Chapters Transcript Video Whats New and Whats Not in the Management of Severe Traumatic Brain Injury Dr. Hoffer discusses trends in management of traumatic brain injury patients. Thank you so much. See if I can uh. Get this up hopefully everybody uh online here. You can see if we go into presentation mode. Great. Um, so I'm Alan Hoffer. I am, uh, from Case Western Reserve University, University Hospitals, uh, in Cleveland, where, uh, I am the director of the traumatic brain injury program. Uh, I don't have any conflicts, but I'm always interested in getting some, so if anybody has any leads, please let me know. So, uh, our objectives for today, we're gonna talk a little bit about guidelines, uh, for traumatic brain injury, uh, and understand how these have helped patients and how our guideline process is ever evolving, uh, but beyond the guidelines, a little bit about how individualized care can help our patients. Uh, now, at, uh, Case Western we always talk about the fact that we view the measure of our success, uh, by how well the people do who came up behind us, so I'm really delighted, uh, to be here and to see Byron, who was my resident and my fellow, uh, who, uh, is, uh, here and establishing his career, and here he is at his, I think this is your graduation, uh, with his co uh co-resident Bear Shamashian, uh, and Warren Selman, who was our chair at the time, but. But I have to really, you know, we're all in a continuum and uh just as I was Byron's mentor, uh, I had. Yeah I was the junior resident of uh of, of Tina Rodrigue who I definitely think left her, uh, left her imprint on me. I was kind. Uh. So you know, the, the evolution of traumatic brain injury care, um, you started as with many things in the laboratory and two are really the most influential people, uh, in the history of traumatic brain injury research, uh, were Don Becker, who was a neurosurgeon, and Tony Marmaru, who was a neuroscientist who both happened to be at the Medical College of Virginia in the 1970s. Now Don Becker actually came from Case Western Reserve University and so here he is as a resident. I recently discovered, by the way, that our university hasn't has a university archivist who has these amazing old pictures of everything. Uh, so here, here's Don Becker on the right with Harry Young, uh, who went on to become the, the chair at the College of Virginia, uh, and recruited Don to be there and. And there happened to be this sort of perfect confluence with, uh, with Don Becker there and with Tony Marmaru. So Tony Marmaru is a PhD researcher, uh, who had really come up with the first models of intracranial fluid dynamics and did a lot of work in hydrocephalus that was then translated to traumatic brain injury where they were really describing the pressure volume relationships uh inside the head, and he was really the first one to talk about the vascular component of intracranial pressure. Uh, and its effects on, uh, it's effects on patients in traumatic brain injury. Well, uh, it took a little while, you know, the, the, the, the research comes out and it takes a little while for it to be translated into clinical practice, uh, and, uh, and it wasn't until the 1980s, uh, that JM Gajar, uh, started to work with the board of the Sunny von Blau Coma and Head Trauma Found Foundation. And really founded the Brain Trauma Foundation, which is, is now the I think the major source of guidelines uh and research, uh, which is very interesting because in so many other things, the leadership or, or the, uh, you know, for the guidelines really comes from the national organizations. This is actually a private foundation, uh, but it's been extremely influential in uh in the care of traumatic brain injury. So the first guidelines, the first evidence-based guidelines, didn't come out until 1995, uh, but it ended up being really a uh pivotal moment for traumatic brain injury care because before the guidelines, You know, trauma was thought of as this pretty much uncurable disease that it had an extremely high mortality rate, you know, we were giving patients steroids because there was brain swelling and we didn't want to uh have vascular congestion of the brain, so we ran these trauma patients very, very dry because we didn't want to, uh, give the body any additional fluids that might get into the brain, um, and then after the guidelines, just by having the guidelines. We cut mortality almost in half, right? So the evidence-based guidelines, we had the crash study that said that steroids were actually bad for traumatic brain injury. We realized the importance of full resuscitation for uh trauma patients and the importance of uh profusion. We stopped uh prophylactically hyperventilating patients and as I said, both in the United States and worldwide these led to a significant decrease in mortality. So now we are up to the 4th edition of the guidelines that this was, you know, meant to be something that would evolve with time, uh, and this is still, uh, sponsored by the Brain Trauma Foundation. Uh, there are other BTF guidelines, uh, such as pediatric TBI, uh, surgical