Transcript Video Panel Discussion 2: Brain Injury Management < Back to Summit23 Brain Injury Management Panel Discussion 2: Brain Injury Management Presented by Professor Chiara Robba, Professor Raimund Helbok & Professor Ha Eun Jin Moderated by Professor Fabio Silvio Taccone Three members of the faculty to be on the site. We have 15 minutes per question before the final session upstairs. We are going to start with questions for our audience, please. If we can have a mic here. Thanks. Hi, Nicole Jeer from the Netherlands. I have a question to all of you about the avoidance of fever. Um You were saying you should do this as long as there is a risk for secondary brain damage. How long is this? One week, two weeks, three weeks, we always struggle with this question in my IC U. If, if I can start uh taking a question, I think it it totally depends on disease and on the disease itself. Um And if we talk about sah patients, we know the critical phase is much much later in in certain patients. And if we look at the v of spasm phase uh associated with infection CRP uh ra in CRP, also fever. And I think that that's a very critical phase. We we, we should, we should be also aggressive in treatment in terms of intraceable hemorrhage. Um There's the very early phase and then also the prolonged phase where certain patients develop peri hematoma edema, massively aggravated. I think that's a target to patient population as well. And we have one study hypothermia in IC H which, which was just not finished, included only a small number of patients. But we saw a signal that actually against the peri hematoma edema, uh temperature management or even hypothermia could, could have a very nice signal, but then you have to treat for for 14 days. So that's, that's right. Um Does that fit to every patient? No? Um but, and, and that's, that's why we come to the discussion, how do we do we properly identify these patients at a certain stage of the disease? And that, that would also be, have been nice to discuss with David Greer. Should we now wait for the first fever peak and then treat so to identify these patients who actually develop fever? Because as he said, what we've seen in rapid trial that many, many patients didn't develop fever. And so that's why you apply a treatment and then um the treatment has a certain side effects and that's why uh it, it really depends on the, on the disease. And um uh and, and I don't think that there is a general recipe for that, but um in, in certain certain diseases, yes, even prolonged for, for 10 days or 14 days. How long you do? It really depends, it really depends on the type of patient, the severity and the type of the pathology because as Raymond was saying some brain injured patients have a very acute phase where you have to be very careful. And then there is a sort of reduction of the severity. And here you have to follow neuroimaging neuromonitoring, but especially the clinical picture of the patients. But for example, in patients with sub aid hemorrhage where you have the risk of vasospasm for a longer window and fever increases the risk of vasospasm. So here probably you have to watch also not just in the very early phase but also later on. There is not a magic number of days. It's really about the pathology and how it is going just to know because you presented your data with very aggressive temperature control. Is it the same that you apply for the duration? Depends on the patient's pathology and clinical cost. Sometimes it goes as long as like 21 days and sometimes it is shortened like five days. So I like to challenge when I do the medical round, I always ask people which is the risk benefit to keep patients with normothermia with all the devices and drugs. And when patients get febrile, they don't degradated clinically, we sometimes tolerate temperature 38. But it's mostly the case after the first week, 10 days of disease. And I think an important point is whether the patient is awake or not, if we have a mechanically ventilated sedated patients, totally different patients to the awake patients. And in the intrepid trial, we included awake patients as well. And that's the question whether this kind of treatment is potentially too aggressive for that patient population. But we will, we will analyze all these subgroups of the intrepid trial and come up with ideas, a question. Yes, to all three of your question. Have you ever evaluated the effect of the regulation and the impact of the temperature monitoring and regulation, temperature control? I mean the status of auto auto regulation of the patient if this can affect any potential favorable effect or unfavorable effects of thermoregulation. So the answer is yes, when you have a fever because of all the path physiological issues that we discussed, autoregulation is impaired. And there are some physiological studies which say that autoregulation is becomes impaired even before you might, you see the increase of the intracranial pressure, which from a physiological point of view makes also sense because first you lose the regulatory response and as a consequence, you as you have a vasodilation and therefore increase of uh intracerebral volume. So if you have a possibility to test out regulation, this can certainly help. Of course, you know, if you want a proper assessment in this context, you will need a software for continuous out regulation evaluation which has a cost. And so not all the units have it with the static methods. It's more difficult probably on the on the opposite side of the fever if you see patients that are severely damaged, were spontaneously hypothermic. These are patients when you monitor blood pressure, they have no variation of blood pressure, no variation of heart rate and they still have impair of regulation because of the severity of the disease. I think the both spectrum of uh temperature reflect somewhere these disturbances of uh hos static mechanisms