Say hello, welcome to this talk about, traumatic brain injury, how to avoid the headache hopefully. So I'm Alice Dugal. I am one of the ECC specialists at D DWR vet specialists in Cambridgeshire.
And today I am going to talk to you about traumatic brain injury, . We're mainly going to focus on the emergency side of things because of of who I am and what I do. But hopefully that will remove the stresses for you for when you see a patient with head trauma and try and and go through steps of things that need to be done to hopefully avoid bad outcomes.
I quite like going through your case when, I'm talking about a subject. I feel like it helps us being grounded and and knowing what we're talking about. And so we're going to follow Chica during this talk.
I saw Chica during my residency, as you can see, she's a little chihuahua. And she belonged to the lady of a couple that was like moving in together, and the male owner had two Great Danes, at home. And it goes without saying Chica the Chihuahua was obviously the boss of the house, and she was bossing around the two Great Danes who were quite chilled, and quite tolerant of her and and her, I guess a dictatorial, fashion.
But, it was going pretty well, except. One night they were in the living room and they just served the dinner for the two Great Danes who went to eat their dinner. And the routine was that Chika would usually inspect their dinner and then decide when they'd be allowed to then eat their dinner.
But it turns out that that one evening, clearly one of the Great Danes did not feel like being told when they were allowed to have their dinner. And they literally just heard a tiny little bit of noise and it sounds like. Chika told them when to eat their dinner and it didn't go well for one of them who probably just tried to like move her away by taking her head in his mouth, but unfortunately that did quite a bit of damage just with one little bite of Chika.
So obviously what we see when when we see Chika for the first time is the massive bruise on her head, and the fact that there's definitely a head trauma there, it's visible for us all. But what we are going to talk about today is what we can do to make the outcome hopefully better and and and how we can treat this. And so we're going to talk about the procedures that we put in place to try and and improve things and and treat things.
So in terms of agenda, today we're going to talk about what is primary and secondary traumatic brain injury and why we worry about it and why it's worth mentioning how we monitor for this secondary injury and how to prevent it and how to treat it. So we're gonna start with what is primary and secondary traumatic brain injury and why we worry about it. So the primary traumatic brain injury is the damage sustained at the time of trauma, i.e., like if you like see a car accident happening, the thing that you will see is maybe that the car doesn't look like it did before, and it's got some scraps on it and it's.
No longer got the paint that it used to have or it's got a burst tyre. But you won't know exactly yet if it's functionally still working. So, the primary TBI is, is what we see and in Chica is obviously this huge bruise on her head, which is accompanied by skull fractures.
And so what you can see quite well on CT, and again this is just like what we can see, it's not, it's not what's happening inside, it's what the problem is. You can see that canine of a Great Dane that's done quite a bit of damage and made a decent hole in her skull there. So all we can do really is assess the damage and try and like write it down in our problem list.
Like there are skull fractures there. I can, I, I've seen them. There's like a massive bruise on her head.
There's maybe a wound if, if it's been a bite like in this case. And all, all we can do for that is support the patient, and discuss with the different teams. So as an ECC vet, I rely on a lot of other teams working with me on, on any case, but mainly for these as well.
And so it's going to be, for example, saying, well, actually I foresee that one of the eyes has maybe like popped out or there's a scleral rupture that I can see on, on the CT and I'm going to need, my colleagues from ophthalmology to help for either treating that eye or further down the line removing it if if it's not working and if it's causing a site of infection, for example, because it's the scleros exposed or or or or fractured really. I'm going to talk to our dentistry team to see if there's any jaw fracture or if there's anything that I need to plan for. But this is all like assessing the damage and trying to plan for what we are going to do about it.
And we're going to give the patient some time to recover because that's really all all we can do is, is time and seeing how things are going when it comes to the prima primary TBI. When it comes to the secondary traumatic brain injury, these are the changes that occur after and in different timings for that, so in the minutes, hours, days that follow the trauma, I'm gonna wanna know like what is going on and that these are those changes that I want to prevent from happening for things not to spiral the wrong way. Say I want to prevent these changes.
It's obviously the most important part for me and the most interesting. I'm sorry, my cat is clearly going to join this talk, and it is definitely the most interesting part interesting part of treatment for me, and in terms of like how the secondary injury works and what is actually going on inside. You get at the time of injury a massive release of neurotransmitters and some cell membrane disruption.
That will also alter the iron levels in there because obviously the sal membranes are disrupted and so the iron are not gonna stay where they should realistically, and because of the swelling, you're gonna get some reduced blood flow which is going to cause some ischemia. And that means that we're going to get some neural damage and cell death where brain is, and some cerebral edoema. And that will lead to increased intracranial pressure, and then that's where the vicious circle starts, because obviously increasing the pressure means that we're going to get reduced blood flow and we're going to cause more ischemia, more neuronal damage, more cerebral edoema, even more pressure.
So really what we want to do is break this cycle. To understand how that works, we need to talk about cerebral perfusion pressure. And you're probably thinking, oh God, I'm gonna log out of this talk if she starts talking about things like that.
But it's really not that complicated and it will help you a lot to understand what's going on in your patients, so bear with me for a minute. Cerebral perfusion pressure is really how much blood I am getting going in my brain. And so for that there are a few things that I need to take into account.
The things that make the the blood go into the brain are mymni arterial pressure, so how much pressure there are in the vessels to get blood going into the brain. And the things that play against me are my intracranial pressure because the more I have pressure inside the skull really, the less perfusion I'm going to get getting into the skull. So that's it, it's literally what CPP is, is mymi arterial pressure minus my intracranial pressure, which is causing resistance to the flow.
