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Hello, everyone. Uh, welcome to our middle education event. Apologies for the delay. I know we are about eight minutes, uh, late in starting, we just had some issues with, uh, slides and, and everything, but we've got slides which is really important. We've got slides and we've got hose with us as well and it's gonna be a great event. So, what I'm gonna ask you to do is, um, pop your questions in the chat. We'll answer those at the end of the event if that's ok. Um, your feedback will be in an email in an hour's time to you and your attendance certificate will be on your medal account. Ok. So, like I said, questions in the chat, you know, I won't have any conditions way above my knowledge. So put your questions in the chat and we'll get around to them at the end. Ok. Over to you. Thank you. Thank you very much and, uh, welcome everyone. I'm really sorry for this always. Uh, we are getting used to it for this, um, informatic issues, but eventually we got it here and it's a huge pleasure to be here to share a couple of ideas with you about traumatic brain injury, which is, which is part of my activity as well with neur oncology and of course, welcome you everyone to London. Um and just to share what is our experience in dealing with this very complex group of patients and with these very complex group of intracranial pathologies. So moving forward, um just a quick outline of my presentation are going to go through a little bit of epidemiology on traumatic brain injury following by the classification from a clinical and from a type of lesion point of view, focusing on some of the most important ones. Then moving to multimodal monitoring and what we can offer. What is the kind of the cutting edge of the management and the research in the management of traumatic injury touching upon some complications with case reports and what what um examples of how we integrate all these um technologies and ways of monitoring and treating these patients in our in our current um setting and then some final closing remarks. So in terms of epidemiology, this is basically made from coming from Western literature, but we know that falls um is now taking the vast majority and occupying the center of the field of traumatic brain injury where we are assisting to decreased number of traffic incidents. Of course, we know that in other areas of the world, particularly where traffic enforcement rules are not very well established yet the traffic incidents, they kind of occupy a much larger fragment of this population. It is particularly significant in both extremes of the of the age groups, which means in the young population, particularly young adults, but particularly in Western countries. Very important as well in elderly population because of the falls because of people that are increasingly on risk factors for severe traumatic brain injury, particularly anticoagulation for aVF for diabetes. So this group of patients is where actually most of the ethical dilemma about the management and is now a hot topic for discussion, but just let's go back to basics and some very broad classification about the clinical severity of traumatic brain injury. And this is the classic one where we can classify any TBI into mild, moderate or severe accordingly to the duration of unconsciousness. According to the classification of on the Glasgow coma scale, most of us are familiar with it. We are going just to recap in a second and as well as posttraumatic amnesia. So the most important of these three, actually, it's gonna be the Glasgow Coma coma scale score where in between 13 and 15, the usual classifies a mild event a moderate between nine and 12 and a severe when a patient requires intubation. Which means when the Glasgow coma scale is below eight, there are more complex attempts to classify TBI particularly with subclassification in mild TBI. I, this is important even though it is difficult to have a widespread acceptation of what are the criteria for these multiple categories of mild TBI. Me personally as a neurosurgeon, of course, mild and moderate TBI is a type of traumatic brain injury patients where we don't get involved as much as in patients with severe and critical TBI, both in terms of treatment and decision management. However, there is an extensive research going on about the sequela of the mild TBI that is most of the times overlooked. Uh mild TBI is of course, much more common and frequent than the others. And patients sometimes suffer with post concussional syndrome, with memory issues with attention deficit in the weeks to months after mild TBI S. And that's why we need to look into more detail about the different categories of mild TBI. So a patient that is slightly confused after a traumatic brain injury, they are not all the same. I think this is one of the key messages that I think it's important to pass on that these patients need support when they come back to the community because at the higher cognitive level, things may not be as good as we initially thought at time of this structure. And the glaucoma, I would say the most important thing um and the message to pass on to some of you, of course, we are neurosurgeons, we communicate a lot on GC S. But those of you that are not from the neurosurgical field or the neuro neurology field, it is important to understand that glaucoma score is not a continuous score. So each number, it's not, the patient is somehow 1012 and this doesn't make any sense. OK. A patient is either GS 10 or GCS 12 because each of the breakdowns and each of the responses are very clearly identified. And you are now more than 40 years since Mr Tisdale published the Glasgow score. So it's a very well established in the trauma community this way of communication. And it's very clear, it is very fast, but we need to understand that it is not a continuous scale, which means each number has a very significant um very significant meaning that it will impact in the decision making process in those, for example, as our, as it happens with us and are at the other side of the line. Um Just a few things that most of us we may not be aware of, which is where is the anatomical location of the different motor response. Of course, out of all the subclassification of a glaucoma score, which is eye response, rubber response and motor response motor is the one that has a higher impact in the outcome and particularly when we come to M two and three, which is abnormally flexion or abnormally extension. It is important to understand that there are some extra pyramidal tracts that are um involved, particularly the rubrospinal tract in patients that are decorticating or having an abnormal flection and patients that are extending. It's more a hyperactivation of the vestibulo spinal tract. So these are not responses that come from the corticospinal tract. So, it is important when we see someone with M two and three, and we try to establish if there is a symmetry or a symmetry in the response, we need to understand that those responses are not coming from the corticospinal tract. And therefore, they provide us very limited information when it comes to supratentorial um health condition of the corticospinal tract or for example, in terms of spinal cord injury, because again, these responses are not coming from the corticospinal tract. When it comes to the different types of, of injuries. And GBI, there is a multitude and even though we always like to kind of do these boxes and to put them and to try to fit the patient into one of these box, external extra parenchymal subdural contusion, intraventricular fracture. The the reality is that in the vast