management, pre-hospital management, field management, uh, in combat related, uh, TBIs, and then we have some upcoming ones that will be coming out soon. So as I said, the latest edition is the 4th edition. Now, the problem with many guideline processes now is that we want these guidelines to be very scientific. We want them to be evidence-based, uh, to show kind of the quality of the guideline and, and it's applicability. The downside of that is there are many things in neurosurgery and in medicine in general for which there is not good data, right? So, you know, some things we think about like when we think about carotid and arterectomy and the NASA trial, right, you had thousands and thousands and thousands of patients who were randomized to one side of the. There are not very many studies like that anymore, and so it's very hard when you're talking about using good data. There aren't that many randomized prospective trials out there, certainly not multiple ones for a single topic that give you high levels of uh of evidence. And so many of the recommendations from the previous edition from the 3rd edition were removed. So here's some examples for hyper osmolar therapy in the 3rd edition there was a level 2. There's a pretty high recommendation about the effectiveness of manitol, uh, and, uh, and, uh, arterial hypotension and a level 3, about, uh, about restricting it because of this paradoxic effect. And when the 4th edition came out and they reviewed the same data, they found out that based on the new criteria for evidence that. Many of the recommendations from the 3rd edition were no longer met the the evidential criteria and so they got rid of them. They said there was insufficient evidence about the clinical outcomes to support its use. Similarly, even ICP monitoring, right, so it used to be ICP of 8, you got a bolt. And uh in the new edition they said, you know, again looking at long term outcomes there was no evidence to support this. So here we have two of like the foundational concepts in brain trauma, right, the bolt and hyperosmolar therapy and all of a sudden we're getting rid of the guidance for people and so while the guidelines were very good in terms of their scientific content, all right, the applicability of the guidelines went down because. We weren't telling people what to do anymore and so there was a uh there was a response to that from the Brain Trauma Foundation, uh, and they said, well, what we are going to do then is for areas where we don't have evidence, we are going to do the next best thing which is expert consensus and so this was the CBIC uh uh conference and so we got together about 40 people from a number of different backgrounds, so neurosurgery, neurocritical care, trauma surgery. Uh, etc. and uh we identified key questions in, uh, the care of TBI patients that were not answered by, uh, the guidelines and We tried to work them all out so that we could give people guidance about what to do, so it was a Delphy style uh consensus process where you had to have 80% or greater consensus for a recommendation to go through, uh, which involved lots and lots and lots of pre-meeting surveys, and then they basically locked us in a hotel for 3 days and told us not to come out until we had something. And the result of that uh was uh was the uh CBIC protocol, um, and, uh, so really the goal of this was to give people guidance. These are not evidence-based guidelines, these are not necessarily standards of care, uh, but these are recommendations based on expertise, uh, so you have this assumes that you are already. The tier zero is that you're admitted to an ICU and you have a bolt. Uh, we kind of didn't want to, uh, address the issue of who needs a bolt, uh, because again that is one of the things that there was no evidence for, uh, and we'll talk a little bit more about that, uh, particular problem in a minute. Um, and we didn't want to necessarily box people in to say these are the criteria you have to have one for, but assuming you have a bolt, you start out with your tier one therapies, uh, which include, you know, uh, uh, uh, maintaining the cerebral perfusion pressure between 60 to 70, uh, some sedation, uh, uh, making sure patients are roughly normal carbic and you can give them some hyperrosmolar therapy. Now we did specifically say again because. This is an expert consensus protocol. There were certain things that you don't have to do everything in a particular tier before you move on to the next tier, right? Uh, and that if you need to, if you feel it is clinically, uh, uh, necessary, you can skip tiers, right? And, uh, uh, and the, the reason to go up tiers is because of what we consider what we call neuro worsening. All right, uh, so then you get to the tier two, where you can do neuromuscular blockade, and we talk about the map challenge which we'll talk a little bit more about in, uh, in the next, uh, a couple of sections, and then tier 3 is where you have things like decompressive craniotomy, uh, pentobarb coma, etc. Uh, so this hopefully helped fill in that gap of, well, there's no hard