that you can observe. So we did a study on pigs simulating avalanche victims. And we went down to 28 degrees and we studied out regulation and there is a certain point these were not injured pigs. And I can't remember the exact degree, but I think at 30 degrees, we saw a signal that, that there was a clear derangement even in the healthy individual. So how does that translate to our, our patients? It's very difficult to say but yes, temperature affects auto regulation, auto regulation. I'm not sure whether it's directly in these 35 degrees or 36 degrees already, but maybe depending on the injury. I have a question for the three of you. Quick question, a quick response and you have one disease each. So we start from here, we discussed a lot about normothermia, but you mentioned it about hypothermia. So I have a question for you, which are the patients with a that you treat with hypothermia if you treat them? Of course, as I mentioned on my slide post CPR status and the patients with a poor comat status and even have intracranial hypertension. After applying the EVD, it means that she has diffused brain swelling. And the other case is the after the cardiectomy because we do the craniotomy for the poor grade S a patient. If she or he have a large or mid shift. In that case, the patients can get gain from the prophylactic hypothermia. So if I understood well from your slides, the use of hypothermia is very early in the manner for that the other patients I applied in pneumo for you. If you apply A T in which patients I applied only in cases of fracture, intracranial hypertension. When you arrive at the tier three therapies, I have to be honest that when I arrive at that stage, we generally go more for the compressive C gray, especially if the patient has a possibility of good uh neurological outcome. And in these cases, I I might use it as a bridge. You have spikes of IP you discuss with a neurosurgeon, you decide to go to the theater, this requires some hours at least in my institution. And in the meantime, to treat this crisis of I can use it Raymond for you. It remains several vascular diseases outside the sage. So I would say ischemic stroke or do you use epiderm? And in which patients? So I think for ischemic stroke, we have very little evidence. And as we, if we, if we apply correct treatment for the malignant isa stroke. We the operation is, is very early in our decision already. Um in IC H I think there is no evidence to treat patients with hypothermia. But we come to the same point. If I have refractory and I consider as tier whatever 34 treatment, I think there could be an option also for a specific patient population where we say that we want to apply all conservative treatments, but we don't want to operate on a certain patient. And there are patients that, that where the family says well, no operation but do everything what you can in conservative treatments. And and I think there are some patients where we can discuss based on ICP um the intervention but not on the physiology of. So we responded partially to the first question from that. At the end, most of the use of hypothermia specific hypo is driven by IC P or brain edema. And most of this disease is a common point. There may be time, we have time for three minutes. So at least one question from the audience. If you have any, if not, I can have the last one, maybe to the three question again. The same question for the three of you, we discussed a lot about controlled temperature and of course, you are very sensitive because we are in a meeting on temperature. Are you reactive? So you react to fever and you start therapy or you are prophylactic, you start immediately to avoid any fever. Maybe we start now from this side, Raymond. So we we conducted in a book, a very early prophylactic study in brain injured patients. And that actually that worked quite well and decreased the nursing load. And that's why we applied prophylactic hypothermia in several patients. Now, based on these data that that would be a nice discussion also with other people around the world, whether whether we should identify the patients who actually develop fever and then say, well, now now is the time to be very aggressive. And I think reactive is more the approach but in very severely sick patients which are sedated and intubated. I think temperature control is just part of the protocol. And and in these patients, I would still choose a prophylactic approach where I know that any, any nos of a difference, it could be co two as well or temperature makes a difference. And then, then I would, I would go for the prophylactic reg and I generally agree with Raimund just a comment regarding the reactive, I generally accept this case is more reactive. But if you just read the guidelines, they say when it's 37.5 start the treatment and this is very action. I think it's very important to see the trend. So if you see a patient who has 36 and then quickly starts to increase, I don't wait 37.5 I react a bit earlier because the trend is telling me that this patient is going to spike. So actually, I prefer to be prophylactic because I always put the continuous body temperature monitor for the patients who admitted to neurosurgical intensive care unit. If the patients have to stay in our unit for more than two days. In that case, I put the body temperature monitor continuously at first. And then I like to use the antipyretics as a regularly for the pain control and uh fever control. But if the patient shows the uh uh like you, like K says, trends up uh to the uh no, I cannot say. So, in that case, I love to apply the TT M device for as soon as possible as soon as possible. So uh we are at 1222 we have uh the last session starting in eight minutes. So we leave you the time to go up and maybe take a break, take some hair. Thanks for everyone to being there. And of course, thanks to the speakers for this great session. Created by