So, if I get more intracranial pressure, I obviously get less flow going in. So, when it comes to the skull, there's the Monro Kin Kelly doctrine that says you have a skull, it's a fixed box, it's got fixed volume, and inside of that you have some brain tissue, which is 80% of what is inside there, some CSF, which is 10% of the volume in there, some venous blood and some arterial blood that composes the rest. Now, it's a fixed box, there is no way of increasing its volume, especially not in an acute setting.
So if you start having an increase in one of those compartments, whether or not it's brain tissue, for example, if we're talking about a mass, which is what is depicted on this diagram here. And then there's no more space really in there to accommodate that. So some of the things are going to have to shift out, and those things are going to be the blood and then the CSF, and then ultimately there'll be too much pressure in there for anything to be perfused or to have any CSF around it, and that's when we're going to have some injuries to the brain and some ischemic injuries most of the time.
So to a certain level, the brain can cope with that because there are some things that the box can shift out, and that is, as we said, the blood and the CSF, but at some point, and you can see this in like the third phase of this intracranial, pressure diagram, then you get to a point where there is no more things that can be shifted out of the skull and there is just too much pressure and it's starting to be the brain tissue that pops out and that's when you get herniation. There is a degree of auto regulation that the brain has, which allows it to cope with a certain level of it. And that is, for example, when it comes to blood pressure, because what we don't want is every time we have an episode of hypo or hypertension, the brain to be the first victim of that without any control mechanism that allows a bit of buffer there.
So, so we definitely have that mainly between 60. 150 millimetres of mercury of of pressure, the brain will still manage to maintain a good cerebral blood flow, as you can see in that like area in green, that is like the area where you still have good cerebral blood flow, even though you have a big variation in the mean arterial pressure. And we'll talk about it a bit later, but there's also an effect of the PACO2, and so your partial pressure of carbon dioxide, and so the more carbon dioxide there is, and the more vasodilation there will be.
And so that will also have an effect on the cerebral blood flow if it's very high, more vasodilation, there'll be like less space in there and so less blood flow. And it's in the opposite direction as you can see when it comes to oxygen, and so the less oxygen as well, the less blood flow we, we are going to have. So.
What and, and you can see in terms of like when it comes to blood pressure, outside of this 60 to 150 millimetres of mercury, the brain will be also affected by these changes in pressure that are a bit more on the extreme values, but, but there will be some damage there. And so when we're outside of these re regulatory like boundaries, really, we, we get herniation of the brain tissue because there's no more space in there. And, and then the brain tissue starts to come out.
The main herniation sites that we see are through the foramen foramen magnum and and here you can also see in the caudal transorial, you will, you will potentially see some herniation in cases of increasing intracranial pressure. So again, these are the things that you would hopefully not see on MRI on CT because like that means that the patient has unfortunately herniated quite badly, but these are the things that we're worried about is, is the moment where there is no more space in there and the brain herniates. Say it.
We have talked about what is primary and secondary traumatic brain injury and why we worry about it. So now I would like us to talk about how we can monitor for those secondary injuries because it's a good thing to say we want to prevent them, but we, we need to know which which ones they are. So I'm sure you've all heard about Crushing's reflex, and that's probably the main thing you're concerned about when you see a patient coming in with a traumatic brain injury.
And as we said, if there is too much pressure inside the skull, if the intracranial pressure increases, I get less perfusion coming into the brain because the blood flow is limited by the fact that there is a lot of pressure inside the skull. So what will happen is that to kind of like maintain still some perfusion pressure to the brain because obviously it's the head of the machine, it needs to work, we're going to have an increase in the mean arterial pressure to try and get the blood to still go in in spite of having too much pressure inside the skull. And that the fact that the min arterial pressure increases, that gets sensed in the body by the baroreceptors, and they will respond to that by decreasing the heart rate.
And so what you will see as a result is bradycardia. So, what we usually say for like Cushing's reflex and what people are always concerned about and always measuring heart rate and obviously blood pressure for in TBI cases is this, is this massive increase in blood pressure to try and like get some perfusion pressure to the brain, which then is associated with bradycardia. Now, I think the main thing to remember is that Cushing's reflex is not something that happens.
On a like for example a mild TBI and the patient is like super bright, I feel like I do get some questions about a patient that comes in and, Don't know, there's a history of, the owners really concerned because they dropped something and it fell on the dog's head and the dog's completely fine, but then when he came in had a blood pressure of 180 and maybe the heart rate was a bit on the low side because it's, it's a big dog. But really consider that usually this is associated with like very poor mentation. It's not going to be your dog running around.
That is starting to like herniate and as a result you get Cushing's reflex. It's not an early thing that you will see in traumatic brain injury. So if the patient looks totally bright and fine, the blood pressure being high is probably due to the fact that they're a bit stressed being in hospital or clearly the owner's very stressed, so they got quite stressed.
And you could have a low heart rate just because the dog is like a big dog and has like a good bagel tone, but Yeah, do you, do you associate those findings with the mentation to make sure that this is what you're dealing with. The patients I've unfortunately seen Cushing's reflex in are already like in a like this gap, for example, on a bed, in like where I can, I am monitoring their mentation and suddenly we we see an increase in blood pressure and and potentially a drop in heart rate, but not the ones that are currently running around. So it's a life threatening stage of intracranial hypertension.
So remember those three things that I've just mentioned, hypertension, bradycardia, abnormal mentation are the three things to to recognise for for Cushing's reflex. It can be associated with irregular respiratory patterns. It's likely because the brain stem gets compressed as well, as you've seen when there's herniation there.