majority of cases, the patient may have a dominant injury. Is it a contusion? Is it an exo hematoma? Is it a subdural hematoma that is the dominant injury after that TBI but multiple other injuries are happening in the background. For example, posttraumatic sub hemorrhage that you can see on the bottom left is by far the most common posttraumatic injury, but is not always the dominant one. So it always happens when you have a subdural matoma, when you have a contusion, when you have an I VH almost always a patient will have a traumatic subrenal hemorrhage as well. So we will try to focus on the treatment for each of these most representative pathologies. But I would like to start by saying that we need when assessing a patient to understand what is the dominant feature, what is the dominant pathology that is responsible for the clinical scenario that we are seeing in front of us and starting with the most common one, which is a chronic subdural hematoma. We can see here good examples. For example, on the left, we can see even a level uh between more acute blood and more chronic blood. And here a very, very significant chronic subdural hematoma with subside herniation, we can see that the midline structures are pushed from left to right with a two centimeters midline shift causing already what we call hydrocephalus because of the occlusion of the foramen of Monro. So the lateral ventricles are not communicating with 3rd and 4th because of the mass effect are occluding these natural communications between the chambers of the brain. Um and therefore, this is a real real emergent situation. Usually, these patients are old patients that are on anticoagulants, patients that had a traumatic brain injury in the past with some acute blood that then became chronic. And when the blood becomes chronic, one or two things can happen, either there is an increase in the mass effect or the blood is subsequently reabsorbed. It is almost impossible to predict based on um on the initial presentation, if that acute blood is going to evolve in a chronic way or it is going to be reabsorbed. And that's why these patients need to be kept under close follow up. Just to give you a little bit of an insight about the physiopathology behind the chronic subdural hematoma. I would say that I would like to draw your attention to this image over here where we have again, it's a subdural hematoma. So it is extrarenal. The parenchymal is pushed by the hematoma but it's underneath the dura mater. So we have skull dura mater, here is the hematoma and then the whole hematoma is outside of the brain. Usually these hematoma, they have two capsules or two membranes, one outer, 11 inner one and sometimes we have blood in, in m in in both sides of these membrane. So that's what we call when, when a sub hematoma has multiple membranes um inside of it. The most common etiology is as you can see these, these veins that are stretched in the central space, particularly if there is a, a trauma that makes sometimes an acute bleed or sometimes just a continuous oozing from these veins that is enough for in a period of a couple of days to develop this collection and then start to exhibit some mass effect over the the brain. And then we'll have either focal deficits related to the mass effect related to the area of the brain where the hematoma is pushing or we may have some more generalized symptoms. As for example, headaches, vomiting or decrease of awareness. It is important to know that as the name implies, the chronic sub hematoma takes days two weeks to develop it's not an acute event. So to sum up our um our ideas about chronic surgery, hematoma, I usually look for a previous TBI, even though particularly in the elderly population, a previous TBI people may not be either aware of it or it is so minor that people don't. And that's why in the other population, you may not have a clear evidence of previous TBI in terms of pathophysiology, bridging veins much more common in older patients, old patients. Why? Because this space becomes a natural space in the old population as the brain evolves or evolute at the later stages of our life, the space between the brain and the membranes will increase, which will increase the stretching of the veins. And they are making this population more prone to have these conditions c head gold standard even sometimes better than the MRI to assess the true impact of the, of the, of the hematoma. And they prefer, the preferred treatment is with tuber holes, which means we do two incisions separating the skin, we perform tuber holes, we evacuate the hematoma that is liquid at this stage. And then we leave a drain. Recent evidence, particularly since the Swiss trial showed that leaving a drain either underneath the skin in what we call a subdural position or underneath the dura mater in what we call a subdural position, have equal efficacy in dealing with the recurrences because these patients are prone to have recurrences of these hematoma. And we have evidence from UK from Cambridge or landmark evidence saying that treating these patients with a drain in situ is better in preventing recurrences rather than when rather than if we don't leave any drain. Moving on. Let's move to the extra hematoma, which is probably alongside with hydrocephalus, one of the few a lifethreatening conditions at this time, critical dependent. So an extra hematoma as the name implies, happens outside the dura mater in this virtual space between the bone and the dura mater. And it's almost always associated with a skull fracture. So why is that we have the jura mater very close attached to the bone and the fracture is very likely to catch one of the rami of the middle meningeal artery, which is the most common source of bleeding for the act hematomas. And if there is a fracture, there is an arterial bleed, most of the times there are some venous ones, but those are less common and they will develop this kind of b concur uh shape hematoma. Some people describe as well as a, as a lemon. And why is this um why is this hematoma has this shape? Because the dura mater is very attached to the, to the skull in certain points of the skull, which are the sutures where the bones come together. And that's why we have one suture here, one suture here that hematoma cannot dissect and you know, bridge that virtual gap between the skull and the jura. And that's why this hematoma develops. For example, if you compare with the subdural hematomas, these are chronic but acute is the same thing because they are underneath the Jura, they don't respect the sutures. And that's why they have this kind of crescent or banana shaped appearance in terms of neurology. Most of the time in these patients, we have uh neurology coming from ipsilateral compression of the brain. However, a very well known phenomena in um the neurosurgical literature is at no one's notch phenomena which is when the pressure is by the hematoma compresses, the brain. In particular, the brain stem against the other side, the other edge of the tentorium. And that's why in 10 to 15% of the patients instead of having contralateral neurology and ipsilateral papillary changes. Actually, the patients have leisure have a clinical manifestation from the compression of the side that is contralateral to the hematoma, which means in the majority of patients with this hematoma, these patients will have contralateral hemiparesis and ipsilateral uh um pupillary dilation. But in 10 to 15% of the cases, they will have ipsilateral hemiparesis to the site of the hematoma and contralateral papillary dilation. This is because of the kernels notch and the compression of the contralateral site at this