evidence here, but, but what do I do when I have this patient sitting in front of me? Well, again, many of these things are based on the concepts of ICP, uh, and a lot of, uh, the data about that we said was, was, uh, sort of, uh, abandoned in the 4th edition. And so how do we move beyond ICP in terms of taking care of our patients and in fact, you know, do you need ICP to monitoring at all and uh this was a trial that was done, right? This was, and this trial had all of the stuff we like to hear about trials. It was a randomized prospective trial. Uh, and this was done down in, uh, South America, um, um, in collaboration with Randy Chesnut where they actually didn't have ICP monitors for everyone. They randomized patients to get ICP monitors and close or close clinical monitoring and frequent, uh, frequent imaging, and they actually found that in that population of patients there was no difference in patient outcome, right? So here we have even our most basic idea about how do we manage these and questioning whether or not it's really necessary. Uh, and I would posit that that, you know, ICP is really, uh, is really kind of an end, uh, uh, an, an end process, uh, measurement that we take because, you know, what do we really wanna know is that we really wanna know about what is going on in the brain physiologically and then potentially be able to intervene, right, to try and make things better. So you know, by the time you get a clinical change, there have already been. Cellular changes that have resulted in tissue changes that have resulted in organ changes, right? And if you're in the cardiac ICU with a problem. You're in there and they've got monitors on you and every single second they can look at your cardiac function, right? In the neuro ICU we once an hour come by with a flashlight and look in your pupils. That's state of the art, right? Uh, so we have a lot of things that we need to do to catch up on our ability to kind of move up this ladder to detect things that are going on earlier and intervene before we get to the point where the ICP is getting higher and we're seeing a clinical change. Uh, and the good news is we're on the cusp of that, that our understanding of the pathophys physiology of traumatic brain injury has allowed for some new concepts and technologies to emerge from what are interestingly very old ideas actually, and I think that this is going to allow us to make many advances in the individualized treatment for traumatic brain injury over the next 10 years. So I think the first and most obvious of these is cerebral hypoxia. It's been known for a very long time that cerebral hypoxia is an independent risk factor for poor outcome after traumatic brain injury. And back in 2005 when I was a resident, they came out with this great thing called Lycox, right, which was the first FDA approved, uh, cerebral oxygen monitor, and I went to James Anderson, who was my attending at uh at our county hospital, which was our only level one trauma hospital at the time. And I begged him, I was like, this stuff is amazing, it's gonna change the world, right? That you know, the initial studies that came out of the University of Pennsylvania showed that patients who had, uh, PBO2 monitoring and a treatment protocol had better outcomes than ones who didn't, uh, and uh they came out with the first PBO2 uh uh uh algorithm for how to treat patients with decreased, uh, uh, cerebral oxygen, and and I said, you know, this is the future, can we do this? And of course, uh. You know, I, I begged for it and he said, Well, is there any data that shows that it improves outcomes? And, well, of course, you know, there was, there was not good data, right? I mean, the, the UPenn studies were small studies they looked at 60 people, uh, you know, they were, they were sequentially, uh, uh, entered, it wasn't randomized and you know, so we've been sort of caught in this trap with, uh, with cerebral hypoxia. Uh, for really two decades now that it's been 20 years of us asking this question, you know, do we still need it, and thank goodness the trials have proceeded and we've been through the boost 2 trial, right, which was, which was the phase 2 trial looking at this, uh, and the boost 2 trial did show that there have been some improvements, but it is still not the large outcome-based study that some people need, so. Very thankfully, we are in the process of doing the boost 3 trial which will hopefully settle once and for all after, you know, 2025 years if we should be using this tool. So I, for one, am very much looking forward to it. I will have to say that at our institution, uh, we drank the Kool-Aid, we are believers in uh in brain oxygen monitoring, so we've adopted that system. But I think once if the data from this comes back, uh, with a positive result that it will uh very quickly become a standard of care and in fact when we put together the, uh, the algorithm, uh, for patients, we did include a separate section for the management of, uh, cerebral hypoxia. So, uh, you know, we had. Recommendations for if you just had an ICP monitor or if