Brain stem is having a lot of pressure on it, so it's possible to see this, irregular respiratory pattern associated with it. And it is important that as a minimum, the level of consciousness is regularly monitored and reported on on your hospital sheets so that you know what you're dealing with and you can see if a patient is deteriorating in terms of mentation. So is, did it come in bright and alert and is it now tended or stuporous or comatose, but it is really important to use those terms that are objective terms so that if you leave your shift, then your colleague who takes over after you.
And will not think like, oh yeah, this patient is a TBI anyway. It came in and it looked like that. Well, no, maybe it came in and it looked actually just obtunded at the time and now it's becoming stuporous and that represents a deterioration of the state.
The other things that you can monitor for are pupil size and PLRs, and there's obviously different combination, and this needs to also be correlated to the state of the eye, because I mean we've seen, I'm sure you've seen also quite a few TBI patients, and they can unfortunately have damage to their eyes and obviously if the eye is not functional and if it's, I don't know, like come out. Or anything like that, then obviously you do consider that that eye doesn't really count into your PLR findings, but it's obviously not great if you've got some level of anzocoria or if you've got bilateral fixed midriatic pupils, and again it's another objective thing that you can document on the sheet so that this patient is closely monitored and that if there's deterioration, then it's being picked up as early as possible. The other thing that I really like to monitor again because it's another objective skill that that we can use and and that is always easy to document on on a hospital sheet and say can you fill this sheet out every every 4 hours, for example, is the modified Glasgow Coma Scale.
So it's a scale out of 18 which will have 3 main components. It will look at the motor activity, brain stem reflexes, and level of consciousness as you can see. You can like print out those scales so that again they can be done every 4 hours by colleagues who will then be able to say actually this is the grade I got when the patient came in so that again if any deterioration happens, you're aware and you're being told, wait a minute, like things have dropped.
We started with a 16 or a 15 and we're now at a 12, and clearly it's time to intervene. And it's quite good as well, if you are using them, and if you're saying I have a TBI patient that's come in and every 4 hours I'm going to, record it's modified Glasglaucoma scale to say where you've put the points. So for example, you could say, well, this patient is a 150 and I've put like 5 at the motor activity, 5 at the level of consciousness, and 5 at the brain stem reflexes, because again, if things.
It's easier for someone else who would be doing this objective grading to know where the points have dropped and to know where where things are deteriorating. So that you can intervene and also make sure that maybe the colleague who did it before didn't have the same appreciation of that. It kind of like gives you an extra bit of safety by saying which bit of of the scale you've attributed points to.
And in terms of prognostic value of it, and there's a study from now 2008 starting to be a bit old, but they looked at the like prognostic value of of the MGCS and They saw that it could predict the probability of survival in the 1st 48 hours after head trauma with 50% probability in a patient with a score of 80 sorry. So if you look on the graph there, you will see that at 8 as a score, you're roughly at 50% of like probability of survival. So that is in, it needs to be taken in the 1st 48 hours.
I guess it gives you a bit of an indication when you get a patient coming in if they have an MGCS of like 5 or 4, it's probably not very good. That being said, Things can change a lot and the outcomes can be, as we'll discuss later, can be very different in head trauma patients. So, and, and this is like a retrospective study, so it's obviously got limitations, and I wouldn't say well.
If a patient comes in with a modified gra glucoma score of 7, I will tell this owner, then there's no point in continuing because we're under the 50% survival. It's just something that like helps you understand what you start with and gives you an idea of what's reported out there. Like every study, like every patient is individual, so it is a tool to keep in mind and know that this is what's been reported and, and help you as well figure out how bad your patient is.
But do not decide of the outcome of your patient just based on that, especially if you've got motivated donors who are willing to go ahead with treatment and, and seeing what the outcome could be in in a head trauma patient. In terms of other suggested monitoring, obviously you want your patient to be as stable as possible. That's probably true for any type of injury, any type of trauma, but in terms of the parameters that you need to monitor, then we've talked about the neuro exam and the modified Glasgow Coma Scale, and the blood pressure is important to maintain.
So with a map of anywhere between 80 and 100, having. A good oxygenation level, because you, you want the brain effectively to have some oxygen and we're going to talk about that, but ideally you'd want an SPO2 that is over 95 if possible. Again, we've we've briefly talked when we talked about auto regulation, about hypoxemia and also the effects of an elevated PACO2, you want these values to be as close as possible to normal.
So, avoid hypoxemia with a PAO2 over 80 millimetres of mercury and a PACO2 between 35 and 40 millimetres of mercury. You want your patient on an ECG to make sure that there is no arrhythmia and that again the heart is doing as much as it can to like get some good perfusion going. You want normal electrolytes, normal blood glucose, especially for us in a patient as small as Chika, we know they're prone to having hypoglycemia.
So again this is something that we'd want to like check regularly to make sure that she is normal glycemic. Having a good respirating effort and a body temperature that is also within normal range. So now we've talked about primary secondary traumatic brain injury, we've talked about how to monitor for secondary injury, and now we're going to talk about how we can prevent secondary injury because that's ultimately what we want to do.
So we talked about this diagram about like how things happen, this vicious circle of having bad things happening at the time of trauma and and the neuronal damage. So what we want to do is break this cycle so that we prevent increasing intracranial pressure and prevent more damage to be done by reducing even more of the blood flow to the brain and causing even more ischemia. So that's where we intervene and we want to prevent any more from happening.