level. So how we perform these surgeries? These most common uh require a craniotomy and not and not um bur hole evacuation. And as you can see, as soon as we open the bone, we have hematoma straight away. And only after the evacuation of the hematoma, we have to run out. So as soon as we do our bur holes in the bone, we'll see hematoma straight away and we can start evacuating immediately. So for example, if you are in a place where you don't have quick access to, to um to a CT scanner, we can always do exploratory bur holes and we always start because of this because 80 to 25% of the patients have neurology have ipsilateral pilar dilation and contralateral motor weakness. This will guide our exploratory burle and then we can extend the craniotomy, just be careful because our craniotomy, you usually have a fracture that is the primary responsible for the hematoma inside, inside the flap. In terms of technical uh nuances for those of us that are um neurosurgeons. For example, I think that this craniotomy was suboptimal for the for hematoma. Usually it is important to do a craniotomy that is slightly smaller than the extension of the extradural hematoma. So then we can use tack up sutures, we can pull the dura to the bone to prevent recurrences of the extradural hematoma. And if you do a craniotomy that is larger than the extradural or the epidural hematoma, you have no physical bone, do the tack up, sutures. A mass, you do a popping stitch which is a stitch in the center of the dura and then you attach it straight to the, to the bone flap when you reposition. But ideally, our craniotomy should be slightly smaller than the hematoma to allow for us to bring the jura in a more uniform way towards the the edges of the bone and prevent recurrences to see if I can move. So in terms of take home messages for extradural hematomas, a true neurosurgical emergency. So, neurosurgeons need to be involved from the moment we consider uh as a possibility in extradural hematoma, always look for arterial bleeding in the middle meningeal artery. Usually, I don't, I don't like to say usually because it only happens in less than a third of the cases. 30%. We have this lucid interval that is classically described. The patient has a traumatic brain injury is ok and then becomes into a coma. A couple of, you know, one hour, two hours after the event, when the hematoma increases significantly the intracrine pressure. So this is AAA classic distinction or difference between extra and um then the city has in the gold standard and again, trauma flood. The next one is the acute subdural hematoma and the acute subdural lymphoma as we discussed before, has it crescent shape instead of that by convex shape and usually the subdural hematoma, the there are two completely different pathologies. It's what we call the subdural hematoma of the elderly people that comes with minor trauma in patients that have um that are, for example, on anticoagulation. And those can have if I'm allowed to say a pure subdural hematoma where we have subdural blood compression of the brain, but sometimes not even traumatic subrenal hemorrhage and definitely no contusions or anything like that. And then we have the subdural hematoma from the young population where it happens after usually um um a high intensity trauma or a high intensity traumatic brain injury. And in those situations, usually we describe them as burst lobe syndrome more commonly on the temporal lobe where we have literally a, a burst of and, and, and and a severe contusion of both the brain. And then we have the adrenal hematoma on top of it. And that's because it's a more severe injury of blood outside the brain. But as well contusion in the brain that these patients, for example, they don't have the lucid interval, they are unwell immediately after traumatic brain injury. So again, from the clinical history, we can have some clues about what type of injury we are going to to identify in the in the CT scan. So this is a different scenario. So for acute subdural, we need to do a larger trauma flap when compared with uh with the actual lymphoma. And as you can see the blood, we only find the blood after we open the jar. Of course, it is safer to open the here because the blood is pushing the brain away from us. So we can open quickly without as much dissection as we would um require to do if we are doing an elective case, for example, and then you can see here very well the contusion in the brain as soon as we take the blood in the central space. So this is a classic case of um of a burst lobe. Again, this is just another example. Once we, once we elevate the bone, we can see it's a very tense dura, a lot of hematoma usually here, the blood does not come or the bleeding point is not the middle menage artery that is extra duro here is usually a cortical artery that as soon as we take the clot starts spreading and we need to control. So take a message we have venous but also arterial bleeding. It's an emergency, a large craniotomy, potentially a trauma flap. Then we have skull fractures and skull fractures become much less common, particularly since the widespread use of helmets um in a motorcycle and particularly in bike um accidents, there are different fractures that we are, we are going to see. These are the ones that we as surgeons are more concerned about, which are the depress fractures which may require elevation. The least of our concerns will be in an acute phase, the cosmetic appearance, even though that should be taken into account. For example, if you have a depressed so fracture in the forehead, um but because there may be laceration of the dura, there may be a contusion in the brain underneath which may be prone to uh seizures. And if there is uh an open wound on top of a depress fracture, there is the risk of contamination and infection that can spread. It's not just superficial but can go uh intraaxial as well. So I'm just gonna to touch upon what are the the main divisions of skull fracture. We have diastatic which are usually high impact because they open the natural sutures of the skull. We can have the breast skull fractures that we may have to inter as well is a particularly high risk. One always be very concerned about the breast fractures. If they are overlaying severe sagittal sinus, it's always at least a two surgeon operation because these patients may lose a significant amount of blood in a very short period of time. Then we have the linear fractures, the ones that usually particularly in this area of the pterion and the temporal um the temporal, the temporal bone, they can produce a laceration of the middle meningeal artery and be responsible for extradural hematomas. And then we have the basal fractures, the one that we are going to look for it. It's not that they are such a surgical emergency or a surgical emergency, but they will, they can have those external signs that to look like, for example, the Bartle sign or the chemosis in the pits bone, they can have the raccoon eyes bilaterally. They can be, they can be associated with cranial nerve deficit or pseudoaneurysms if they happen in the prus bone or in the sphenoid bone. So those are the ones that we may not need to do anything acutely. But the patient may have more um or maybe more impaired. For example, you can have facial palsy in a fracture in the pits, you can have auditory impairment that require a follow up. So if you are in a kind of a a setting, these are the ones that we need to look for the signs, not to be out acutely, but to know how to, how to follow up these patients in the community and what kind of support they will need. Then we have the fourth classification for fractures