Thank you very much, Sophie. Hi and welcome. So, obviously, we're talking about traumatic brain injury this evening.

We're gonna go through the normal brain physiology. I think it's really important to talk about how the brain normally works, talking about that cerebral perfusion pressure, cerebral blood flow, intracranial pressure, and how they all work because then when we come to that, traumatic brain injury, pathophysiology, we're gonna Integrate that and think about how those are affected, and then how that is in turn going to affect those patients. So then we'll come to patient assessment.

We'll be talking about clinical signs, clinical exam, and what we're looking for, and what we might expect to see, change over the course of treatment, as well as, You know, diagnostic imaging and tests that we can perform on our patients both in the triage, scenario and, more into their critical care stay, in hospital. And then we're going to go through treatment options, the different tiers, and then a quick brief look at contraindications as well. So let's look at the path physiology of the brain.

So first, I'm gonna look at the definition of traumatic brain injury. So we've got, brain damage due to contact injuries. This can result in contusion, concussion, laceration, and intracranial haemorrhage.

And this brain damage may also be due to hypoxia leading to progressive neuronal damage. So when we think about, most of our traumatic brain injury patients, they're gonna be, multifocal or polysystemic patients. So more often than not, these patients have been involved in a road traffic collision, Or they've had some form of concussion, you know, I see, dogs that have, run into walls, even those that have for us down in the south as well especially is falling off cliffs, you know, any, any injury that results in that concussion, contusion, concussion.

If there's any lacerations, and hypoxic events would be examples such as drowning, electrocution, respiratory arrest, and that would then lead to that progressive neuron damage that will come to you in a little while. Do you look at cerebral perfusion pressure. It's really important, to maintain the, blood flow through the brain, and keep that intracranial pressure, at the right level.

So the cerebral perfusion pressure relates to the net perfusion pressure that drives oxygen into the cerebral tissues. So it drives this oxygen in, and it normally rests at a 50 to 100 millimetres of mercury, as a normal value. So it's the difference between this mean arterial pressure.

This is often the one that we will monitor, because intracranial pressures, you can, Measure it non-invasively and invasively, but often this is just in human hospitals. So often what we're looking at is this mean arterial pressure, and this can really be affected, by the cardiovascular system having a knock-on effect. So as we've talked about those motor accidents, that they're often affected, cardiovascular, so often these patients will be hypovolemic, and that's going to have a knock-on effect on the cerebral perfusion pressure.

So we look at this equation here, we have cerebral perfusion pressure equals mean arterial pressure minus the intracranial pressure. I'm And then so, but as I said, it depends on the cerebral perfusion pressure and The cerebral blood flow depends on this and also on this cardiovascular resistance. Any cerebral hyper perfusion, in the early stages of injury, is going to be significant, if the cerebral oxygen, consumption isn't matched.

So this is why we just need to keep this blood flow at a constant rate, and we need to keep these values within normal values, otherwise, the there's going to be hypoxic injury to the brain and those tissues. Can we talk about cerebral blood flow, this supplies the oxygen and the glucose to the neurons. This is essential for, ICP homeostasis.

It's self-regulated through auto regulation, and this is despite changes to blood pressure and cerebral vascular resistance. So this will constantly trigger this, auto regulation to maintain the cerebral blood flow. And so when this auto regulation is triggered, and this is triggered when there's an increase in blood pressure, an increase in cerebral vascular resistance, and this causes a cerebral vasoconstriction, and a decrease in, The cerebral blood flow so will lower your cerebral, blood volume.

And so like I said, this is critical to this ICP homeostasis. This is the most important thing to keep those neurons and those ATP regeneration growing. So we have intracranial pressure, so we've mentioned this a couple of times.

So the intracranial volume is the net worth of the brain parenchyma, cerebral blood volume and the cerebral spinal fluid. And so whilst this skull is a rigid structure, it does need some, some degree of intracranial compliance, and, and this is just to allow, the fluid to exchange, and also to allow some protection, because if it was just rigid and solid and the brain moved around, then there would be a degree of injury every time that patient moved essentially. So there is some movement, but obviously, fractures are gonna cause more movement than, is necessary, and it's gonna change that, compliance and the intracranial volume.

So when we're talking about I'm maintaining this intracranial pressure, and the blood and the CSF will be shunted to the body to maintain this. So if there's going to be an increase in the ICP, and then all this blood and CSF that's in the in the brain will be shunted into the body to manoeuvre and allow for for that. Intracranial compliance.

Raised intracranial hypertension, it compromises of cerebral perfusion over time, and this causes, ischemia, and so, Usually in our trauma, there is some parranal damage, and blood leakage in, and this is gonna, potentially exceed intracranial compliance capacity and then in turn increase the ICP. So we talked about, you can measure, ICP and the normal values are 95 to 10 millimetres of mercury. It's quite an expensive way to, measure ICP and Currently, there's not many hospitals that will be able to do this either invasively or non-invasively.