How do we do that? Well, that's where I told you we are going to go away from the major things that we saw on CTN on Tika, and we're going to focus on the bits that are surrounding her. And as you can see, we are focusing on fluids here and the blood pressure cuff because the fluids and the monitoring of the blood pressure are going to help me prevent hypertension.
And we're going to talk quite a bit about how to monitor the blood pressure and and how to try and like maintain it at the normal level. And also oxygenation. We've again briefly mentioned it in auto regulation, we're going to need a good level of oxygenation for the brain.
So why do I bother telling you so much about this? Well, because hypertension and hypoxia are really badly affecting patients with traumatic brain injury. And so this is like human studies because they always do things like much bigger than we do with like loads more patients.
And they looked at the impact of combined pre-hospital hypotension and hypoxia on the mortality in major traumatic brain injury. So what you can see here in terms of on this graph of the death rate, you can see that patients that presented with a TBI and hypertension only had a death rate of 20%. If they presented to the hospital with hypoxia only, they had a death rate of 28%.
If they unfortunately had a combination of both, we're looking at 44% mortality. So that's pretty huge. And so if it is something that we can avoid and if we can try and maintain a normal blood pressure and normal oxygenation levels, we're effectively, hopefully trying to prevent our patients from dying.
When they looked at the adjusted odds of death in patients that had both hypertension and hypoxia, it was more than 2 times greater than those that presented with either hypoxia or hypotension. So really the combination of the two is, is really what we want to avoid in, in traumatic brain injury patients, but also if we can avoid either one of them, it's, it's obviously even better. How do we prevent that?
Well, obviously we need to monitor the blood pressure so that we can pick up the moments where it potentially becomes too low or too high, and you're going to need to have serial blood pressure monitoring on your patient. For that, ideally, if you have a way of doing invasive blood pressure by placing an arterial catheter. In the patient and having constant monitoring on the screen, then that's ideal because if there's any change there, if there's a bit of hypertension, a bit of hypertension because you're starting to go on the wrong way towards Cushing stride, which you're obviously trying to avoid.
You'll see on the screen immediately it will be there, but for us, for example, a patient like Chika, we already didn't have enough venous access as it is, let alone arterial, so it's a luxury that we didn't have and it's also something that you might not be able to do in practise. But if you are, then these patients, especially if they're in a cot and if they're non-ambulatory and quite bad. And, and if you have access to this, then there are ideal patients to use invasive blood pressure in.
We couldn't do that as I told you, so we used non-invasive blood pressure with Doppler, and you can use oscillometric if that's what you're using. The main thing is do it regularly and monitor these patients. Don't, don't do it like twice a day if they're in a state where they're tended comatose stuporous either if their mentation is altered and you're worried about them.
If you can do it every 1 hour, do it every 1 hour. If you can do it every half hour, and then as you become more reassured about the patient, then you maybe you can space out those measurements. But in the initial phase, it is extremely important that we are able to spot the moment if they become hypertensive.
How do you treat the hypertension? Well, if they're hypovolemic, which again in case of trauma, they can definitely have lost some blood in in different places, then you can use a bolus. So depending on what patient you've got, you can use either a crystalloid solution like Hartmann's.
Or saline if if this is what you tend to use. And when it comes to a bolus, I would usually in dogs and also in cats, but depending on how careful I am with like fluid overloading them, so obviously you want you want to avoid that. But we'll go 10 mL per kilo over 10 to 15 minutes in a dog.
Maybe I will start with a 5 mil per kilo bolus in a, in a cat, and then if I see good response and I think they're hypovolemic and, and their blood pressure is increasing after I've given the bolus, I can always repeat it rather than starting big and then ending up with a fluid overloaded patient that you can't take back the fluid from. So. That is a good 11 to do.
And if you have like a bigger patient, for example, who is not dehydrated because you could weigh like really have, for example, a big dog that has that is well hydrated and just had like an acute trauma, and you can also use hypertonic saline. For fluid resuscitation and to help with your hypovolemia, and in which case you'd use between 2 and 4 mL per kilo of hypertonic and again that would be over like 15 but up to 20 minutes to give that. You will see a transient hyponatremia after that, but it's not usually a problem.
Obviously if you've resuscitated your patient, and they're no longer responding to fluids because they're no longer hypovolemic, or you've reached the stage where you, you've finished your fluid resuscitation and, and you're down to still having a hypotensive patient who is fluid resuscitated. It's time to use vasopressors. Again, this is a human study, looking at early vasopressor utilisation strategies and outcomes in, patients with TBIs, and they do recommend using the vasopressors if you've got persistent hypertension after fluid resuscitation.
They saw that the most reported vasopressors being used in in this study was phenylephrine and norepinephrine. My vasopressor of choice will usually be norepinephrine. If you have vasopressin, then by all means that is also a very good one to use.
We do like norepi because it, increases like the tone, without usually having too much of an effect on the heart rate. So if it is what you're used to using, by all means, like clearly phenylephrine and norepinephrine were both very used in in this study. In terms of effect on survival, this study looked at, vasopresses and TBI and the were trying to quantify their effect on mortality.
And they did find that patients that had vasopressors were like more likely were more likely to die where we had more of them that were in non-survivors. However, there's obviously the bias that patients who did require vasopressors are probably the sicker ones because in spite of fluid resuscitation. Vasopressors, so it is, it is really likely that we are dealing with a sicker population and so obviously they will be, the ones that will are more likely to die.
