Oh, thank you so much for having me, and welcome everyone to traumatic brain injury. I really enjoy managing TBI. It can be such a rewarding problem, no matter what sort of case comes your way, you never really know what you're going to end up with, which, is, is, is quite a novelty in emergency critical care.

And it really allows us to use all of our critical care monitoring tools. So, definitely something I enjoy. So, The reason why traumatic brain injury is so important is it's estimated to have a really high mortality, especially of, as we know, the bulk of our information we get from humans, and anywhere in the ballpark of a of a third to a half.

Of traumatic deaths in humans, due to traumatic brain injury. And half of these deaths, are going to be prior to hospital admin. OK?

Now, obviously, we see a very different population, OK? Now, the cases that we're seeing are going to be much more likely to be due to the more common things, which are high-rise syndrome, RTA's, being the big two, to be honest, and less, less so, animal trauma injuries. Now, It's really important to note that head injury does not necessarily equal traumatic brain injury, OK?

Traumatic brain injury is defined as an alteration in the functioning of the brain that's manifested as abnormal mentation or an altered level of consciousness, or other forms of neurologic deficits that result from either the blunt or penetrating injuries. TBI is a pretty common emergency that we see in cats and dogs. These sort of injuries, as I said, can be the result of any sort of trauma, the most common being high-rise animal attacks and road traffics.

Unfortunately there's very little information about prevalence. Outcome and prognostic indicators, I'll go through a couple of papers a little bit later on, but there's, it makes our monitoring and planning of the patient really quite difficult. It actually means it has to be incredibly extensive.

So, first off, we'll start touching on a little bit of general management of the emergency patient, and then we'll go into the specifics of the TBI patient. Now, the reason we're triaging is to ensure that where each patient receives the appropriate treatment at the appropriate time, OK? The goal is to ensure that any form of life-saving treatment is administered in a timely fashion.

And once you get, the more experience you get, the more you'll realise that one day you'll have one case in the waiting room, the next day you'll have 30 cases. It's, it's all just a little bit of potluck, and this is why your triage is so incredibly important. Now, a very brief history is a really good starting point.

We don't want to get into the long-standing information, what the dog ate 3 years ago, it used to eat chicken, that sort of thing. What we want to know is, initially the signalment. So, what breed are we dealing with, what sex, what age?

This is important to help starting us off with a differential diagnosis and a prognostic list just to get started. We then need to know why the animals presented. For example, if it was a trauma, when did it occur?

What was the form of trauma? Have there been losses of consciousness with that trauma? Or has it been changing of a changing level of consciousness?

Those sort of questions are quite important. And then the last thing we briefly want to know is, for your initial triage is, is there any relevant concurrent medical issues that we want to know about? It's then that we'll go on to the next phase after our triage, once we've decided this is the patient we need to see first.

We'll go to a more focal physical exam, focusing on, Anywhere, 3 to 4, major body systems. Now, the reason I say 3 to 4 is, for me, the, the 3 major body systems of most significance would be the cardiovascular system, the respiratory system, and the neurological system. But as an emergency patient, you might often pop in urinary, if that's relevant to what's going on, but it's certainly not relevant to us today.

In general, if a condition is acutely life-threatening, then one of these three systems will be affected. So, the initial exam involves checking for signs of imminent respiratory or cardiac arrest. We should then be evaluating the airway and breathing, checking the perfusion status of the patient, and then ascertaining if there are any other life-threatening injuries.

It's here that we're also checking for evidence of haemorrhage that needs rapid intervention. Abnormal mentation, seizure activity, or spinal cord injury, OK, because this will again change how we manage this patient in this initial setting. So neurological assessment's going to allow us to identify deficits in the neurological system and to start to localise lesions.

It also helps us to tailor our therapy, our initial therapy, quite specific to the patient. For example, we'll discuss this in a little bit further later. But a patient with traumatic brain injury will have fluid administered differently, both type and volume, to the way that we manage a patient with septic shock, to the to the way that we manage something such as a GI problem like parvovirus.

The, the additional benefit of the neurological assessment at this time point is To give us a vague assessment of our mentation state, and we'll talk about this in a little bit more detail in, in a couple of slides forward. And both of all of these things should be reassessed constantly. So, we've made a decision on our quick neurological assessment just after triage, but as we go forward with our therapy, and when I say repeat it regularly, I'd be doing that every couple of minutes, revising what we're doing and potentially changing our therapy as needed.

So, starting off with how we can assess our patient's neurological state is the modified Glasgow Coma Scale. Now, this has been, the Glasgow Coma Scales from human medicine, and we've modified it, so modified Glasgow Coma Scale. We've adjusted that for use in, in dogs and cats.

This is a really good scoring system that we use in the initial neurologic exam, and then also serially, like I mentioned, to grade our patients. This is really important for multiple reasons. It helps us to evaluate prognosis.

It helps us to assess a patient's response to therapy and time, and make us, make decisions on, are we needing to alter our therapy? Are we needing to revise with an owner about, potential prognosis? This is the most important part of this.

Now, there are 3 main areas of the multiified Glasgow Coma Score. It relates to motor activity, brain stem reflexes, and level of consciousness. The total score of the, the Glasgow Coma Scale is up to 18.

Each of those three categories, will give a number scale of 0 to 6. So, the highest being the most normal. So a score of 18 would be a neurologically normal patient.

Whereas I don't recall if I've ever, ever had a 0 in a, in a live patient, but that's certainly your most moribund patient, the lower the score. So level of consciousness is a really reliable measure of abnormal cerebral function, OK? So, consciousness levels can range from normal to obtunded slash delirious to stuporous.