you had ICP and PBO2 monitors so that you can look at cerebral hypoxia in the setting of elevated ICP or even in the setting of normal ICP, uh, and that of course came with its own algorithm, uh, so I think that will be uh probably the soonest change uh that that we'll see in the management of traumatic brain injury. The second thing I want to talk about is cerebral auto regulation. So there's always been this discussion, this debate in neurosurgery about what's more important, intracranial pressure or cerebral perfusion pressure and uh. If you believe in ICP control, uh, you're very worried that if a patient is uh hypertensive that you're gonna get vascular engorgement, and this is going to worsen your intracranial pressure and conversely, if you're a CPP proponent, you say, well, if you have hypotension, then you're gonna have ischemia, and that ischemia is gonna worsen uh cerebral edema and that's gonna worsen your ICP. So who's right here? Uh, and this is a debate has gone on for a number of years, and here's a very interesting study. All right, here are two centers, one in Sweden and one in, uh, Scotland, and, uh, the difference between the two centers was that one primarily did ICP management and one primarily did CPP management and it turns out that the difference between where you did better depended on your state of auto regulation. So if you were at the CPP center, you did better if your auto regulation was intact and worse if your auto regulation was impaired, and if you were at the ICP center, it was the exact opposite. You did worse if your auto regulation was intact and better if your auto regulation was impaired, right? And uh, so why is that? It's because if your auto regulation is intact and you raise your mean arterial pressure and your cerebral perfusion pressure, your brain will distribute that perfusion to where it needs to go, and you will have better perfusion of the brain, whereas if your auto regulation is not intact and you raise your mean arterial pressure. You're gonna get vascular congestion and all that's going to do is increase your ICP without relieving any of the metabolic uh needs of the brain, uh, that you have. And because of that, you know, the 4th edition of the of the guidelines said that, of course they recommended if you're going to remember one number, right, you're gonna remember 60 for your CPP, but they put in this little caveat that said that the optimal uh CPP threshold is unclear and may depend on the auto regulatory status of the patient. And we addressed that again in uh in our uh consensus algorithm with this, uh, one little thing here that we slipped into tier two and what that says is, all right, uh, that you can perform a map challenge, right, you can also perform an oxygen challenge. Now what that means is that someone, the intensivist or the neurosurgeon or someone is gonna walk around the ICU with a syringe of pressor. And you're going to give it to the patient and you're gonna look up at the monitor and you're gonna see when you raise the mean arterial pressure does the ICP go up or does it stay the same or go down? Now that's not so great, that's not very scientific, right? And you know you're doing it once maybe twice a day if you're doing it. Um, to determine this thing, but it's very, very important because it's, uh, it's gonna tell you how to optimally manage your patient. Well, uh, we are starting to get better at, uh, at, uh, doing this, and this was the cogitate trial, um, uh, from, uh, from England, and what they did was, you know, we collect this data already, right? If you have an ICP monitor and you have an arterial line, every single second or every single heartbeat, you have a data point. And you can sit there and watch and you can look at the changes in ICP and compare them to the changes in arterial pressure and you can determine the relationship between changes in blood pressure and changes in ICP which really tells you what your auto regulation is. So the data is there, it's sitting there, we're already collecting it. It's just that you have to analyze it and so that's what they did. They basically developed a software that does a bedside real-time comparison of these things and tells you what the state of auto regulation is and so here they are for two patients was basically looked at their continuous state of auto regulation and then what they were able to do with that is they were able to make optimal CPP maps for patients and so they could determine at any given time what was the optimal CPP for that particular patient. Uh, now, remember, the traumatic brain injury is a very dynamic injury, uh, and so over time, uh, you know, you could see even in individual patients that the optimal CPP for an individual patient at a given time, uh, could differ. Um, and, uh, so this is, uh, this is really I think the beginning of something very new, but interestingly again data that we've had for a very long time that we just haven't done anything with, uh, but I think I know some of the, uh, ICP, uh, monitor companies are now starting to integrate, uh, software