in the craniofacial complex. And the ones that we are always more concerned is the 43 where we have a complete dissociation between the skull and the face. This will require always surgical treatment. So just some notes. Uh and I'm very happy, II mean, I don't know, but I'm very happy to share some of the slides if you want. Uh in the end, I'll take everything that is patient sensitive. And I'm happy to share. This is a nice um way of thinking about um the skull, about skull fractures. So all these be very concerned about the breast open, what we call compounds, uh compound skull fractures. They require nurse exploration pretty much all the time linear. If it's in the vault, usually you have some scalp hematoma but nothing else that we need to be kind of aware of the buzz ones. Nothing that needs usually surgery in acute setting, but always be concerned about what's happening in terms of neurology, how this patient may need support in the community after discharge. So this is an example of a nasty fracture. As I was saying, a fracture going over the superior sagittal sinus. This is a critical, this is a very difficult surgical management. We need to be prepared with two units cross match. We need to have an experienced anesthetist on the room, an experienced surgeon on the room. And we need to have before we start operating, we need to know step by step what to do if we have taran bleeding from, from a venous size, growing skull fracture, a problem particularly in the pediatric population. If you can see here fracture, acutely fracture, a couple of months later, basically what's happening is there's a kind of a sudden meningocele and the bridge in the membranes, but it's contained usually you have Arachnoid or PMR just overlaying the CSF space but because of the possibility of the brain, there is a like a water hammer effect and this water hammer effect keeps pushing, pushing, pushing, pushing this collection here, bringing the skull edges apart. And you have particularly in a skull that is so flexible and mobile as in Children, it's very, very easily. You have these growing skull fractures that you require opening, require tidy and resuturing of the dura mater to avoid this water hammer effect and sometimes to do a coroplasty to cover the bone defect. So skull fractures, urgency maybe, ok, we may or may not have to have neurosurgeons involved. Very careful with sagittal sinus bleeding. I always tell these to all our trainees and to myself, you know, if I'm going to operate one of these patients, even as a consultant, I always have another person scrub with me. It is very important. We need to have a very clear plan before careful with delayed epilepsy, particularly in the breast skull fractures where we have contusion, careful with growing skull fracture. So don't discharge these patients particularly in the pediatric population because we may have to do craniectomy, cranioplasty. We may have to do a little bit of construction work with small plates. So always be prepared and creative to minimize, to minimize the the the deficit and the cosmesis deficit that you may have intraventricular hemorrhage quick. Uh uh Word about it, it's usually a sign of a high energy trauma. For example, as you can see here, as I said before, it's never an isolated injury. The dominant feature is the I VH. But also we have here very well are traumatic uh subretinal hemorrhage. So we deal with these patients with an external ventricular drainage that it's a catheter that we put in the ventricle that allows at the same time to have idea of the intracranial pressure. But as well deal with a problem that will develop soon after which is the hydrocephalus blood and particularly a cast of blood in the ventricles will not allow for the normal circle of the CSF that is produced in the cry plexus to the outlets of the fourth Luca and more to allow the subarachnoid space to to absorb the CSF. And therefore, these patients may suffer with hydrocephalus, which in the acute setting can be treated with an external ventricle drainage. There is some evidence and some new evidence, for example, for trials run in the UK has missed the trial. And then we can put some thrombolytics inside the ventricles to help just for this clot to be reabsorbed. And then we can eventually aim to remove the EVD or if these patients become chronically dependent of an external ventricular system to drain the CSF that is produced. Then after the blood has been reabsorbed, we can just put an internal system and we put a VP shunt. There are different ways of me intracranial pressure in these patients. The most common by far are the intrarenal. This one here and the intraventricular. However, we can have subretinal bolts, epidural bolts, but they are less reliable. We'll talk in a second about a little bit more about um ICP and this is what this patient had catheter in the ventricle to deal with uh the hydrocephalus. So interesting. It is commonly associated to diffuse axonal injury that we talk in a second. But the surgical treatment in this patient is minimal. It's mainly ICL where we provide with an ICP probe or an external ventricle drainage information and a treatment way to manage raised intracranial pressure in this population. And this is a good example of diffuse axonal injury where we can see a very unexciting ct scan, but a patient is incredibly unwell and this happens usually after a high speed um trauma and with a severe acceleration, deceleration motion at the time of the trauma. So if we put this patient in the, as you can see here, this is at two star or wy sequence that is very sensitive to paramagnetic material, we can see these microbleeds in the cortical sub cortical area in the corpus callosum. And I'm sure it went all the way down in the brain stem, which means that in these areas that are very more prone to, to stress and to share effect, we have just a disconnection, an injury, a sharing between the white matter and the cortex. And that's why these patients are very unwell with poor neurology and they may have a very poor neurological recovery in the long term despite a kind of blunt initial ct scan. So again, every time you have severe neuropsychological impairment in an otherwise unexciting CT scan, or if the patient is just not waking up and you don't have a clear explanation, sometimes the MRI can provide you imaging clues for what's gonna what is happening with this patient. Um I would like just to start dropping a couple of ideas about Mo Kelly and about the intracranial pressure compliance and the way the way the pressure um goes up and down in the brain. So the Moholi says basically that intracranial pressure is uh a mixture of CSF blood and blood parenchyma and one of these compartments goes up. The other ones of course goes down and they go down in the only exiting point from the cranium, which is a fro micro. That's why in cases of severe raise intracranial pressure, you have tonsillar herniation and compromise of the blood supply to the brain. Usually the first space that reduces its volume. In cases of an increased pressure is the CSF followed by the venous blood and then followed by the arterial blood. And that's when we have ischemia. So if we have a growing volume, a mass, for example, a hematoma inside the brain, what we see that initially, our brain is able to compensate with these mechanisms and blood is increasing. CSF is growing, then the venous compartment is growing as well from inside the skull. But as the volume of the hematoma increases our ability to compensate, decreases until a point where there is a steep increase in the intracranial pressure. So of course, if this patient comes to