Some people would call that semi-comatose, and then coma. Now, obtundation is a reduced state of mental function. So the patient would respond to normal stimuli.

So they'd respond to you talking around them, to light, to touch. Delirium is a form of, of, obtunded mentation where a patient is disoriented to their, to their surroundings. Now, Stupor is defined as an animal that only responds to noxious stimuli, so they'll be laying and not responding to light and touch, but when you are, Pinching them to do your neurological exam, that will be a, noticeable response.

You'll get a noticeable response from them. And then coma is unconsciousness. So where a patient doesn't respond to any stimuli.

Decreasing levels of this consciousness scale really indicate abnormal function of the cerebral cortex or the brain stem. OK? Focused to those two areas, cerebral cortex and brain stem.

Then we come to the next components of, so I've got brain stem, conscious, oh, you can't see all of the conscious things, consciousness scales there. I'm sorry about that. And we've also got motor activity and, brain stem reflexes.

Now, motor activity is assessed by evaluating the gait of the patient, and the posture of the patient. And brain stem reflexes are evaluated using ocular responses. And this can include, and will include, depending on its level, it will include the PLR, the eye position, pupil size, pupil symmetry, and, importantly, the oculocephalic reflex.

This is, this oculocephalic reflex is a evaluation of the animal's eye position in relation to the head position. And it's a test of specific cranial nerves. It tests cranial nerves 36, and 8.

The way you perform this test is to hold the patient's head steady with their eyes open. You very infrequently have to hold their eyes open. This is a more of an extrapolation of human medicine.

So, hold the patient's head steady, and as you move the patient in a smooth motion, The eyes should be slowly flicking back towards centre. And that's a normal response, OK? If they continue to move, so the eyes stay in the exact position of where the body slash head is turning towards, then that's an abnormal response.

And that's when you have inappropriate brain stem function, which can be associated with quite a poorer outcome. There's actually a linear relationship between the modified Glasgow Coma score in both humans and, importantly, cats and dogs, and that's related to the probability of survival. So, for example, a patient with a score of 8, so 8 out of 16, will have a 50%, 50% of those patients will survive.

Whereas patients with a score of 4, so a much lower score, remember that's associated with a poor neurological function, this would have a 20% chance of survival. And then at the opposite spectrum, a patient with a score of 14 would have a 90% chance of survival. It's also really important to consider other factors that could potentially affect your modified Glasgow Coma score, but also can affect multiple components of your neurological exam.

So there are some things that I do very quickly before I give pain relief, because that's often something we're doing within the 1st 5, 10 minutes of an animal arriving with us. They get after a trauma, they're getting analgesia, OK? But there are some things that I would like to have a quick look at first, and The why we do that is opioids will inhibit the response, to certain stimuli, in particular, your spinal reflexes and your mentation changes can really be impaired, especially in a traumatic brain injury patient.

Other factors that can affect your Modified Glasgow Coma score could be fractures of long bones. So the presence of these injuries has the potential to reduce the motor response, making a patient seem more impaired than it really is, OK? And cardiovascular instability.

So a patient in shock, hypotensive, hypothermic, would potentially inhibit much, what appears to be much more severe neurological responses. So now, let's look at some anatomy and physiology. There's a small portion where this is a little bit dry, but I just really wanted to touch on this before we focus on our treatment a bit.

So, blood flow to and from the brain is really important for many reasons. The, the, the biggest being that a significant portion of the cardiac output is received by the brain, OK? 15 to 20%.

Now, When we take a next step down away from cardiac output, there's a really tight relationship between intracranial pressure, cerebral blood flow, and your cerebral perfusion pressure. So what is cerebral perfusion pressure? This is the gradient that moves blood flow, blood into the brain.

So when cerebral perfusion pressure is too high, The intracranial pressure will increase, when it's too low. It will become ischemic, OK? Then let's look at cerebral blood flow.

What is that specifically? That's the blood supply to the brain over a given period of time. This relates significantly to the cardiac output that I just mentioned before.

And then what is intracranial pressure? This is the pressure inside the skull. It's made up by the solid tissue, so brain parenchyma.

It's also made up by the fluid component. So blood vessels, what's in the blood vessels, and your CSF. So, cerebral blood flow is going to be determined by cerebral perfusion pressure and the cerebrovascular resistance.

That's that's, that is that second equation we have there. Now, cerebral blood flow is further determined by a combination of factors such as blood oxygen levels, carbon dioxide levels, but most importantly, it's going to be determined by arterial pressure. So coming back to this bottom equation, cerebral blood flow is determined by the gradient of the blood entering the brain, and then the resistance of the vessels that make up, yeah, the resistance of the vessels.

And, and that is determined by many, many factors, some of which I mentioned, the car the carbon dioxide, CO2, but also by natural regulation of the body. As you know, all vessels have a certain level of tone when they're healthy and functioning. So that can be a determining factor factor.

This cerebral perfusion pressure is determined by the mean arterial pressure and the intracranial pressure. Now, this helps us to understand the body's compensation that you see in traumatic brain injury, specifically the intracranial pressure and the mean arterial pressure. By looking at this top equation, you can see that if trauma causes Swelling, for example, or haemorrhage, or something that increases the intracranial pressure, then perfusion to the brain is going to decrease just by basic maths, OK?

Because that second component, that ICP, is too high, if the mean arterial pressure hasn't changed, then perfusion's going to become inadequate. OK? This is worsened if you think about a general patient that's been in trauma.