that will calculate the auto regulation for you, so it'll have an input for your arterial blood pressure information. Uh, from your bedside monitor and it will, in addition to telling you what the ICP is, it will tell you what the auto regulation, uh, status is, uh, for that patient. So I think again in the next 10 years, uh, we will see that get put into clinical practice. So the third thing that I want to uh talk about uh in terms of uh some of our upcoming trends is spreading cortical depression. So again, here is a very, very old, well known phenomenon. This was first described in the 1940s by Aristoes Lea, who called it spreading depression because it was an electrical silence, uh, in the brain and what was really happening. Uh, was that, uh, you know, you have your injury, you have this initial cytotoxic response, uh, and that really heralds the oncoming of a metabolic crisis. I remember all of our neurons require a transmembrane ion gradient to remain charged and the process of reestablishing. that is dependent on ATP dependent pumps, and when you do not have enough energy and you can't re-establish that relationship, number one, you lose the electrical activity because you can't repolarize your cells, and then because you've altered the transmembrane gradients, you also get cellular swelling. Uh, now what the spreading depression is, it is a slow, right, spreading at 2 to 6 millimeters per minute, right? And that's compared to our normal fast electrical changes that we see with neuronal discharges, but it is a slow, uh, persistent depolarization wave that extends out of, out of the brain. Now normally when our brains are in metabolic crisis or when they have metabolic needs, the body's response is to vasodilate. Alright, and that's where we see where, you know, our auto regulation and so when you have this sustained depolarization that's the indeed the initial response that you maximally vasodilate in your brain. So after this wave of electrical silence, uh, or uh, or depression, that's followed by a wave of hyperemia as the body tries to meet the metabolic needs of the brain. Now even. At maximal dilation, if it's still not enough to meet the needs of the brain, you can have ischemia even if you are well perfused, right, those those uh those those micro vessels can only dilate so much, uh, so even if your CPP is optimized, you can still have ischemia from that. Alright, uh, and here's an example, uh, if you look at uh at regional cerebral blood flow so that you have, uh, your metabolic activity, you have then the spreading wave of hyperemia. The bigger problem, however, becomes if you have sustained depolarization like we see with these spreading waves, because then what happens is that uh you go from having hyperemia. To going into a refractory state of vasoconstriction. So you have hyperremia that's followed by a wave of allegemia, and then you're really in danger of ischemia. And here is an example, a laboratory example of spreading ischemia in the rat, and you can see this drop out of the microvasculature as this wave goes past and is sustained. And so we've all seen patients in the ICU you right whose ICPs are normal and maybe their brain oxygen is normal, but they're still in terrible condition and this may be one of the reasons why, uh, that, uh, they have these spreading waves and we're not meeting the metabolic needs of the brain and, uh, so even if you're. ICP and the things that we measure are normal, they can still have significant damaging processes. Well, how can we detect these? Well, historically you would have to lay an electrode strip across the brain, which would mean taking the patient to the OR to implanting one, and that's not something we would normally do for a patient who needs a bolt, right? You're not gonna take them to the OR and do an operation for something that you could do a bedside procedure for, all right, uh, but now, uh, certain groups, and this is, uh, data from the University of Cincinnati from uh Jedd Harding's and Laura Nuea. are actually putting in depth electrodes through bolts so you can get a multi-port bolt and you can put a number of different things to them. You can have your ICP your PBO2. They are putting in depth electrodes and interestingly, even though it is a single electrode, so you're not seeing it's not a strip where you're seeing it pass by, but it's, it has multiple leads on it and because you are never putting that in perfectly perpendicular to the brain. What you can see is that as the wave goes past each of these leads, even though it is only a fraction of time delayed, you can see this slow wave passing by the different leads that are in the cortical uh cortical ribbon here, uh, and so we're starting to get the ability to detect this bedside, uh, now of course you need to have, uh, uh, the EEG support uh to be able to to see this and read this. All right, but, uh, it turns out there is actually something that we can do about this. So, uh, uh, talking about uh uh cortical spreading depressions, uh. They looked back at all of the things that had any effect on