Transcript Video We Have A New Consensus < Back to Summit23 Brain Injury Management We Have A New Consensus Presented by Dr. Andrea Lavinio Uh So Andrea Vino is um a senior consultant in the SCU. Adam Brook, very well known for this long time experience in manager of acute brain injury patients uh working with Devin Menon and others. And Andrea is uh um also great interest in TT M and has been really the leader of this group working on different projects trying to implement the consensus in the management of temperature in uh ischemic stroke. And sh first and now we are working on a new consensus on TB I. So I think that the lecture is going to give is we have a consensus. So I don't know if Andrea is online. Yes, he's online. So, Andre, if you can hear me, it's recorded. OK, perfect. It's recorded. But so you cannot hear me but you will, you will hear his talk. Get some. Yeah, the problems. Thank you very much for the invitation of sharing the work uh undertaken by a group of us on developing consensus recommendations for temperature control following stroke, saracho hemorrhage and intraparenchymal brain hemorrhage, which was published uh on the British Journal of Anesthesia. Earlier this year, we start off by sharing this diagram uh of brain physiology, uh which we have developed to describe uh what we do um as neuro intensivist um in trying to protect the brain from physiological insults and what you have there on the X axis, you have oxygen delivery to the brain which is cerebral blood flow multiplied for the arterial content of oxygen. And this can be hampered uh either by uh hypertension, hypoxia, intracranial hypertension, uh or conversely, um in some circumstances, if you have malignant hypertension or profound hypercapnia, uh you can have a hyperperfusion of the brain or hyperemia. And on the Y axis, you have cerebral metabolic rate and this is increased uh by fever and seizures. Uh and it can be modulated or decreased either by sedation of hypothermia. And so, in this diagram, you see that there is um uh the band there of coupled metabolism and brain, which is uh normal physiology for the large part of it. But you can also have uh when you move to the left uh reduced perfusion. And if that's not associated with the reduction in cerebral metabolic rate of oxygen, uh uh you may encounter hyperperfusion or ischemia. And so you really want to be in a couple of hypoperfusion uh uh hypometabolism when that happens. And this is uh represented here. So you have uh starting from the 0.1 at the center of the image, you have patients with normal physiology and when, for whatever reason, um due to shock hypoxia, intracranial hypertension or vasospasm. You have uh a a moment of hyperperfusion. You have to modulate um metabolic rate of oxygen to protect the brain from injury. And you do that by reducing um um temp brain temperature uh or by sedating patients. Obviously, we do all of those things at the same time as we try to re-establish uh uh uh brain perfusion. So, in this context, uh we we, we, we focus primarily on the temperature management uh aspect and we know that uh temperature I I is a vital uh uh variable modulating uh um uh uh host of functions in the body. So at the top left of the screen, we see that we can reduce metabolic rate of oxygen and um uh we can reduce IC P and also we can um modulate inflammatory response. But we know that uh in the top right, uh that fever as um uh uh uh a physiological uh um uh uh importance in uh uh responding to infection and enhancing immune immune response. Conversely, uh the negative in the bottom left. If you drop uh temperature, you know that you have higher infection rate. And this is something that we normally observe uh when we call our patients in our IC us, um especially chest infection, um uh represent the burden of complication in these patients. But also you have shivering uh and the side effects associated uh with measures to control uh shivering and rebound hyperpyrexia. Is also a potential uh complication of hypothermia. However, in the bottom, right of the screen, we see the cost of tolerating uh uh fever. Uh and that's particularly true in patients that have acute encephalopathies. Uh you have lower uh seizure threshold, you have uh overall CO2 production that's uh increased. And so, if patient has um say a brain injury and chest injuries, that's very difficult to control. And ICP hypertension crisis with brain hern nation reduces ischemic time. If you have compromised brain perfusion is an issue and overall patients are more prone to developing secondary brain injury when they have abnormally elevated temperature. And so it does make sense uh to think that temperature modulation would be uh a key aspect uh of um excellent care in patients that suffer a stroke. Um be it hemorrhagic or thromboembolic because it does modulate uh um um uh rist ischemic time, edema inflammation uh and in patients with mass effect, um uh I it may help control IC P. And so uh many of you will be familiar um with the literature. Um There are uh uh uh a long series of reasons and rationale why temperature management is key. However, the optimal temperature targets methodology and duration of treatment. Uh uh I I is