However, maintaining good, good blood pressure as we've seen in those previous studies is of the utmost importance. So if you have fluid which has stayed in your patient and there's still hypertension, you should use vasopressors. I've put a just a, a little recap from, Sacom on like the vasopressors that can be used.
So like it's more for you to, to have a reminder on, on the effect in the beta 1, beta 2, and alpha 1, alpha 2 effects. And the reason again why we love Norepi is because we've got. That alpha 1 and alpha 2 effect, which will increase the blood pressure and won't have too much of an effect in terms of increasing the heart rate.
But if you do have a pressure, a patient who doesn't have, good, good perfusion pressure and you feel like the heart is maybe needing a bit of positive otropy. You can also use some dobutamine if if that's required, some maybe some chemo in cats. And it's kind of like making sure that once you've examined your patient and once you've identified maybe the reasons why you've got hypertension, you can use the vasopressor that that you're happy with and that you're used to using because because you know what to expect.
Then in terms of oxygenation, again we want to avoid hypoxemia. There's many reasons why these patients could be hypoxemic. They will have been, have had traumatic brain injury, but unfortunately they're usually quite small patients.
If, if we're talking about a road traffic accident, for example, there, there's a good chance their thorax. A hit as well, so you could have a, a big pneumothorax there that is causing hypoxemia. You could have some pulmonary contusions, and, again, the way to kind of like help you diagnose them is maybe to do a point of care ultrasound of the chest if this is something that you're used to doing.
And if you see those be lines all over the chest. Keep in mind that that means that you've got a degree of wet lungs and that could be obviously haemorrhage, which is effectively what pulmonary contusions are, and these are good reasons for our patients to be hypoxemic. So they do remember that even though they do present for a traumatic brain.
The rest of the patient has also been through trauma and so you could be dealing with hypoxemia for other reasons and some of them are fixable. For example, if you have a pneumothorax, then it's very important to drain that so that we get some good oxygenation going and and the TBI doesn't get worse. In terms of how to treat the hypoxemia, why you need oxygen, I think you you had gone that far yourselves and and you knew where to go.
But they, there's good ways to supplement oxygen and bad ways to supplement oxygen when it comes to RTBI patients. In terms of good choices, a mask is a good one. Obviously the reasons why there are good choices and bad choices is because we don't want to use a method that will increase even more the intracranial pressure.
And so a mask is a good one because unlike this patient wasn't a TBI patient, but you wouldn't want to put any pressure at the back of the neck and and push them into the mask, but having the mask in front of them to give oxygen is totally fine and it's not adding any pressure. The oxygen kennel is obviously great, it's got limitations in terms of size. You can't put a Newfoundland in there, but, it's got a very good, way of measuring the oxygen in there.
It's got some control of temperature of CO2 as well. So if you do have a smallish patient, it's very good to place them in an oxygen kennel because there will be no external pressures in the way you oxygenate them. And it's got limitations when the patient do feel a bit better and and this dog felt extremely strongly that we should not oxygenate her.
So just as an example, but usually when they are at the bad moments of their traumatic brain injuries, they're in no state to do that. So they are a very good choice for for oxygenation. The things to avoid that are good methods of oxygenation for other patients, I'm not telling you not to do that for any patient.
I'm just saying for those TBI patients, so, anything where you take a collar and, and try and increase the oxygen within the collar is a great method, not in cases of TBI because you will like put some pressure around the neck where the collar is, and that will potentially make the TBI worse and increase the intracranial pressure, . Just a side note here, if you do use this method for another reason and unrelated to TBI, always make sure that you do leave a bit of an opening as it is in this picture for the CO2 to get out. And we'd sometimes see patients coming in with those and there's no opening for the CO2, and obviously then they can asphyxiate in there.
So please make sure that you always have a little opening there. The CPAP helmets are great for some patients, but again, in this case, really not a good idea. There will be an increase of intracranial pressure.
I think it's quite visible in this picture that you can imagine that even though there's a better pressure of oxygen, there's probably also more pressure on the skull. Same for anything that goes up the nose and will tickle them, make them want to sneeze, and all of that increases the intracranial pressure. So no cannulas that go up the nose, or even prongs.
I'm sure we've all like seen many dogs trying to like pull at their head, and remove them, so all of this will increase intracranial pressure, so even though they are great methods of oxygenation for other patients, do avoid them in your TBI ones. In terms of blood products, do we need to use them ever with traumatic brain injuries, and the answer is potentially, depending on the patient, there is a recognised TBI induced coagulopathy. Again, we have more data in humans than we do in dogs and cats, but we, we do know.
That our dogs and cats get coagulopathies of trauma, and the question here is, do they get it with TBI and the likelihood is yes, because you get disruption of the brain blood barrier and you disseminate some brain injury systemically by releasing some brain derived molecules into the circulation. And they, these patients get, hypercoagulable and also hyperfibrinolytic at the same time, so that results in a persistent and delayed intracranial haemorrhage and systemic bleeding as well. So basically it's kind of like consistent with the pathology of the DIC and so as a result, they can get this.
Coagulopathy and require some blood products if if they are coagulopathic. So worth monitoring if you can see that they've got ongoing bleedings again, always monitor their lungs because it could be that they first come in and they have like no signs of pulmonary contusions whatsoever, and then 24, 48 hours down the line, you scan their chest and they're covered in beelines even though they're not fluid overloaded, so. The lungs definitely can bleed after the trauma, so you keep an eye there if you're starting to see a patient whose PCV is dropping and you're worried about coagulopathy, but you're not quite sure where the bleeding is.