it and very interestingly, ketamine can help reset uh that electrovascular coupling and reestablish the uh re-establish the microvascular blood flow and so now uh the University of Cincinnati. Uh, they are doing a, a trial looking at ketamine to help patients with cortical spreading depressions, uh, and see if they have any outcome. So I think those are three big trends of things that are coming that will help us individualize care for our patients. So what's next? Uh, well, the next thing coming out from the Drain Brain Trauma Foundation, uh, are some new guidelines for penetrating head injury, uh, and, uh, so we finished these up. We, uh, are now in the process of going through the, uh, going through the guidelines, uh, committee of AANS and CNS to to get approval from them, um, so it was very important, the last penetrating. Uh, guidelines came out in 2001, and, uh, especially, uh, in this country we see a lot of, uh, uh penetrating injuries, especially gunshots, uh, with a very high lethality, uh, and of course from the military perspective, uh, uh, there have been a lot too, and I think it's really our experience in recent conflicts in Iraq and Afghanistan have taught us a bunch, you know, it used to be thought that these are almost universally fatal, uh, and, uh, so there was a lot of pessimism about treating these patients. Uh, but I think we learned from our conflicts that rapid treatment, uh, and, uh, getting these patients quickly to the OR doing decompressions, it is amazing, uh, the people that you can actually save. So as I said, the previous guidelines were in 2001. They were done by an independent group, uh, and here's an example of the, of the classifications, uh, for of evidence, uh, for guidelines that we were using back in 2001, um, but again with our recent military experiences we needed to update these. Um, and, uh, and create some, uh, treatment algorithms, uh, so we, uh, this time we learned our lesson from the 4th edition guidelines. So, uh, instead of just doing a guidelines process and, and then having people say, you know, there's nothing in here it's useful, we actually combined the two processes this time so we did an evidence-based guideline process and a simultaneous consensus process to fill in the gaps. So this was a joint military and civilian. Uh, effort, uh, with the support of the Brain Trauma Foundation and the Department of Defense again very important for it to be multidisciplinary, uh, so that, uh, everybody had a seat at the table and had their say in the process. So we had people from uh neurosurgery, neurology, plastic surgery, trauma surgery, rehabilitation, emergency medicine. Uh, and we aimed at addressing penetrating, uh, TBI in diverse environments whether you're talking about, you know, in the United States at the United States, low and middle income countries, uh, in battlefield environments, etc. uh, so we want to create a product with the best evidence and opinions available. We identified 46 key questions that addressed pre-hospital care, surgical care, and perioperative and critical care. Uh, we did our evidence-based process and our consensus process. We also thought it was very important to develop some algorithms and a tool kit. Uh, so the way we do that is with a peacoats, uh, literature search and so this looks at this is, this is now the, the standard of how we do guidelines, uh, uh, uh, design. So we're looking at populations, interventions, right, comparators, outcomes, uh, timing and setting, and, uh, instead of that little three line thing that you got from, uh, in 2001, this is what, uh, this is how we determine the strength of evidence now. Um, uh, and that this is only the first half. Here's the slide with the second half, right, so you know we can break down all of these papers, we can determine the strength of evidence and the risks of bias, uh, in these papers, and then again we had our consensus process with our level C recommendations, all right, uh, and then we made, uh, an algorithm and tool kit to facilitate these, so there's an overall major injury pathway. There are algorithms for surgical management for cerebrovascular injury, uh, and very importantly, uh, one thing I want to highlight is the futility assessment, and I bring that up because I think even though we have made a lot of advances in uh our care for patients with, with, uh, penetrating head injury and head injury in general, we still have a major problem of nihilism of thinking that somebody who comes in that looks bad and we go and talk to the family and say this looks really bad, I don't think we should be doing anything. And uh so it turns out in the United States, uh, one of the major, well, the major cause of death after a head injury is withdrawal of care. Now, when we talk about prognostication. We, the neuro experts, it turns out even though we're, we're really good, but Nobody is that great at prognos early prognostication. So here are examples of multiple studies where they've looked at neurologists, neurosurgeons, neuroradiologists, and it seems like we're only about 50% accurate