If they have, if they're in shock, OK, so not only will you potentially have increased intracranial pressure because you might have some bleeding or some swelling, but you've also got a hypotensive patient. So the mean arterial pressure is less. So therefore your perfusion is even worse, OK?

So, in traumatic brain injury, this, the intracranial pressure can be increased by quite a few things. Edoema, swelling, hematoma, or haemorrhage, compression of the vessels due to a mass effect or vasospasm. OK?

Due to cytokines or due to pain, poorly controlled pain, OK? The next most important factor that affects cerebral blood flow and traumatic brain injury is the systemic hypertension and shock for the reason I just mentioned, OK, coming back to affect the blood flow. So increases in intracranial pressure are often responsible for quite significant deterioration in the patient that we can see initially or as we go through treatment, OK?

The brain is enclosed in a rigid box, it's got a very fixed volume, and increases in the volume of its contents cause this change in intracranial pressure, causing it to increase. As this tissue compartment volume increases, other things must change to compensate. They must be decreased, and this is known as your volume buffering of the brain.

The only factors that can be altered are the CSF volume or blood volume, which, which will decrease to prevent further increases in intracranial pressure. Compensation for increased brain tissue initially involves this shift, but eventually, it has a maximum level that it can compensate for. Beyond that, we, you will start to get significant decreases in blood flow to the brain.

Once this capacity is exhausted, the intracranial volume's going to get quite significantly increased with your increased intracranial pressure, and then that's when you get significant changes in your clinical science. Unfortunately, the clinical signs that we see with intracranial pressure being increased often are evident in veterinary medicine quite late in our cats and dogs. What, what, and this is known as the Cushing's reflex.

Generally, when this is present, we have quite advanced changes in the intracranial pressure, and the patient's either imminently going to or potentially has already herniated a component of the brain, OK? And those things are lethal. So we have to tailor our therapy that I'll talk about later on, to try to prevent this happening, this Cushing's reflex happening, or any of these changes happening because it's very hard to come back from that, OK?

So, what is the Cushing's reflex that we're looking out for? This is reflex bradycardia after the body has become hypertensive, so after they've developed systemic hypertension. How does this occur?

So as the intracranial pressure increases, the body responds, as we've discussed earlier, by reducing the cerebral perfusion pressure, which then leads to reduced blood flow. The body detects this with Barrow receptors all around the heart and increases the blood pressure. This will then lead to more receptors detecting this and responding to this high blood pressure by reducing the heart rate.

So it's quite late in the cycle that we see these changes, OK? Now, what's auto regulation? That's another component of, response that the body has, OK?

Another safety mechanism really. It's a physiologic response that refers to the capacity of cerebral circulation to adjust its resistance to maintain a constant blood flow to the cerebral cortex, OK? Regardless of changing systemic blood pressures and changing cerebral perfusion pressures, it stays the same.

This means that increase, for example, mean arterial pressure will, Increase the vessel tension causing obstruction of the vessels. The range through which the body can do this is a mean arterial pressure of 50 to 150. If you have a look at that red line.

Above and below this range, the cerebral blood flow will reflect the body's mean arterial flow. OK? So in really high blood pressure and really low blood pressure, blood flow to the brain will mimic that.

But we have this safety mechanism within a decent range, 100. To, to manage these acute changes. And it's a really vital tool in trauma.

Unfortunately, it's it's impaired in trauma, OK? So that's another reason that traumatic brain injury has the potential to be so lethal. So let's start talking about primary brain injury.

This is the injury that the brain or skull, has from direct trauma. So 3 forces can cause this. You can have acceleration, deceleration, or rotational forces.

And these forces cause injuries such as haemorrhage, contusion, edoema. OK? In our patients, they're, they're presenting to us with this trauma already occurred.

OK? So we, we, we don't, we're obviously seeing them as their post-primary and the what our goal is to do our best to prevent as much secondary as we possibly can. So there are many types of brain injury and, and of varying severity.

Concussion is a brief loss of consciousness and is not associated with an underlying histopathological lesion. And this is why, as I mentioned in our early conversations with owners, I like to know if there's been a loss of consciousness, because it's very brief and it can be missed. And it often is, to be honest.

Most owners don't see the road traffic accidents or, or, or they frequently don't. So, it certainly can be missed. Brain contusion is a little bit more severe.

It's where there's parental haemorrhage and edoema, or and or edoema. And you'll see clinical signs ranging from mild to severe. These are differentiated from concussion in that the unconsciousness stage lasts a little bit longer.

And you can see contusions of, of varying locations. So if they're at the site of the com site of the impact, they're called, coo lesions. If they are on the opposite hemisphere of the trauma, then that's contracoup.

Lesions, or you can have both, potentially, where the brain has been significantly displaced within the skull, during that trauma. Laceration is a more severe injury as that is occurring and causing a disruption of the brain parenchyma. And haemorrhage can occur either axially or extra axially, either of which can cause compression of the brain.

So axial is when you have haemorrhage within the brain parenchyma, and extra axiala is when it's in the space around the brain, OK? So, subarachnoid, subdural, or epidural. Now, let's talk about secondary brain injury.

And this is, this is, this is the one thing that we can be most focused on. So, traumatic brain injury is going to trigger biochemical events, and these events have the potential to lead to neuronal cell death, and they will, to varying degrees of severity. This is the beginning of secondary brain injury.

Now, Many factors can contribute to this, and most patients will have all, or certainly some of these occurring. There's a release of excitory neurotransmitters that affect the electron pumps, and when these pumps are abnormal, so your ATPA's pumps, when these are affected, you've got damage to the cells. When you've got these pumps affected, you've also got energy depletion and vice versa.