It's, it's a good one to, to check as well. So this little patient, had presented to us, post trauma. Her PCV was in the 20s, but again, once I've made sure, once I've gone through these like 1st 48 hours, knowing that there's not going to be necessarily some more complications, more bleeding, I know that she's going to need surgery because that eye, as, as you can tell I'm sure is nonfunctional and she will need surgery to remove it.
So again, there's going to be some blood loss there, and so if I'm at a borderline level in terms of PCV and I know that these patients will then need to go to surgery, then they will be transfused before surgery so that we make sure that they are more stable and avoid potentially some pre-op or intra-op hypertension which could be due to anaemia. So again, consider what procedures are needed and whether or not you're going to need blood products for them. These products, if you're dealing with a kind of a DIC type scenario like a TBI induced coagulopathy that is similar to DIC, you might need.
Poor blood or you might need blood, like red packed cells, some plasma and some platelets to kind of like cover for all the things you're losing during trauma, but just think about what you need and what the clinical signs are to decide which product is most appropriate. For extra bleeding, we do tend to, use tranexamic acid as well in cases of trauma. So the, CRS 3 trial in humans, like these are like big trials, looking at specifically the use of tranexamic acid in humans, in TBI.
Tranexamic acid is this drug that basically we, we always say like the, the first clot tends to be the best clot, and the way our body works is we obviously create clots and then they also need to go when we no longer need them. So there's fibrinolysis and tranexamic acid will prevent. This fibrinolysis from happening, so we kind of like maintain this first clot for longer or in patients who do tend to maybe be hyper fibrinolytic and break down those clots a bit too quick, we're trying to maintain them for a more normal amount of time.
So in humans they recommend giving it within 3 hours of head trauma because that's when they've seen some improvement in survival. Because it reduces head injury associated deaths, they, we tend to give it at 10 to 20m per gig, slow IV, or if you give it per us, obviously in patients that are doing better than, the ones that are maybe tuberous or comatose from, from their TBI, do not try and tablet, obviously a dog who, who's not, bright and, and fine to swallow. If you do give it IV, it can cause nausea, and again, vomiting is bad because it increases intracranial pressure.
So give at least more potent before to, to avoid the nausea associated with this, IV injection of tranexamic acid. Also ensure adequate ventilation. So as we've discussed when we looked at this auto regulation diagram.
If the PACO2 increases, we're gonna get vasodilation. If we get vasodilation, there's more blood that's pooling inside the brain, and that means that we're taking more space for blood and so the intracranial pressure increases, and I think you've got the hack of this now, we don't want that, we don't want an increase in intracranial pressure. So you need to make sure that the patient is ventilating adequately.
So. You can obviously if, if there's a problem with them, check their gag. If they don't have a gag, then it is important to intubate them, and you can have an inline monitor monitoring the on on on the capnograph to know what your entitled CO2 is and see and check that it is within normal range.
And the other thing is obviously to monitor your blood gases, whether arterial or venous, whichever you're more used to, and, and what you. And check that you are within normal. So, as we said, we're kind of like thinking about somewhere between 35 and 40.
There's an argument to say that you could even be a bit lower, so you can have a certain degree of of vasoconstriction rather than vasodilation in the brain and avoid the increase in intracranial pressure. But basically anywhere in your, in your 30, 35 is ideal in terms of of your PACO2 to avoid any more increase in intracranial pressure. If not, and if your patient is intubated, you can obviously use an envy bag to ventilate them to try and manually decrease their, CO2.
Hopefully it's kind of like transient and, and you then get a patient who is spontaneously breathing. But if that's not enough, it's when it is possible to end up on the ventilator for a TBI because, because basically the, the PAO2 is too high and they're hyperventilating. So this was a particular bad day, I'd say of my residency where we had like two big dogs on ventilator.
But it's just like, yeah, do you, do you think that is really important and, and that if they are not spontaneously ventilating for longer than you are happy manually ventilating them, it might be time to talk to the owners about potentially referring them if that's what they want to do for mechanical ventilation or unfortunately, if it's not an option, then that's when more bad outcomes happen. But do keep an eye on that ventilation. Then there's like simple things that we can all do to try and avoid intracranial pressure increase, and that is things like elevating the head.
So this patient that had the TBI is in the oxygen kennel and we've just put a pillow under the mattress to have this kind of like 30, 45 degree angle to to increase, the, the level of the head and all of that is to obviously decrease the intracranial pressure. Or if the patient wants to, and as you can see, my cat is doing it very well herself when she wants to enjoy the sunshine and like anything that you can do to incline their head and keep it higher is good. What you don't want is obviously doing that, is increasing the intracranial pressure.
And so you don't want to put any pressure on the neck. So anything that you put under needs to be under the board that you will use as as an inclination bench, if that makes sense. You, you really don't want to put that, that, that thing just under their neck and then cause some jugular pressure and an increase in intracranial pressure.
And it turns out that if you don't know exactly what the 4530 to 45 degree angle that you're looking for is, you can use cans of food to put under there and that will do the trick. When it comes to analgesia, let's not forget that they've been through a trauma and they probably have one hell of a headache. I think it's a, a, a good way to say things.
So don't forget to give them some pain relief. I think there's like sometimes a concern with like using opioids because they will potentially cause some bradycardia, which is already a problem when you're thinking about like cushings or things like that, but as we said. It it's not the patients that are like doing well that will have crushings and also it doesn't matter ultimately what what will happen when you give the drug, you do still need to give them some pain relief because pain is going to negatively affect the outcome.