medical management here, this is usually a very tricky condition to be because the patient is very unstable and we should try and optimize while we still have some compensatory mechanisms and compensatory reserve. When this is exhausted, the compensatory reserve, then a small amount of increase in volume leads to a sudden increase in the CSF pressure which again, sometimes even just release a little bit, the pressure is enough to bring the patient to a safer end of the curve, but it's still a very unstable situation. And that is why, um, in terms of dealing with ICP medical management is usually at the foremost treatment. And we should, if there is a lesion that should be resected or that should be evacuated, we should attempt that and then deal with patient on a medical way. And then there is a role for the decompressive craniectomy. Um, we have the deer study that was negative and these were patients that were randomized and they had a primary decompressive craniectomy. So they were not through a trial of medical management to deal with at the risk of intracranial pressure. They were just decompressed at time of admission to the hospital. Then we have the Rescue ICP where that has just been published um that decreased mortality in the group of patients with um decompressive craniectomy with an increase of patients with poor outcome, which is what we kind of expected. Um but this decompressive craniectomy was done for secondary injury. So it was not done at primary treatment only in refractory ICP S to the best medical management and it was a control arm against um thiopentone. And then we have the recently published paper on the rescue ADH that proved no benefit in terms of overall survival and neurological outcome of primary decompressive cardiac to me at time of surgery for an acute compared with patients where the bone was kept in place. And the main difference was of course a higher degree of surgeries, a higher number of surgeons in patients where the bone was was kept in place and more complications related with coloplasty in patients with primary compressive cronies. So those these were kind of surrogate or kind of predictive outcomes related with the army you have been randomized to. And the final lesion I would like to touch upon is a sinking skin flap syndrome, which is a cause of delayed deterioration in patients that are actually recovering well after initial management of traumatic brain injury. So as you can see here, these patients that have a bifrontal decompression, which is something that according to the brain trauma foundation, when the evidence to support. This surgery is not quite there. But again, for certain indications, for example, these patients with very symmetrical injury in the both frontal lobes, we felt it was AAA good indication but a couple of weeks it start deteriorating because as the swelling comes down, you have the severe sinking of of the flap because of the effect is also by the external um atmospheric pressure on the brain. And the treatment for these patients is we need to proceed with an emerg. I don't like the word emergent but we did expedite or urgent cranioplasty to try and restore the the intracranial pressure. Moving now to a quick word of uh multimodel monitoring, which is the second part of my presentation. And I always like to start with this slide uh from the team from Cambridge where a very nice paper where they said basically that and the main conclusion was that regardless um the protocol that each institution may have to deal with these patients, it is better to have a protocol than not have a protocol at all, which is protocol driven therapy has been proven to improve the outcomes of in neurocritical care after traumatic brain injury when compared with, you know, a management without a clear fixed protocol. And that's why you know it of pave the pave the way for people to start working in protocols. Uh The like concentrating cohort these patients in the same critical care units to improve the expertise in dealing with these patients. And therefore, as a group, we can improve um the outcome uh of of these patients, I would like to start with the ICP, which is probably the first um and one of the most widespread use techniques of, of multi model monitoring. Um Basically, this is the, the normal ICP curve, which is P one higher than P two higher than P three has some similarities with um the BP curve, but the P two happens in between. So this is when you know, when you have the, the blood going in the brain, this is the compliance curve, the way the brain deal with that sudden increase of pressure. And then this last spike, last notch is the closure of the aortic valve. And this should be the normal morphology. And that's why having a number on its own without having the curve for me as a surgeon doesn't help me that much. I like to see the curve. Actually. Sometimes I become suspicion of the number. If I don't have a curve, you know, there are different numbers. Usually we should treat definitely when the ICP is below 20. Some patients in some trials, for example, rescue ICP was below 25. But you know, it's not like at 19, we are all relaxed and at 21 it's an absolute emergency. I think we need to understand the trend of the pressure and we need to look at the curves. So the curves will help us to interpret the number. And if I have a curve where P two is higher than the other two, means that this patient is already in the face of the curve where he is not compliant at all. And that's why I need to be very aware and probably aggressive in the treatment of a patient with that has a curve in this shape. We will have a couple of waves that are normal or prognostic um um variabilities of the waves of ICP and the numbers, but where we may not need to work necessarily upon it. So starting from the end, the sea weight are just fluctuations, small fluctuations of of the, of the CP related with the breathing pattern. Then we have the Lundberg B waves that can be slightly higher fluctuation that can last a couple of minutes, but usually the fluctuation is still less than 10 M 10 millimeters of mercury. And then we have what are the cannon waves or the lumber A waves? And these are usually sudden raises in ICP way above than 10, sometimes up to 50 millimeters of mercury that can last up to 10 to 30 minutes and they don't respond to anything we do. And then without us doing anything, you know, the ICP just gradually comes down. And these are the poor protic waves of mis compliance and a autoregulation of the brain. But again, we need to be aware that sometimes we can rush the it has happened to all of us, we rush the patient on to theater, for example, to do decompressive cy. Whenever a patient gets to theater, the ACP is back to normal values. That was a Lundberg a wave um that, that we were witnessing, then we have the CPP and this this context of cerebral cerebral um pressure perfusion that then will open the path to the more new concept of pressure relativity index. But the CPP, the classic teaching is that we are able to route to regulate the BP in our brain between 5100 and 50 millimeters of mercury. What does it mean in between this range of pressure? We can just with dilation or constriction of the veins, maintain a constant blood perfusion. So we are protecting the brain from hypotension and severe hypertension when we go way beyond these numbers, that's where our autoregulation is this. You know, we can't keep it and that's why it becomes we will have even with maximal dilation. Look, there is no increase the the blood flow in the brain is decreased. And here with the maximum constriction, still, the BP is so high that