Energy depletion in this trauma can cause problems with these pumps. So we have some real electrolyte abnormalities. Not that we're seeing in the blood when we take blood samples, that we're seeing that you're not even seeing.

It's happening at a, at a cellular level, OK? You can also have ischemia, production of inflammatory mediators like cytokines. Production of reactive oxygen species that can be further exacerbated with haemorrhage, because components of, of, of our blood vessels can make that worse.

And, we can have accumulation of nitric oxide that, that causes other problems, that causes vasodilation. So all of these things can contribute in varying different ways to worsening injury to the brain, to the secondary brain injury. Now, primary and secondary injuries lead to worsening of cerebral injuries, OK?

And that's as a result of, of, of one part of this is impaired cerebral perfusion pressure that we've spoken about already. Recall, this is the force that drives blood into the brain, OK? And this blood supplies oxygen and nutrients.

Now, The Munroe Kelly doctrine describes intracranial dynamics, and it's actually pretty straightforward. It's basic maths, really. So, it describes the total intracranial volume that we've touched on a little bit.

The sum of the brain volume, the sum of the intracranial volume is when you add brain volume, so parenchyma tissue volume, plus CSF volume, plus blood volume, plus any mash mass lesion. Sudden increases any of these, so Such as increasing your brain volume with edoema, or increasing your blood volume with haemorrhage, OK? Sudden increases in any of these, due to primary or secondary injury can lead to significant increases in your intracranial pressure.

Why that's an issue is untreated or unresponsive intracranial elevations lead to brain herniation. Brain herniation, as I said, is not something that we can have a significant impact on. We certainly are a lot more crude in veterinary medicine, so there's a lot that we cannot do in human medicine.

There'd be more surgical interventions that could be performed, or even medical procedures in an, in an emergency state to, to spare the brain tissue, OK? We are a lot more crude and don't have The capabilities to do this. So that's why our, our preventative mechanisms are really important.

The, these various forms of herniation are classified solely based on their location. So transtentorial, the foramen, which is very common, false and calvarial. Now the clinical point at which we initiate therapy with head trauma and the extent of the appropriate therapy.

And the length of time that all this, this therapy is necessary is really poorly documented in dogs and cats. So the effectiveness of treatment and the prognosis for any animal can be really, really difficult to assess. So I wanted to touch a little bit more on the neurological exam.

This is the part where I am, I would, And I've put it at this point in the lecture, because, as I said, our, our first assessment are the body systems. And then when I've realised that my priority is, is a brain injury, I'm focusing on a mini neurological exam. And then I'm spending some time stabilising my patient, OK?

With my various treatments that we'll talk about at the last part of the, the lecture. And then we're coming back to make sure we have a complete neurological exam, so that I haven't missed anything in my evaluation. And part of that is, is a component of your physical.

Exam as well. This is when you're go back in, going back and noticing, oh, although I've got a traumatic brain injury, my patient, that is their priority. They've also got a fractured femur that I have to do something about that at some point.

It's just not going to be for the next day or so, kind of thing. So, a complete neurological exam is not really brief and is best done when the patient's stable. And the reason we're doing this is so that we can, for multiple reasons, we can localise the lesion, we can determine a prognosis.

Those sort of things. OK, so let us consider a full neurological exam. The core components of a full neurological exam include mentation, posture, gait, cranial nerves, and spinal reflexes.

We've discussed levels of consciousness already when we were talking about the modified Glasgow coalco. I just wanted to add in, A more severe grade of consciousness that we've not really mentioned. And I guess this is not the most severe, because the most severe would be, dead patient.

But the next stage would be a con, a, a live but brain dead patient. And this is referring to an absence of cerebrocortical activity or no brain stem function. And that's when we're using our modified Glasgow Coma score and our brain stem reflexes like that, oculocephalic reflex to make decisions.

So the difficulties we encounter, oh I, sorry, I should have put that slide up there. So the difficulties that we encounter in cats and dogs is how to decide definitively if a patient no longer has brain function. It can be actually really difficult to advise an owner on what to do.

And one of the most common things I'm saying to owners with traumatic brain injury is, I don't actually know what's going to happen. I don't know how your animal. Going to respond.

This where it is right now at admit might be the best it's going to be, and that's not appropriate for life. However, things could be very different in a positive way in 1224, 48 hours. OK?

And that can be frustrating in both respects, it can be difficult to manage when you have a cost constrained owner who kind of wants to know early if this is hopeless. So you potentially are making decisions on euthanasia really early in the game, when you don't really know if that's quite what you need to do, or you could be at the opposite spectrum, really frustrated with yourself or with the situation, because you don't have a crystal ball, and we don't have access to a lot of these tests, to say to an owner, I wish I had euthanized your dog two days ago because he's actually the same, and you've got a huge bill now and you don't have insurance. So, you know, it's actually really quite frustrating.

In an ideal world, we'd have access to a lot of tests that we don't, such as this bear test. So, this is the brain stem auditory evoked response test, and it's used to check for brain, brain stem function. OK?

And they use it in comatose patients. Obviously, here it's being used differently in a, in, for, auditory responses in a very conscious patient. But what it's doing is it's an electrical wave that's generated by the transmission of a nerve response along an auditory pathway.

Clinically though, we're relying on brain stem nerve responses. This vestibulocochlear, it's one of the most useful tools you can have that I've described on how you perform that a bit earlier. So now let's talk a bit about posture.