Anyway, and so they found in this human study looking at opioid use in traumatic brain injury that there was no effect on the intracranial pressure, the cerebral perfusion pressure, or the map with an infusion of an opioid. They did find that there was an increase in intracranial pressure and decreases in cerebral perfusion pressure and map when they were bolusing, which is potentially what we tend to do more in veterinary medicine. Where we will use our methadone 0.2 mix per gigQ4 in, in those patients, but, you can still use it, maybe give it over a longer period of time and say, well, I'll, I'll give my methadone over half an hour, or if you're happy to use a CRI, then they did find that maybe fentanyl was associated with a lower intracranial pressure in this study.
So if you're happy to use fentanyl and and you're happy to use it as a CRI, then it might be the best thing in those patients. But again, I wouldn't say I'm not gonna give this patient methadone because I'm worried about bradycardia or increasing intracranial pressure, and so I'm gonna leave them with the pain because this is definitely gonna negatively affect the outcome. Avoid any procedures that increase the intracranial pressure.
So we've talked about oxygenation methods, we've talked about the CO2 levels, but also think about things that, are, for example, jugular samples because you're going to put pressure on the jugular and as a result. Or increased intracranial pressure at the time, and this is not something that we want. Same for anything that goes up their nose and feeding tubes.
We want those patients to be fed ultimately, and most of the time they are not necessarily in a good state, which means that they are not going to eat for a while. And in a patient like Tika it's really important that they do. But think about things that matter the most, and in the 1st 48 hours if they are not great, the risk of increasing the ICP is too high, so prioritise things that will not increase the ICP.
It was a real challenge with Chika, because as you can see, we're already all over a few veins, and we needed to check her blood glucose regularly. We needed to check that she was having a normal PCO2, say like blood sampling in this dog was becoming really difficult. And so we still had to put a central line in her without putting any pressure on her jugular.
So we had to do a cut down, which is represented here on this image where you basically without putting any pressure, try and like do the cut down and find the jugular to to cannulate it. And she was a very tricky patient for that, but at least it allowed us to to get venous access that was a bit longer lasting than her peripheral IVs. In tiny tiny patients, think about intraosis catheters, that can be placed in kittens and puppies as well, for, for access.
So now we're gonna go to the last bit of it, which is how do we treat our increases in in intracranial pressure and. The main things that you need to remember is that any patient with TBI is at risk of developing seizures, so do you have a seizure plan on for your patients, even if that means that when they come in you write on the sheet, if there's a seizure, give 0.5 ms per kg of diazepam IV if that's what you're used to using, but just make sure that you've thought about that, .
In terms of studies, in terms that's in dogs as well, they found that 10% of dogs with TBI developed in hospital seizures. So it's not nothing, 1 in 10 presenting with a TBI will have seizures. Depending on what you're used to using, like Keppra, as in levetiracetam is a good one that you can start them on.
Load them when they arrive, and then you know that you've got that going and, and that is your seizure prevention like sorted and done. Obviously if they do have a seizure, that's more ischemia and more increasing intracranial pressure. We really don't want any of that.
So, so do monitor them. In terms of reducing cerebral edoema, we use hyperosmotic agents. The way they work is they create an osmotic gradient that moves water out of the interstitium and into the circulating blood volume.
So effectively we're kind of imagining that it's sucking out that extra, water and, and putting it back in circulation to get rid of it. That will overall reduce the intracranial pressure and promote good cerebral blood flow. What you can use is hypertonic saline, or mannitol, whichever you're more comfortable with, it doesn't matter what you stock in your practise.
Mannitol can be a bit tricky because it needs to be maintained quite warm. It forms crystals and it needs to be given through a philtre because of that you don't want those crystals to go in circulation, so that does require a bit more preparation than hypertonic. If you do give it, we tend to give 0.5 to 1 gramme per kilo over 20 minutes.
And hypertonic saline, you don't need any of that. You will get a, a transient hyponatremia following this. We would give between 2 and 5 mL per kilo over 15 minutes if using it to decrease intracranial pressure.
There's the whole debate always about which one to choose. In our hospital, it tends to be that the neurologist really likes mannitol, and us in the ECC, we really like hypertonic saline. We, it, it, it remains very civil.
I'm, I'm just gonna say, but we, we do have like our preferences. The terms in terms of like meta-analysis and like big trials in humans, they have historically recommended using mannitol as a first choice hyper molar agent, but actually when looking at at RCTs and meta-analysis, there's no difference in improving function and outcome. And reducing ICP and mortality between the two, but they did say that they had a preference of using hypertonic saline for refractory intracranial hypertension, which for me means like it's probably working better, but that is obviously the bias of the person who prefers hypertonic.
Mannitol does have a few things to do if using it, and you need to be a bit more careful in terms of, Basically, really kidneys because it can cause an AKI if you're not using it in a uvvolemic patient. We do like to look after our patients and their kidneys. So again, that's not me saying do not use man at all, just do make sure that you're following these precautions, and you'll have them all here on the slide anyway, but it's just to to make sure that your patients you make to avoid any AKI and to make sure that your patient is passing urine.
So, these are, these are the precautions to, to keep in mind if you, if you do use mannitol. It, it can also have an effect of on ongoing intracranial haemorrhage. So if you are suspecting that there is some, which again in our patients is a bit hard to judge, but if you've just done a CT on it and, and there's evidence of ongoing haemorrhage on CT, then maybe go for hypertonic, .
And place a urinary catheter, monitor their UOP, their trauma patients, they could become hypotensive. Do not give them NSAIDs at the beginning because you don't really know how they're going to go, and if they become hypertensive and have had NSAIDs, then their kidneys are potentially going to be very unhappy. And you know, I'm, I'm an ECC person.