we can still um increase the flow in the brain. The classical teaching is that when you have a traumatic brain injury, we lose this capacity. And that's why there is a almost a linear correlation between uh the cerebral blood flow and the perfusion, the cerebral perfusion is the minority of BP minus the intracranial pressure. We know that this is not necessarily which one. Again, we come back from the landmark work from Cambridge with the developing of this pressure reactive index. And we also have the oxygen reactive index which is basically in each time point. Understand what is the best intracranial, what is the best um BP target for the reactivity of the brain in that moment in time. Which means for example, now I may have a very good BP to keep a very good ICP and blood perfusion. That can be it, I don't know, for example, 100 then a couple of hours later, actually, I may need 120 of millimeters of mercury to have the same, the same sweet point in between intracranial pressure and cerebral perfusion. And basically this is a very continuous, it variates the patient adapt, has his responding to his traumatic brain injury. And our as as our intensities likes to ask, what is the CPP target? We always need to be very aware that the answer for a CPP target A is variable and it needs to be calculated every moment in time. And that's why most of the times we as surgeons, we protect ourselves. And we, we mention um we mention uh an interval of CPP instead of a single figure, a single number. And the preliminary data shows that patients that have a better P Rx that have a, a more um constant and uh and adapted um cerebral autoregulation have better outcome. Then we have the P two ability to measure the intracranial and tissue oxygenation. There are a couple of trials boost two was a phase two trial that shows some potential benefit of P two, even though it was not powered for outcome measure. Then we have the French study that showed no benefit because again, we are just measuring the oxygenation in the tissue around the probe. So it's not an overall measure of the brain. It's very focal. And that is one of the criticisms. But this trial was impaired by a lot of technical problems related with with the probe. And we are still waiting for the large boot tree and bonanza trials that eventually we are hoping to provide us with level one evidence um from the RCT about the use of tissue oxygenation measuring when the pressure increases, the tissue oxygenation decreases. This is one of the ways there are multiple ways. But again, we may have, for example, to hyperoxygenate patients to target uh blood transfusions to these markers. There is a lot of things that go a little bit beyond the scope of this presentation that we can do based on the feedback and information we are getting from the P B2. And I will say the the last kind of um technique that is still very experi not experimental but research based is the use of microdialysis and how we can and with the analysis of the brain metabolites, particularly glucose lactate, pyruvate glycerol, have an understanding in terms of prognostication uh of the traumatic brain injury and how we can modulate our treatment, particularly, for example, glucose management just to give an example to and the ratios and to the redox state of this patient, which is the information that the micro dialysis will give us. There is a consensus stated uh from 2014, again, very leaded by um and by the people from Cambridge about the potential um uses uh of the micro dialysis and how to interpret the the results in the metabolites coming from it. Then coming pretty much to the end of these, I would like to, to show you one slide about what are potential complications. And don't forget, as I said, that neurosurgery intervention is not restricted to the acute face. We may have infections particularly if we have fractures that were just closed, primarily without surgical exploration. So always be aware that can be a problem. Patients managed initially with evds or external venal drainage can develop ventri colitis that they require as well. Um Management we can have post uh or delayed hydrocephalus. So in patients that have blood intraventricularly or in the subarid space, they may have circulation and reabsorption problems in the CSF that may not be apparent as they come to the hospital, but they just become a period a couple of weeks later. And these delayed hydrocephalus may require CSF diversion. So every time you have a patient that is recovering well from a TBI and seems now that it is becoming static or deteriorating, always have a low threshold to we scan to rule this complication. And we have posttraumatic epilepsy. As you know, there is no evidence for prophylactic um for prophylactic uh antiepileptics in TBI. However, patients with focal laryngeal lesions. And again, let's put again here, some emphasis on um penetrating brain injury, contusions. They seem to be slightly prone to have this sort of um complications. So last slide, some closing remarks, this is an example of a case I did recently. And this is just to give you an idea of how these things become complex and integrated. So it's not just to open the skin to do a craniotomy. This was a patient with contusions with the sub that we wanted to put to the multimodel monitoring. We have here a probe that is responsible for IC PPB O2 temperature information. And we have here a probe responsible for microdialysis. And we also have some subdural um probes that are going to give us information about the electric activity of the brain. The concept of spreading the polarization that um my colleague, Doctor Sharon Jewel and Professor um Anthony strong in our unit are leading the field in terms of the investigations and we in theater to provide them with the tools that then will help to do the management of this patient for the next week or two weeks in ICU to maximize um the outcomes. So TBI is complex. It's complex. Acute insult that requires a multidisciplinary team to deal with this. It's not just surgery, it's just not trauma, it's not just i it's everyone together. Um the treatment goes beyond the acute management and don't forget that some pathologies are time dependent as for example, extradural hematoma, but we may have delayed complications that require surgical intervention such as infections or delayed hydrocephalus or the sinking skin flap syndrome. This is very important regardless um the the capacity that means your, regardless of what you have access to in your institution protocol guided treatment. That is the that is the cornerstone of traumatic brain injury. Ok. I think we always need to have this reality check. Where is my practice? What can I do? But if this is what I have access, we need to have a protocol. So there is a standardized treatment of these patients. This is what alone will improve the outcome um of these patients. The current research is is focused vi would say in um in secondary injury in terms of primary treatment. Ok. We still treat an EK today as we were treating 40 years ago, more or less. But the the cutting edge of the research is what after the patient leaves theater with a severe traumatic brain injury, what is happening? Uh And again, just to reinforce that neurosurgery involvement is either in acute but also in the delayed and chronic um stage of TBI management. Thank you very much. I'm open to any and every questions you may have. I'm very happy again, as I said to share some of this information, to share more information if I had in a more updated presentation that I couldn't upload to you today. I'm very happy to hear from you. Oh, we've got some questions. Oh, thank