Posture and body position at rest should be evaluated and determined as being normal or abnormal, and should, could include some of the following categories, head tilt, head turn, wide-based stances. Those are in your more upwardly mobile patients. They're not really the TBI cases, OK?

This is more your generally neurological abnormal patient. These other postures are more relevant to traumatic brain injury, so decerebral rigidity, the cerebellar and shift Sherrington posture. Now, as you can see here, I've got a couple of Different images.

That can be quite difficult to differentiate between. So decerebrate rigidity is a posture that you see as a result of a rostral brain stem lesion, so the midbrain. It's characterised by rigid extension of all four limbs and episthetonus.

Epiotonus is extension of the head and neck backwards, like this dog on the left, the, Weimar runner. This posture is associated with a stuporous or comatose mental status. So, rigid all four limbs, abnormal mentation, which is different to the cerebellar rigidity.

You see epistotonus, you see the four limbs extended. But compared to the decerebral posture, these hips are flexed, and there's increased tone. You've got flexion of these back legs.

So there's increased tone in the ileosoas muscle. And the mentation also remains normal. These postures caused by an acute cerebellar lesion.

It can actually be episodic, so you can have varying severities during the course of your, treatment of this patient, not necessarily related to A deterioration of the mental state, if that makes sense. And then you've got a shift Sherrington posture, which is more of a, a spinal dysfunction. So myelopathy.

You see this with acute, severe, thoracic or cranial lumbar spinal cord lesion. So T3 to L3. And this posture consists of extensive hypertonia of the forelimbs.

So, increased tone of the forelimbs, a flaccidness to the pelvic limbs, OK? And you should have a normal mentation. The posture's seen with acute and severe lesions, but it's not necessarily associated with prognosis, which we used to think.

So now let's very briefly touch on gait. I don't want to make things too complicated, but, since you'll be constantly thinking about upper motor neuron and lower motor neuron evaluation for your modified Glasgow Coma score, for your localising of your spinal lesions, we need to understand a little bit about it. So, gait generation requires these two systems to interact, the upper motor neuron and the lower motor neuron.

Now, The upper motor neuron system is confined to the CNS and it's responsible for the initiation and maintenance of normal movements, OK? It also supports the body against gravity by providing tone to the extensor muscles. OK?

The lower motor the lower motor neuron system connects the CNS with the muscles to be innervated, meaning the upper motor neuron pathways are responsible for stimulating the appropriate lower motor neuron response, OK? And that induces posture and protraction phases of locomotion. Now, ataxia, that's defined as in coordination that results from either insufficient sensory proprioceptive input to the gate centres in, in the CNS, or a failure of the regulators, the central regulators of motor function.

Now, there are many types of ataxia, an example being cerebellar ataxia, where there's a cerebellar lesion causing abnormal regulation of motor function. So let's touch quickly on paresis and paralysis. Mainly because it's, it's a significant component of the neurological exam.

But to be honest, in the detail, is a bit beyond the scope of this lecture on TBI. Paesis is the loss of the ability to support weight and all the ability to generate gait, and it's seen as weakness or decreased strength of your voluntary motor movement. Now, paresis means that some voluntary movement is still present.

Which you compare to paralysis, which is severeparesis, OK, it's plegia, it's an absence of voluntary movement. Now functionally the spinal cord can be divided into 4 regions. And we use these spinal reflexes to help, help us localise lesions.

OK, that's why it's a significant component of your neurological exam. The four regions of the spinal cord are C1 to C5, which is the cranial cervical. You've got C6 to T2, which is the cervicothoracic.

T3L3, the most common we're going to see, thoracolumbar and L4S3, which is lumbosacral. Remember, the loss of function of any neurological system develops in quite a predictable manner. And you'll use this most relevantly in spinal reflexes, and you lose it in the following sequence.

First you lose postural reactions, then voluntary motor function, then you lose superficial pain sensation, then you lose deep pain sensation. Now, the first cranial nerve, cranial nerves. Part thereof are relevant to your modified Glasgow Coma score.

But once you've had the opportunity to do your full neurological exam, these can be really important to help you localise your lesion. Are you seeing lateralized changes in your cranial nerves, which helps you to look at a solitary lesion? Are you seeing diffuse absence of responses, which is either multifocal or diffuse changes?

OK? So the first cranial nerve attaches at the most rostral part of the forebrain, so right at the front as the olfactory bulb. This extends all the way back to cranial nerve 12, that's attached right at the back of the caudal medulla or blongata.

And all the others attached in sequence between these two endpoints. It's really important for you to perform an evaluation of all the cranial nerves. As I said, it helps you localise your, Differential list, and it helps you decide what is our next stage of diagnostics.

Are they warranted? Are they going to yield us anything? Or is it, if you're not doing any diagnostics, which is often the case, is it, is it changing the way we're intervening with our therapy because we're seeing a lack of response to therapy, or are we simply using it as way to monitor the patient and their resolution of their disease.

OK, resolution of their clinical signs because things are slowly improving. So there was an absence of a PLR one day, and now it has returned, might be sluggish, but it's there. So now let's have a chat about therapy of TBI.

There are many stages to treating the patient with TBI and and should include, A sort of a multi-factorial approach really, we want to stabilise the cardiovascular system. As well as the neurological stabilisation. It's very important to remember that no imaging is used during the early stages, and in some circumstances, it's not used at all, be it due to availability, or it's simply of no purpose, OK?