If you tell me that there's a problem with their kidneys, I imagine worst case scenario that they're going to end up on dialysis, and we don't really want that. It costs a lot of money and it's not very accessible. So please do as much as you can to look after those kidneys and monitor the EOP, and, and see how, how your patient's doing, especially if you're using magnitor, but just in general it's a trauma patient, it's important to monitor their kidney function and their urine output.
The reason why we love hypertonic saline is because it kind of like does two things in one for us. It also, on top of being a hypo osmotor agent, it also helps with fluid resuscitation, as we've talked about when we said, what do we do if they're. Hypovolemic and and what do we give them?
Hypertonic saline was in there in one of the solutions. So you'll get an intravascular volume expansion in excess of the volume infused because you're effectively trying to pour some interstitial water intravascular. And it rapidly redistributes into the interstitium, and so the volume expansion is quite short lived.
We like things that we can like reverse in case it's not the right solution. It will also have some immunomodulatory effects, which is all beneficial in in a trauma patient, and it will improve rheologic properties, so that means that the blood will potentially circulate in a better way. And again, that is something that we want because we want some great blood flow going to the brain.
And it will also improve myocardial function, and just in general the, the cardiac function. So it's got some very good properties. I quite like this human paper because I was thinking actually we, we are really like using .
Ambulances and things like that. So for us, even though we are not all our patients are in mountain areas, the time for us to then have an animal post trauma presenting to our practise is probably in human terms, the time that it takes them to be taken from the mountain into a hospital. And this is just a reminder that like patients with TBI and hypertension have the like highest mortality and so that's why I will potentially reach out for hypertonic a bit faster than I would for mantle because I would then.
Suddenly have the hypertension side of things and the TBI side of things kind of sorted in one go and and this was 24% mortality in in those patients in in with TBI in the mountains, for the ones that had TBI and hypertension, 10% if they had TBI only, and 1% if they didn't have TBI. We no longer in terms of treatment use steroids, to treat, TBI. I think that's potentially something that, was done in the past.
We know that it's definitely not beneficial in traumatic brain injury patients, so do not reach out for those. The reason for that is. Again, big studies in humans looking at the outcome of patients with TBI treated with steroids, and the risk of death was higher in the steroid group compared to the placebo group.
And same for the risk of death or severe disability at 6 months follow up. So do not reach out for those, they are not helpful in this situation. In terms of recovery and outcome, this is, a little, well, this is a study that uses a scoring system that you can use on a CT if you CT a patient with TBI.
And you give them a score depending on what you see. So again, you do the CT of cheeka, for example, and you see some hemorrrrhage, that's one point. Obviously we had a depressed fracture, that's another point.
And what they found on, on this scoring system is that if performed, so it was performed up to 3 days after the injury, with a cutoff value of 2, they had 100% sensitivity and specificity for short term survival. So if the patient had like 2 or less, and 100% sensitivity and 80% specificity for long term survival. And, and they also looked at the modified Glasgow Coma Scale with a cutoff value of 13 or more, and again they had 100% sensitivity and specificity for short term survival and 100% sensitivity and 80% specificity for long term survival.
So basically if you have a patient presenting to you that you do a CT on and you get a KCTS value of 1 and An MGCS value of 15, then the likelihood, according to this study is that you're probably going to have like a good short term outcome and long term survival. It's just an extra tool to use if you do perform a CT on these patients to know, potentially like give clues as to to the owner, as to how potentially well the patient is going to do. And, in terms of the reason why I put these wonderful pictures of my cat first, because I can't help but put my cat in every presentation, but also because I feel like I get asked a lot when I see a patient with TBI about recovery and whether or not what's the likelihood of them doing better.
And in spite of what she would make you think of this, she can't write and she can't read clearly because she's drinking from a dog bowl. And we don't, we don't have the same things that we assess on our patients that are done on humans. If, if a patient with TBI in humans.
If we're asking a doctor, is are they going to recover, we mean, are they going to be able to go to work? Are they going to be able to drive? Are they going to be able to be the same human that they were before?
Whereas for our, our cats and dogs, we hopefully have a bit less expectations, and we need to think about that. And, and if owners are asking us like, are they going to recover. We, we have to keep in mind potentially they, they could have a good outcome because all we want is them to be back at home and be able to sit on our laps and in my case interrupt my presentations when I'm trying to talk about TBI, or like be our animals that that we have at home, but, but the functional outcome that we're expecting from our animals is not as high as the one we're expecting in humans, so.
If owners are motivated and if they want to treat, no matter how bad they are, obviously if if they're terrible, then you make your decisions. But it is possible to have a good outcome for these and do give them time and see how they're doing because they could really improve with time and and be back to being a totally fine pet who who will do all the things that. To do at home.
So if, if you have those patients, please do give them time and try and monitor those things that you can make a difference on oxygenation, blood pressure, and, and, and, and see how they are doing after all of that because it could be way worth it. And most of the time when you discharge a TBI patients, you have to tell the owners actually you'll be the one to tell me if this is your dog. Back because I, I've had a cat who can eat and be cuddly and breathe and be fine here, but whether or not your cat is back to you, who they were before is mainly the, the owners are, are going to tell you that and, and some of them could say like, actually, yeah, that they're back to doing most of the things that they were doing before, which is sleeping in front of the TV, which is totally fine.
So thank you very much for your attention. This, little TBI patient is now well protected as you can see. Please feel free to email me if you have, any questions about this talk.
I'd be happy to answer, and I hope you found this helpful.