goodness for that. Uh So I am actually going to start our Q and A and the first question will pop up at the bottom of the screen. Can you see that? Mm Yeah. Yeah. What's that? So what thank you, Mustafa, what are the effective strategies for preventing uh traumatic brain injuries? That's a very good question. So, and as I said, as I showed in that um in that uh slide of, of the epidemiology that is a slide after, after, after a lot of, of public health uh public health um measures have been put in place. So let me give you the example, for example, in London now, uh inside London, we cannot drive above 20 miles per hour in the majority of BS. So I think the traffic regulation was key to change the epidemiology between western and non Western countries to be honest with you. Um Also it is important to um to tailor how many patients are on anticoagulants and on aspirin patients, we still have a lot of patients that come on primary prophylaxis with, with anticoagulant therapy that they don't know exactly why. So I think we need to work closely with our primary care physicians to, to, to understand and to try to optimize the patients that need to be on anticoagulant or antiplatelet therapy. Um And the last thing I would say is the widespread use of helmets that has changed completely. For example, it's rare nowadays when we have an extra meto, pretty much all the trainees want, want to go and to help and to and to be part of that surgery because a pure meto became rare because the helmets protect from the fractures. And usually when you have a car accident, it's true that people are not wearing helmets inside the but usually for the head to be impacted if you are wearing, for example, a belt, it needs to be such a severe trauma that it goes way beyond the extradural space. So it goes on the subdural contusion trauma, you know, it it becomes a completely different, more like a um a burst lobe syndrome and not an extradural. So the helmets on these on their own drastically change the type of focal injuries that we see. And the last thing I would point, this is highly controversial mainly in Western countries. And I think for example, UK is a very good example, which is, you know, if we have elderly people and healthy population living uh in accommodations where they have a lot of stairs very steep as it's the classic example of the Victorian houses in UK, you have a lot of falls and unfortunately, we see that often and often in this population. So maybe we need to act with the communities to try and raise awareness that elderly population, they cannot live in this sort of accommodation. I know that there is a lot of wishful thinking here but to try to summarize the answer to your question, we need to act in multiple ways which is traffic enforcement. I would say primary care education and working together with our colleagues. But as well in terms of community, in terms of society, how to adapt in the elderly population. So we can act on multiple fronts. Gps and community to decrease the severe of TB in the elder population, road traffic enforcement to reduce the TB in the young population. He was as a follow up question uh for sports as well. So as you may be aware, I mean, in UK, we have, we have some restrictions particularly related with rugby. I know that in us there is all everything is very well um uh reg in terms of in terms of um NFL and in terms of, for example, there are some certain maneuvers that you can't do. For example, that came out with the classic one is a spear, right? We can't do a spear anymore when you do because of the cervical injury. Uh There are some rules, if you have a concussion, you need to do certain things outside of the pitch before you are again allowed to go inside. So there is certain certain things that we can use to, to to help our colleagues in terms of uh of sports prevention. Now, I think in the end of the day, the more you want to make the sport safe, I think our intervention as doctors will mainly be as if an injury happens. How or when can that sportsman or sports woman go back to the sports practice. You know, we have developed the the helmets in box, we have developed all these rules about what can be and can be done. We can work together with the federations to improve the protective equipment during the sport. But at the end of the day, the pa if not the patients, but if um this um people want to practice that type of sport, I think they need to accept the risk. For example, dementia dementia in box. Ok. It's quite, it's well known and sometimes it's very difficult, for example, um there is a theory that if you use the helmets in box, for example, you are allowed to have or you can tolerate higher impact because of the cushion effect of, of those protections of the head. And therefore actually you have a higher risk of developing, of developing long term sequela from box such as dementia, even though the helmets protect for the short term. So sometimes it's not clear cut and even acting on something. Now, we can actually produce um uh a different type of problem a couple of years long down the line. But I think in the end of the day, we can help with the protection, but we cannot prevent people from, you know, from playing the type of sports. Um Thank you. So I'm going to the next question, George and can you please do a quick vision on the ICP measurement? And what do you expect from fresh graduates to know about it? Thank you very much. So ICP, you know, and when I started sometimes uh when I started as a young trainee, I remember, you know, doing my round before going to bed, you know, go to ICU, I see a patient ICP of 80. Now I'm very relaxed and then ICP of 22 bring this patient straight for the compression and that's why I put the emphasis on understanding the curve. So the number is an indication but you need to know what's happening with the trend. And that's why I think, you know, as for example, a junior doctor as someone that is starting in the hospital, you know, don't just say, oh what's CP of that patient? 17 fine. No, no. What's happening in the last 12 hours is the ICP slowly creeping up. If that's the case, don't wait for the magic number of 20 to start acting on it. No, no, you can start optimizing. Let's check the sodium, let's check the oxygen. Let's check the temperature. Is there anything that we can start acting to avoid the patient? No, you are in the period of the curve that I showed where there is still a compensatory mechanisms going around. So you can still be very effective uh in medical management. And to be honest, some of my colleagues may say, don't bother me unless the patient is ICP above 20 I disagree with that approach. I like to know what's the trend, what's happening. So in terms of communication with ICU, I can even tell, look, raise the BP, let's see what's happening, increased transfusion, we can do a lot of things. So I would say the key thing is above 20. You need to let someone know because that is where the patient needs most likely a surgical intervention, but be aware of the trend and act on that ICP. If it starts raising with small things that can avoid uh a much major intervention, that would be for example, a decompressive craniectomy. Um Hi NTI, thank you for a question. If a patient on G A PT come with a severe TBI, do you correct before taking for surgery? Absolutely. Absolutely. So usually if a patient comes or I II like to know and, and, and this is controversial and there is no clear evidence for that. But if I'm operating on a patient with a trauma that I have very, no history about or um for example, I know that he's on some sort of anticoagulation or if it's uh I just do a