I certainly have access to, to the specialised imaging such as MRI and CT but I am not using it as much as, as, I guess I, you would initially expect in traumatic brain injury, because a lot of the time it's simply academic, the answers it's giving you. What I really care about is the patient's response to therapy. And often, by the time you think that you've deemed the patient safe to have a general anaesthetic, To go through these, this imaging, you're kind of thinking, well, things are getting better, so it, it, it is, at this point, it's academic.

It maybe becomes more relevant to do these more specialised imaging if there's a failure to respond or a deterioration, OK? The most useful imaging tool, would be either MRI or CT. Not only can we evaluate more with, with a CT, we can use this to assess the entire patient as well.

Remember that large changes inside the head can be detected with CT, but many smaller lesions can be missed. A more accessible tool is survey radiography, and it's really useful in a trauma patient. Recall that CT is basically a 3D version of radiography.

So, survey radiographs are really important, OK? The most important thing to note with TBI is, as I said, just don't rush. And it's actually the case with any emergency patient.

Be sensible with your imaging tools and don't rush into them. And often the most useful is the less invasive hands-off approach and you can use ancillary tools such as point of care ultrasound to help you give, give some information. OK, so maintaining adequate perfusion and extracranial stabilisation is really important, and the, the main reason being to prevent secondary brain injury.

Hypovolemic shock is going to be really common in your patients with TBI, and volume resuscitation goals should be pretty aggressive to target a mean arterial pressure of 80 to 100 millimetres of mercury. For patients without electrolyte disturbances, I think a normal saline is a good initial choice for fluid resuscitation. The reason being it contains a small amount of free water, .

And it's the least likely therefore to contribute to cerebral edoema. Other options are synthetic colloids. Or sometimes people use them as a combination with their saline.

Patients that don't respond to volume resuscitation require vasopressor support. So don't be shy to start these. Don't chase these patients that are hypertensive with significant amounts of fluids.

I would be starting vasopressor therapy, and in general, my first choice is norepinephrine, if I'm going to use a vasopressor. My second choice, would Would be dopamine. And I would use dobutamine, catecholamine, as a, as an appropriate choice in a patient that potentially has, Cardiac muscle dysfunction, so there is a unique population that you would benefit from that, but my tend to be my, my drug of choice would be, would be norepinephrine if I needed a vasopressor.

We'll talk more about hypertonic saline and Manatol in, in just a minute, for fluid choices. So, techniques to decrease cerebral blood flow really or cerebral blood volume are really important. And the reason we're doing that, as you recall, is to reduce high intracranial pressure.

Now, we can do this with positioning of the patient, so we'll The target you're aiming for if you are going to elevate the head is to elevate it by 15 to 30 degrees. This, the benefit of this is to increase venous drainage, now, Be, be really careful to use a slant board. To do that.

And you could use anything as simple as a cage divider or anything that's not going to bend. We want to be the reason we don't want to use something like a pile of pillows is because, yes, you're elevating the head, but you're doing it at the expense of blood flow. To the brain, OK?

So you're occluding the jugular veins, or you're including veins in that whole region, OK? So you, you, when you bend the neck. Remember, also the elevations, you can do, you can go too far.

So elevations of over 30 degrees can cause a significant decrease in cerebral perfusion pressure. Another thing you should be managing to help with your, cerebral blood volume is to manage hypoventilation if that's occurring. We want to try to prevent that, and that will lead to reduced cerebral vasodilation and decreased cerebral blood flow, OK, if you don't.

You should aim for normal capnia with an arterial CO2 of 35. To 40, which equates approximately in your venous blood samples, which you're most likely going to be due of of about sort of 45 give or take. In animals with acute intracranial hypertension, short-term hyperventilation is advocated in some patients, and you target a, so in, in that situation, you're targeting a lower CO2, 25 to 35.

The reason this is done is to reduce cerebral blood volume and intracranial pressure, but The reason we don't do this regularly is, it's hard to know when the exact time, when is the right time to stop. And that the negative of that is if you're doing it for too long, it can decrease cerebral blood flow and that will lead to ischemia of the brain. So cerebral ischemia and, and a worsened outcome.

So back to the our hyper osmolar therapy. Now Manitol can decrease intracranial pressure, it can increase cerebral perfusion pressure and blood flow, and as such it can then have quite a significant beneficial effect. On neurological outcome in patients with TBI.

It also has additional benefit of free radical scavenging. Remember we mentioned that free radical scavenging, free radicals can lead to secondary brain injury. So it could be a bit of a multi-factorial benefit.

The most rapid effect of Manitol is it's real logic effect, where it decreases blood viscosity. And by making the blood less viscous, then you'll increase blood flow. And by increasing blood flow, you're increasing 02 delivery to the brain.

After this, the osmotic effects are seen where water's drawn out of the parenchyma and into the intravascular space and where potentially resolving edoema. The negative effects of Manito, so this is potential for some people quite controversial. The negative, effects of Manatol include increasing permeability of the blood brain barrier, and that allows it to leak into the brain parenchyma where it can make edoema worse.

You can reduce this by giving it as a bolus rather than a continuous CRI. Treatment should always be followed by isotonic crystalloid. Or some form of ongoing fluid maintenance therapy, we want the the goal being to maintain intravascular volume.

Now, hypertonic saline, I, I would say that's probably my choice. I use that to both volume resuscitate my patients that are in shock with traumatic brain injury with the additional benefit of, being a hypermolar agent. So, and that's why it, some people feel it has an advantage over Manitol.

So the sodium in hypertonic saline doesn't freely cross the blood-brain barrier. So the hypertonic saline has a similar, similar reallogic effect and as an osmotic effect to Manitol. In addition, it also improves the hemodynamic status, OK?