with our prognostication, and there have been lots of other efforts things to try and refine this, right? So radiographic criteria and so here's the Rotterdam score, uh, which looks at degree of brain compression and lesions and blood, all right, uh, to try and predict uh the mortality and. You know, from many of our studies from crash and impact, we developed calculators to try and, you know, calculate the risk of injury. Of course these have problems, right? these are based off of a study population. Uh, they don't account oftentimes for the overall degree of injury and there's very limited parameters of prediction. We've tried to use biomarkers to try and figure this out. Right, but the problem is, is that for all of these things they do not have, I think, a high enough, uh, specificity to truly say if somebody is going to survive or not, and you know what I think of my favorite examples of this comes from, uh, the hemorrhagic stroke literature. So this is very, very well established. Uh, this was the uh the paper by Claude Hempel in 2001 that described the ICH score, right, our standard score for uh for measuring in cerebral hemorrhage mortality. Um, that's required by, uh, for certification as a, as a, a primary or comprehensive stroke center right here are the things that you can get and uh all of the all of the factors that can lead to worse outcome and the mortality for, uh, the 30 day mortality for your ICH. So this looks bad, right if you're. years old and you have a 4 by 4x4 centimeter hemorrhage, right? So that's, that's 30 ccs and maybe some intraventricular blood or maybe you're not. You are an ICH score of 3 and you have a 77% of 30 day mortality. I'm not talking about functional outcome, but just mortality after 30 days. Well, that sounds absolutely terrible. OK? Now, I think the place where we need to start though, all right, is by talking about this idea of pessimism or nihilism even for brain injuries. So there was another group that went back and they repeated the exact same natural history study that the Hemphill group did in 2001, except there was one difference. The only difference was they would not withdraw care within the first five days, so there's no therapeutic intervention. Alright, for the hematoma, they just wouldn't withdraw care and interestingly, what they found was they cut mortality almost in half. Just by waiting 5 days and when they went back and looked at uh you know when they had had gone back and looked at some of this data from the ICHJ what they found was that there were people who had, you know, some slightly higher ICH scores 3 or even 4, you know, who actually didn't have bad outcomes and and the opposite was true too. So you had, you know, yes there were plenty of people who did as expected, but there were people who had. You know, higher ICH scores who actually ended up doing well and there were people who had low ICH scores who didn't do so well. Uh, so there's a lot of, uh, there's a lot of crossover. And uh you have to remember that recovery from neurologic injuries is slow and that many of the things that we have used are really surrogate measures. So if you're talking about in-hospital mortality, 30 day mortality, 3 month mortality, even 6 month outcome are really surrogate measures for long term outcomes, and we saw that come into play in the rescue ICP trial. So this was the randomized prospective trial looking at secondary decompression for a refractory ICP. All right, uh, uh, so what they saw, so these were patients who had refractory ICP taken for, uh, for decompression, and at 6 months, the 6 month data showed that yes, you improve mortality, but you had more patients in the, uh, in the severe disability group. Well, that doesn't sound great, right, that you're saving patients' lives for them to be severely disabled. But if you look at the 12 month data, what we see is that some of those people in the severe disability group then transition into the lower disability group. So if all you did was look at 6 month outcome, you would have missed this. You wouldn't have seen this. And in fact, there's even more data from the rehabilitation uh literature that shows that patients, even if they haven't regained consciousness by the time they go off to rehab, a significant number of them do it while they're in rehab. And Beyond regaining consciousness can also have improved function. So it brings up, I think, a very important point of establishing goals of care with patients who are early on in their, in their course and you'll know I'm particularly not talking about end of life care because that's that's a bias, right to say that, that, uh, you know, you're going to, uh, this is really to determine, you know, your end of life. It's not determine what is the patient's goals of care. And one of the big problems I think that we have, uh, in the neurological world is we have this dichotomous outcome trap, right, that the, the family says what's going to happen to them and if you say. This is gonna be a bad outcome. The family says, I don't want it. And if you say a good, this is, this