tech test or what that will give me a very broad idea of how is the coagulation of the patient and what do I need to correct? Um Also, if I give FF PS of factors, I always give F FP after a discussion with our coag team in the hospital instead of going, for example, straight away for um for uh recombinant factor seven only if the coagulation team said, look, it's really high risk. I think you should consider factor seven. That's when we go for it. Otherwise we just go for F FP. Um But I would say as a tip, if you have access to the rotten test, you know, it takes like half an hour or so just to put and you will see the Poisson the F and you can see if you need to correct platelets, if you need to correct fibrinogen, if you need to correct factors. I think it's very useful, particularly when you know nothing about the patient or when someone tells you, oh he was on. So and so medication he stopped maybe 2 to 3 days ago. You don't know exactly you want to make sure you're doing the right thing, just do it. Oh, I think there was a question. Uh that was there is pain on us. Uh uh Yes, no. Uh II just press on the, on the um, but I II can pick it up from here. So if you uh just to ask for a gunshot injury to the head with a bullet pet, um lodged in the gray matter without pressure or peripheral effects. It is advisable to consider surgical removing. So this is a very interesting question because we had a case, not that different a couple of weeks ago. So I think that there are a couple of again, there is no clear right or wrong. Either there was a paper published in neurosurgery about the systematic review on this topic. Um I think there are a couple of things to consider young patient that is likely to require MRI S in the future. If the bullet is located in a non eloquent area, I think that there is a rational to at least have a discussion with the patient and saying look, you are young. It's likely that at some point in your life, you are going to have need for an MRI. This bullet will probably not allow you to have an MRI. It's non non eloquent area with surgery. All this carries a risk, but the risk is not very high. Therefore, what you think about as going just to remove the bullet and then you can go back in normal investigations in the future if you need. I think that there is a point for that if the lesion is located in a very eloquent area, then my advice would be not to remove, then there is the risk of infection and everyone is concerned about infection. So the risk of infection with high, like with um military kind of weapons is very low because of the high speed and the shearing effect. So we just sterilize everything under way in low velocity. Um Bullets, of course, the risk of infection is higher. But if you know the entry point is quite far, if there is not a the risk of fracture or a skin opening on top of it. Uh I think that I would personally take the risk of dealing with an infection again in a delayed way if it comes up a couple of weeks, a couple of months later down the line instead of um of going try to remove a bullet just to prevent infection that we don't know if it's gonna happen and that may end up with a patient with a severe deficit. We do have a follow up question. Hang on. Let me see if I can get this up again. Uh from George. Right. Yeah. So is there enough evidence on the indication of decompressive craniectomy if the ACP below 20 but not compensated curve? Also, what are the current neurosurgical gaps? In the evidence that can be answered by low budget studies that we can maybe implement in low income countries. That's a very good question. Thank you. So let me start from the beginning. I would say that not even when you have ICP, a refractory ICP above 20 there is evidence for decompressive ectomy rescue ICP. It's, it's literally how you want to read the trial, right? Which the rescue CP said is that above 20 patients who do the compressive ectomy have less mortality, but a higher poor neurological outcome when compared with thiopentone. Um So that's the first question. Uh evi evidence for the compressive craniectomy with ICP above 20. Definitely there is none I can be very open about it in terms of gaps, uh gaps for, for this, for in terms of low budget studies. It's interesting. Let me bring a trial that I have not brought in the past, which is the best trip trial. You some of you may be aware, it's a trial that was done by Randall Chestnut in Washington, but actually with patients recruited in South America because from ethical, from an ethical point of view, it was not allowed to be run in the US. So basically, patients with traumatic brain, severe traumatic brain injury were randomized for ICP guided management versus non ICP guided management. Of course, this trial was heavily criticized, maybe it was a little bit even beyond this talk. Um And this basically the outcome was that ICP guided management was not superior or was not better than non ICP guided management. And this um made the argument that ICP guided management of severity B is no level one evidence for it. So in terms of questions to be answered, I think that's the question of the behavior of the curve and of the ICP curve particularly, you know, as, as we were saying, we have a, a fixed number, but with that number, we can have a compliant or a noncompliant curve. So does the outcome of the decompressive craniectomy at that stage is impacted more by the number or my or more by the compliance status of the of the brain. Um Also in terms of the management that you can do if you see a trend up to ICP of 20 this is as well a little bit uncertain. So for example, there are trials looking at transfusion, what should be the target for the transfusion. The reality is we don't know. So I think if you ask my opinion, what is what we can do in terms of low budget studies to, to study into ideas for studies, I would focus on actually on the ICP below 20 in this management of these patients that have, that are still in the compensatory phase of the curve and what we can do to, to improve the outcomes. And in this case would be to avoid further surgical management or to avoid decompressive ectomy. So kind of kind of two different protocols with different strategies and to see which one is best to avoid decompressive ectomy or to avoid what people would call the final stage of ICP management. Yeah, perfect. I think that's it. Unless Georgie is gonna get back to us with a follow up. Follow up. That is brilliant. I think that's up. Oh, hang on. That's user. That's it. That's us for Q and A. Thank you so much. Um It was completely over my head, but hey, the delegates enjoyed it. So that's fantastic. And obviously they've learnt a lot from what you have said. So, thank you so much. Um The delegates just to let you know that your feedback form will be in your inbox. If you can complete that there is a part on your feedback that asks about further topics. If there's further topics within this uh speciality, then let us know because I will be passing all this on and uh to your date and we can see whether or not he can come back and give us another teaching session. So thank you all so much. If you can complete your feedback form, then your attendance certificate will automatically be on your meal account and you can download that. Ok. So it was lovely to see everyone. Lovely to have your questions. I think everyone seems to have appreciated. It said nice uh presentation. What we'll do is we can get a copy, uh, if we can, oh, it looks like George would be more than happy for, to have more neurosurgery events. Look at that, uh, George, is it right? Where is it you're from? Is it Syria? Is that correct?