So it has, as well as those two things, it also has additional immunomodulatory effects and beneficial vasoregulatory effects. And additional to this, because the sodium's redistributed within the body and safely, readily reabsorbed in the kidneys, hypertensions are less likely sequelae than Manatol. And for many reasons, reasons, it's often a better choice for patients with high intracranial pressure and systemic hypotension.

Oh. OK. So, other components of therapy, diuretics such as rosemide are not generally recommended, as they're associated with volume depletion and systemic hypertension.

And that's going to lead to a decrease in your cerebral perfusion pressure. So I would avoid rosemide unless I was dealing with a patient in heart failure, so needing it for other reasons. Corticosteroids are currently not recommended, they're associated clearly with the worst outcome.

Also recall that patients with impaired perfusion are being, are in this TBI category that we're dealing with. So, corticosteroids will be further potentially contraindicated. And also just be simply consider that you might want to use a non-steroidal in the next day or so.

Good pain control is really important, OK? It helps you control intracranial pressure. It prevents increases in metabolic needs.

In the initial stage of TBI, I would say the most appropriate class of drugs will be an opioid. I tend to use a formul agonist, so such as methadone or fentanyl, so that I can titrate it quite rapidly. Always start with a low dose and titrate up.

So I would potentially give, methadone 0.1 mg per gig, or I'd give fentanyl 1 or fentanyl 1 or 2 mcg per kilo. And remembering that fentanyl will eventually need to go on as a CRI, and I do that if I've got a significant concurrent orthopaedic injury, I probably would start off with methadone first.

I tend to avoid non-steroidals. To be frank, I avoid non-steroidals, full stop. You know, the patient population I see, most of them, they, in general, shouldn't be having non-steroidals.

So it's certainly not a drug I reach for readily. But I would recommend avoiding them until your patient's cardiovascular stable, OK? And you can confirm that they've got a nice normal renal function.

They're often indicated a little bit later on in therapy, so maybe after a day or so, once your patient is stable, and you're going to need some form of ongoing analgesia, again, if they've got some sort of orthopaedic injury. Management of ventilation in these patients is often required as well, or can be required. Treating hypercapnia is the main indication for mechanical ventilation in head trauma, I would say, but it can also be indicated due to hypoxemia, respiratory fatigue, if they have significant brain injury, they could be breathing very abnormally, so significant, tachynia potentially, and these can make them fatigue over time.

Not, not initially, or potentially they've aspirated because they are very mentally inappropriate, they're recumbent, and they've got a reduced gag, and they've vomited. And then aspirated. Oh, sorry, I think.

Went too far. Yeah. So, the Human Brain Trauma Foundation states there's insufficient evidence to recommend, barbiturate coma, OK?

What they do currently recommend is a mild to moderate therapeutic hypothermia in severe TBI, OK? And they do this for 2 days. But in general, I think the advice you need is to not allow hypothermia to continue, OK?

This will increase, if you've got significant hypothermia, you're going to get a high metabolic rate. And every 1 °C increase in temperature will lead to, a 5 to 7% increase in your metabolic rate, which is quite significant, and that's all going to lead to secondary brain injury. Post-TBI seizures are really common in humans, but they're poorly documented in veterinary medicine.

What I can say is prophylactic anti-convulsant therapy is not indicated. However, animals that are seizuring should be treated as you would treat any other patient with seizures. No drug would be indicated over the other.

Blood glucose should be closely monitored. Hyperglycemia is associated with severity of head trauma in dogs and cats, and it's likely to be inversely related to outcome. OK?

And the reason we suspect this is the case is it worsens secondary brain injury. And don't forget the other things. Always come back to your Kirby's rule of 20.

What's happening with urine production? Is the patient recumbent and is it urinating normally, but it's laying in it, or it can't pass urine because it's got abnormal tone to its bladder? So do I need to put a urinary catheter in?

Why, where am I at with nutrition? It's been recumbent for 3 days, therefore not eating. Should I be doing something about feeding?

Take care to remember that feeding tubes. Will initially be contraindicated because it will increase your intracranial pressure by placement of these tubes, OK? But it's something to think about, potentially you could consider parental nutrition, OK?

Soft bedding, turning, physiotherapy, so you don't get bed sores, eye lubrication because they're not blinking. These patients really commonly get really nasty eye ulcers, so that's certainly something to also think about. Part of your ongoing diagnostic tests, ongoing monitoring can include quite a lot of different tests.

In general, these recumbent patients with TBI have a multi-parameter monitor on them. So I'm monitoring heart rate and rhythm, respiratory rate and effort. I'm looking at the SPO2.

If they're intubated, I'll be monitoring their CO2, ETCO2. We should be monitoring their blood pressure hourly. Coming back to our Cushing's reflex, keeping an eye on their temperature, they're more inclined to be hypothermic.

However, if they're not in oxygen, they can often get hypothermic, urine production, like I mentioned, and nutrition, we've already touched on. Don't forget this modified Glasgow Comaco. This isn't something I do every couple of hours or once or twice a day, every hour, until their mentation is Either close to normal or normal, and don't forget your pain scores, pain scores of mentally inappropriate patients are very difficult, however, I would never not do it, OK, you just have to often make decisions thinking, You do have an orthopaedic injury, you are comatose, you must need analgesia, I have to be sensible and give you some, but I also have to be sensible to not give you too much, give you give something I can reverse readily like I mentioned.