is gonna be a good outcome, the family is gonna say, do everything. All right, but that is a trap and that's a problem and I think we can learn actually from our neurology colleagues a better way of doing this. So if you are asked to do a prognostication for someone who has coma after cardiac arrest, the neurologists have developed this very nice tool, and what they've done is they've identified specific factors that have a poor prognosis, right? So if you're in myoclonic status epilepticus, if you've lost your brain stem reflexes, these are bad things. They've developed things that are clearly associated with a good prognosis, right? If you're following commands, you're tracking things like that. If you do not have either of those things, they say you have an indeterminate prognosis, and I think that we need to start doing things like this with traumatic brain injury, and there have been some efforts here is a paper from the track TBI group where they specifically identified again one of these worst outcomes if you have a 1 cc lesion in your brain stem as a result of your injury. That is one of these factors, and I think we need to identify more and more of these factors. That are associated with good and bad outcomes so that we too can have that indeterminant category. Now the reason uh that we did this again and this is coming from the this is the futility assessment toolkit I mentioned coming from the up uh upcoming uh uh new penetrating TBI guidelines, right, is that when you talk about discontinuing aggressive care, it should be because there is true futility. Not because it looks bad, but because you have identified certain things and for the penetrating head injury, uh, that includes, you know, bilateral blown pupils that includes a trajectory through what we call the zona fatalis, which is right above the brain stem, the bilateral thalamide, basically, uh, things like that, um, and that's going to contribute to our ability to better prognosticate and to help these patients. So, you know, in my practice I've gotten away from uh this simple good versus bad prognosis and I give uh patients, families, I talk about a range of outcomes. I talk about the best possible outcome, the worst possible outcome. And then what I think is the most likely outcome and so the best possible outcome I get basically from the imaging, right, that if there are structures that are clearly damaged, I can say, OK, that is going to be a neurologic deficit, but if there are things that are not clearly damaged that may be affected by inflammation or irritation, things that may be reversible. You know, the best possible outcome means that those those areas will remain functional. The worst possible outcome is obviously that there is widespread injury, even things that you can't see necessarily on on imaging, and then the most likely outcome allows me to fudge a little bit, right, because there that's where I can include individual factors about the patient, their age, their general medical condition, other things like that. Uh, when I talk about the most likely outcome, so when you talk about these range of outcomes, you have to then compare that to what is considered via the patient's surrogate and acceptable quality of life. So if there is some overlap in that range of possible outcomes, then you should be considering long term support. Now when you do that, it's very important, I think, to educate the family about what that means, right, that you know, when, when you say that they have a chance to survival, that doesn't mean that in 30 days they're gonna wake up and go home. Right, they may need a peg and trach and to be in an LA and may need months and months and months of care to get to that point at 12 months where they may have that outcome that they would want and of course they may not, and they have to understand that it's a long haul, but you can also tell them that if they ever get to a point where it's clear that the patient is not going to make a recovery, they can change their path and go on a different thing now. If it's clear that uh uh that there is no possible uh uh overlap between what they want, that's when you're talking about instituting comfort care measures. So I just threw at you a whole bunch of things about TBI care. The good news is that it is always evolving and always changing, uh, and that, uh, even though we have some very old concepts we've been able to apply new technologies and new strategies to be able to use them in new ways. So I think we're going to be seeing over the next 10 years a lot of individualized therapies that are coming out, and I'm very excited about that. Uh, being somebody who, uh, is dual trained in neurosurgery and neuro ICU because I get to do all of their ICU care and play around with all these bedside monitors and things, um, but that, you know, these are severe injuries and recovery can be slow, but the potential for recovery is amazing. Thank you. Published February 6, 2025 Created by Related Presenters Alan Hoffer, M.D. Neurosurgeon
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