. So they failed all those different tiered management. Now let's take them to surgery. Does that make a difference? Well, in both the studies, the burden of ICP was lower in the groups that got the decompression, but the burden of complications was also higher in the patients who underwent decompression. But on a case-by-case basis, choosing the right patient, working in a multidisciplinary group, coming up with the right trigger, how do you prevent complications? What kind of rehab do they get? That systems of care approach will make a difference, but both these trials don't necessarily speak to what happens after the ICU. So practice updates for TBI. I did not touch on tranexamic acid within three hours. Crash three, patch trauma, you take your pick. I'm going to continue giving TXA. ICP monitoring alone is not enough. We've included some data in the chapter and also in the extended version of the talk, which is going to be available to you. And tiered management is recommended. I'm going to wrap up with status epilepticus. We don't have a lot of time. So time is brain, also for status epilepticus. Know what your first line, second line, third line is going to be. When are you going to institute it? Just like everything else in critical care, symptomatic management and what is the underlying etiology. So you've got to do this. You've got a parallel process, figure that out. Just treating somebody status epilepticus symptomatically is not going to improve outcomes. So it's important to look for that underlying etiology. And then patients who have these rare kinds of syndromes, this new onset refractory status epilepticus or FIRE syndrome, do you have that multidisciplinary neuroimmunology team on neurocritical care? Do you have plasma exchange? And are you going to use IVIG, steroids, et cetera? You've just got to be intentional. What is the underlying etiology? In addition to ramping up your treatments. So ESET, again, this is classic now. We know Keppra versus phosphonate versus valproic acid doesn't matter what you choose as your second line, just choose the right dose. The biggest takeaway from ESET was 60 milligrams per kg of Keppra maximum 4.5 grams. Like that's the biggest takeaway. It doesn't matter what you give, just choose the right dose, give it early, try to break that status, time is brain for that too. And ketamine is an important medication to keep in mind for status. It's going to antagonize NMDA receptors. It's going to attack glutamine. So it's very synergistic with GABA. And when to institute ketamine, that's controversial right now, but there's going to be some studies that will help you guide that. In my practice, by the time I'm using midazolam at 0.6 milligrams per kg per hour, I'll add ketamine. So we spoke about a lot of different things. You have the chapter with you. There will be an extended version of the talk. Neurocritical care is exciting. My biggest disclosure here is I love neurocritical care. So I'm looking forward to your questions, but thank you so much for listening. Thank you.

neurocritical care

subarachnoid hemorrhage guidelines

ICP monitoring

thrombolytic therapy

decompressive hemicraniectomy

traumatic brain injury management

multidisciplinary care