Now, when it comes to our diagnostic tests, you've, you've got your baseline, baseline blood tests that are pretty straightforward. I like to see my red cell concentration on my patient daily. I like to know what their electrolytes are doing because they're on fluids.

I want to know what their blood gases are doing. You don't need to rely on arterial blood gases to see how they're ventilating. You just need a venous, so you can look at their CO2 and decide if that's above 40.

That's OK, like we mentioned that number already, but if that's above 50, I need to be keeping a bit of a squinty eye on that because I could be trending towards inappropriate respiration, OK, inappropriate ventilation. Depending on how my patient's progressing, I might consider coagulation evaluation. So looking for lung worm, looking for, PTA, PTT, and platelets.

Has my patient got a, not a red herring, but a secondary issue that was irrelevant until they suffered a trauma. So have they bled significantly in their brain because they actually happen to be brewing a concurrent coagulopathy that was only relevant till they've had something invasive occur? Pocus, point of care ultrasound is really important.

Every day on my, recumbent critical patients, anything in ICU is getting a chest and abdominal pocus. You're doing this in traumatic brain injury to be making sure you're monitoring other components of trauma, really, to be honest. And there's not a great deal that you'll be using a point of care ultrasound for in for a primary brain injury, OK?

And we've already mentioned survey, radiographs, and CT. Oh, I got my slides back to front. I've already gone through that in detail.

The anticonvulsant therapy, glycemic control therapy, and, and corticosteroid use. So, I just wanted to touch on prognosis a little bit. Now, it's really difficult to predict in traumatic brain injury.

Pupil dilation, loss of PLR, and deterioration in your level of consciousness is a Actually a poor prognostic indicator, OK? In human medicine, a high blood glucose admin and a persistent high blood glucose is associated with a poor outcome. It has also been associated with the same in veterinary medicine.

It's not been well validated as an independent predictor of outcome, OK? So it's often associated but not generally the only tool that we use. This paper here looked at the prognostic value of clinical and laboratory values and scoring systems in dogs with head trauma.

Some of the risk factors for non-survival included a low low SPO2, low pH, low bicarb concentration, or a high potassium, high lactate, high BUN and high animal trauma triage score. These things are associated with poor survival. The most useful information for, as a predictor of non-survival in this paper was a decrease modified Glasgow Coma score, OK, and a score less than 11 was highly sensitive and specific for predicting death.

However, I think what's really important, not related to this article, but just in general, really severely affected animals, like I said in my first slide, can have a really favourable outcome, OK? Especially young animals, they can be quite outstanding. I've treated many a stuporous, delirious, comatose cat that's gone home, either a few days or a few weeks later.

This next slide is a perfect example. Give these animals time if you can, and you can do this in a really cost-effective way. This cat here, Monty, presented to me during my residency after he was hit by a car.

He had a higher, modified Glasgow Coma score under 10, OK? After he was stabilised, he eventually, only imaging wise, had bedside imaging, so bedside ultrasound. He also ultimately had a feeding tube placed, an O tube placed after a couple of days, a good week of intensive care, but he walked out the door 2 weeks later.

He walked out blind, and then 3 weeks after that, he had vision. So, over time, and with a lot of care and, and support at home as well as in the hospital, he went home. And it wasn't really an exorbitant bill.

And when I say exorbitant bill, we're in the realms of 3000 pounds. So, it's not small, but bearing in mind we were a referral hospital. So these are really cases that I would give.

TBI, I really, really give them a go. Any questions? Thank you so much, Kerry.

That was great. I've not got any questions through yet, so if anybody would like to ask any questions, just pop those in the Q&A box for us. We have, just while we're waiting for those to come through, there is, a survey which you should all have popped up on your screen, for feedback on the whole Wiki about stream.

So just while you're all thinking of lots of great questions for Kerry, thank you so much. That was a really good talk, really interesting subject. And some really good explanations of how the anatomy and physiology link back to sort of the clinical approach and understanding the process as well.

So thank you very much for that. Oh, that's OK. Thanks for having me.

Yeah, it's fantastic to have you. Just there's some chats coming through saying, thank you very much for a great webinar. Not got any questions.

Oh, very comprehensive in one hour. I completely agree. That was a huge amount of information.

And I think that's probably why we've not got many questions, because actually, it was a really comprehensive overview of the topic. So, thank you very much for that. So don't forget to, click on the link to access the virtual goodie bag.

And I just want to thank everybody again for attending this Wikibat stream. Thanks also very much to Webinar back for inviting us to host the stream, and also massive thanks to JHP Recruitment for their kind sponsorship as well. Thanks to everybody for attending, and enjoy the rest of Congress.

There's still lots of good stuff to come. I'm going over to the wildlife stream now, if anyone's interested in wildlife. And I'd just like to thank Kerry again and also Stephen and Balash, our earlier speakers for a fantastic stream.

Oh, thank you so much for having me. It was great. You're welcome.

Oh, I've got one question now, just right at the end. How long do you give methadone or opioids, and can they subdue mentation? Yeah, absolutely, yeah, really, really good suggestion, they, they do, simply they do, subduementation, so I tend to start off conservative, so, so a non- TBI patient, I give methadone, Either 0.1 to 0.2 every 4 hours.

In TBI, I might go 0.1 6 hourly, or I might do 0.05, so a super low dose and see what happens.

And if I get an appropriate response, then great, I'll stick a 0.05. But if I think it's not enough, I'll trickle it up.

So yeah, yeah, good suggestion. I would delay it a little bit. Lovely, that's great.

Thank you very much. Thanks for that final question there and thank you everybody for attending. Thank you, thank you.