unclear. Uh So at, at, at this point, we know that we, we have some rationale for a broader approach, probably uh uh patient and, and, and type of condition uh is key in determining the dose and duration of temperature uh control. So I if you have patients on the left that have a very tight brain or where you know that perfusion is compromised, then you might probably want to be at the lower end of temperature. And then if someone has comp compensated acute uh neurological injury, then you might be content with no theia and then in patients uh that are septic and have no acute injuries, they probably should uh be allowed to develop a fever as, as a response to infection. And you determine their place on that axis based on clinical information. And we are fortunate enough in our near IC U to have a wealth uh of physiological and clinical data for these patients ranging from imaging to uh neuromonitoring. However, we wanted to put this information together. And so uh in October uh uh um of last year 2022 we called for a group of experts from Knox to come together and we met on the 11th of October uh in London uh to use uh AAA Delphi process. Delphi process is a serious uh It's a strategy that was developed by uh uh the oil industry um to, to, to solve complex problems. So you would get a host um oo of experts and you would break down the issue in the smaller parts and you would cycles of uh um questionnaires. Um and uh you would revise the, the, the way you formulate each question and uh take the responses until you develop uh a set of consensus uh recommendations that you can act upon. And so we did exactly this. Um in this case, uh we um approached the British Neurons and critical care society and we had a, a group of 19 experts on neuro critical care um that came together to try and solve this. And we went through the whole process that's outlined there. And our work was published by the BG A earlier this year. And that's the final paper with the uh um name of the authors there. Professor Raba um uh was one of them and she'll be here um to answer questions afterwards. So, thank you, Kiara for that. And these are the consensus recommendations that the group came up with. Um And the many of them will make uh a lot of sense for most of you, but it was useful uh to have them in black and white and to set standards of care uh that could be replicated. And first of all, uh temperature should be monitored continuously. Uh And in those places that don't have access to continuous monitoring, then it should measure at least hourly. And next, some centers will use uh um um um brain temperature with intra brain temperature monitoring, with intraparenchymal um uh probes. But in, in most centers, core temperature is considered to be an acceptable um um monitoring. Um whereas uh surface temperature monitoring is not um acceptable. Another important point is that uh automated devices for TT M uh are indicated for high quality temperature control um especially in this case, uh for the treatment of the neurogenic fever, uh which we'll talk about in some more detail um in a few minutes. Another point was that that was hotly debated was whether uh uh controlled normothermia with an automated device should be started uh in all patients that are um um a admitted to our I use um uh following stroke or sno and hemorrhage. And the consensus was that this should be used reactively after the patient has developed fever um for, for practical reasons, uh uh primarily but also um because of uh costs associated with treatment itself and shivering. So the second uh bit of recommendations is about how to use uh target temperature management in this context. And the first was the target temperature and the target temperature in this group was identified as being between 36 and 37.5 degrees. The temperature variability has been identified uh um as a cause of burden of neurological insults in these patients. So, temperature variation was also set uh at a maximum of half a degree per hour and less than one degree for 24 hour period. And then for the duration, the duration of uh TT M and temperature control should last for as long as the brain is perceived to be at risk. And this is uh consciously left open to the interpretation of the treating clinician. And again, the use of an automated uh device uh is desirable to maintain temperature uh within those set parameters that we just identified. It was uh uh agreed that uh neurogenic fever that is a fever uh that the patient develops in response to a uh uh uh a brain insult. Uh rather than an infectious uh process can uh adversely affect patient outcome through the mechanisms that we have described. So, increasing cerebral metabolism, reducing seizure threshold, et cetera. And that this is important to prevent and treat it when identified. And we've identified it by monitoring temperature continuously, relying on core temperature monitors and to treat it in a way that responds to protocol care locally. And we've said we, we, we did mention earlier that this should be initiated reactively. And we've identified here a temperature of 37.5 as core temperature to begin temperature control in terms of shivering. Um We uh um uh had agreed that shivering was important to control. But um as in the second line, you see, there is the first area where we didn't find any consensus. We were trying to um probably help shape protocols for shivering here. But um it turns out that it's not as simple uh to define what the best first agent or second agent should be in that, you know, that paracetamol is very safe and broadly used. Uh However, if its effectiveness uh is limited to some extent and many of these patients will be sedated already. So, uh a neuromuscular blocker would be most effective and, and uh the the best way to control shivering in these patients. So, um uh we were unable to, to come up with a, with a simple uh a set of rules that can be applied to uh the very heterogeneous uh patient population we are dealing with here. Uh And, and we, we felt that the expertise, the local expertise will probably best placed uh to determine the appropriate agent to control shivering in, in, in, in those circumstances, we identified that controlled rearming should occur and this could be passive rather than active. Um We, we have uh in con consistently with the previous recommendation agreed that controlled rearming should be uh uh slow. And um we uh agreed on that rate being less than one degree per day, which was the same rate of maximum variability that we should tolerate in these patients. And that normothermia should be applied uh for as long as the brain is perceived to be at risk uh in these patients. And the last area um that we were trying to define is how to measure outcomes in this patient. And we f we, we, we found that this was beyond the scope of what the group uh was trying to achieve in that context. So, in conclusions, uh Uh After reviewing the literature and discussing the topic broadly with a set of experts um uh from the Neuro Anesthesia and Critical Care Society of Britain. We concluded that temperature as you know, modulates cerebral metabolic rate of oxygen. Um uh seizure threshold and inflammatory response following stroke. Be it hemorrhagic or embolic uh core temperature should be monitored continuously and maintained between 36 and 37.5 degrees uh using automated feedback control devices and that TT M should be commenced within one hour uh of first fever identification uh obviously alongside the good practice. So um in infection control and it should be maintained for as long as the brain to be perceived at risk uh of secondary injury. And that rearming should be controlled to reduce, reduce the risk of uh um rebound pyrexia, which is quite common in these patients. And this uh guidelines were endorsed by NC and uh um uh were published earlier this year on the BBJ A and just to give you uh a, a snippet of uh uh more work that's been undertaken uh about one year later. Exactly. Uh we met with an even broader uh group of experts to repeat the same work uh on traumatic brain injury, which perhaps was even uh e even more controversial. And uh uh in this case, uh we reached out to ex experts both from Knox in the UK and uh the European Society of Intensive Care Medicine and both Professor Raba and Professor Helber were, were part part of this work so that they'll be able to discuss this uh uh with you extensively. And um the, we, we are just drafting the paper, but I, I think I'm in a position to tell you the uh two interesting aspects that will emerge from it uh uh as a preview. Uh And the first, uh the first bit is that uh there is an update of civic guidelines uh which is going to be impactful in practice. Uh In the 2019 recommendations, we had uh tier zero, prevent fever. And then in tier three, uh um prevent or con consider my lipo theia. Uh the modifications that emerged from this um uh consensus um meeting was that uh um controlled normothermia should be included in tier one and that's going to affect a large number of patients. Uh The uh other um um insight that emerged from the this work is that when doing temperature control in these patients, we should really um individualized care by thinking about uh uh the source of fever. So some patients will have a fever that originates to a physiological response to sepsis. And some other patients will be developing fever because they have uh this regulated temperature control. Uh And conversely, we have patients that have very tight brains, they are very high risk of developing secondary brain injuries. Temperature is uh allowed to go above physiological levels. Uh And at the other end of the spectrum on the X axis, you have low risk patients. I'm thinking patients in the sub acute phase uh of severe TB I, for example, where um infections are common. And so there is uh on the left in the blue box, patients have very tight brains in the hyper acute phase of temperature where temperature control needs to be extremely strict. Uh either control normothermia or even uh um uh uh therapeutic hypothermia when IC P is not controlled with first or second line treatment. But in the um in the lower risk of acute phase uh of TB I, we have patients um that develops sepsis where perhaps uh uh permissive uh pyrexia um should be tolerated. I thank you very much for your attention and uh um uh I, I leave the audience to Professor Rob with many things. Created by