So you just have a quick look at this equation and break down, where our patients that come in with traumatic brain injury, the different areas, So as I've talked about the traumatic brain injury, they often come in as a polysystemic trauma, and these patients will be hypovolemic and potentially have some form of systemic hypertension. And this is going to change your mean arterial blood pressure, and Often in these patients that have a direct head trauma, so the ones that have got, contusions, or even lacerations, there's going to be haemorrhage, and edoema, so, cerebral edoema, and swelling of the brain, so it's going to change that in cranial pressure. So in turn, these are going to change that cerebral perfusion pressure, and again, will in turn.

Decrease that cerebral blood flow. And then it becomes a bit of a, vicious circle in that that decreased cerebral blood flow. It's gonna cause a decrease in oxygen and glucose supply to, the patient's brain to the neurons, and that's gonna cause hypoxic damage, which, as we looked at in the definition.

This is then gonna cause further brain damage. So we're gonna look at the, the pathophysiology of the traumatic brain injury, but now we've gone through, this equation and a breakdown of, cerebral perfusion pressure and intracranial pressure, perfusion, and then now we can have a look at, the pathophysiology of the actual brain injury. So when does traumatic brain injury occur?

So primary is the ones that we'll often see, they come in after this event. So there's not much that we can do to change this primary event. And the aim of treatment is to prevent the secondary, traumatic brain injury.

So, Primary is acceleration or deceleration, or impact. And as I've reiterated, it may be a polysystemic trauma. And so it's often really important to consider the patient as a whole and not just to look at the traumatic brain injury, and considering, we'll come to treatment, but things like if your patient has lost a lot of blood from elsewhere, and that's why the hypovolemic, do we need to be replacing like for like.

And so this, impact, like I say, we can't avoid this impact that's already happened. We're now going to be trying to prevent this secondary traumatic brain injury. And this is the one that's, quite severe in terms of it, it's hard to reverse the effects of the secondary, brain injury.

And this is a delayed non-mechanical damage, and it's due to cerebral ischemia, and increased intracranial hypertension. So both these together will cause, an accelerated, degeneration of these cells. So when we look at the primary injury path physiology, so you have this direct damage.

So whether it be that they hit a collision in a car, they've run into a wall, fallen out of a building and hit their head, even, I think sometimes we, these patients that come in with just a small laceration on their head, it's important to remember that it is a brain injury, that's a, a direct tissue damage. And whilst it might seem like a small laceration on the outside, it's always important and imperative to, look for those clinical signs, to continue monitoring those clinical signs for any brain injury, because we want to try and stop. Any secondary brain injury from occurring.

So once this direct tissue damage occurs, we're gonna have an impaired regulation of the cerebral blood flow and metabolism. So as I've said, the cerebral blood flow is going to be reduced. This means that there's not going to be as much oxygen, carrying haemoglobin, reaching, the neurons, and so we're going to have a hypoxic event, and this metabolism is going to be slowed as well.

So we're not going to be able to, get rid of this lactic acid. So there's going to be an accumulation of lactic acid. And with this then becomes an increased membrane, membrane permeability, and leads to an edematous formation, in these membranes, because there's, the exchange that normally happens isn't gonna occur, and this fluid is just going to sit there, so, you're gonna get cerebral edoema.

And from this, we then get, these ATPs, stores depleting. So, adenosine triphosphate. They're gonna degenerate and so they're gonna go into, adenosine, diphosphate, adenosine and monophosphate, and then down into nucleotides, which are then unable to, Regenerate to ATP, and so this is going to cause a failure of energy dependent membranes.

And so from this then your cerebral blood flow autoregulation is going to be impaired. So you're not gonna be able to get that cerebral blood flow back up to regenerate and, you know, give the oxygen and glucose to the cells and, and restore that metabolism. So once we've had this primary injury, we then come to the, secondary.

Injury. And the path physiology for this one. So once we've had all this, reduced cerebral blood flow, you know, your ATP is depleted.

We're going to reach this terminal membrane depolarization. So from this, these are going to depolarize and there's gonna be an excessive release of excitatory neurotrans neurotransmitters. So glutamate and aspirate.

And these are gonna activate the, NDMA, and voltage-dependent calcium and sodium channels. These channels are going to be open and there's going to be constant firing, and in turn, this is gonna cause a catabolic intracellular processes. And this then breaks us down and there's going to be a release of free radicals at this point.

And so we know that free radicals are bad, and they cause an inhibition of DNA repair, and fragmentation as well as the DNA. And this DNA I'm Fragmentation and the inhibition of the DNA repair, will cause cell optosis, and necrosis to all these vascular and cellular structures. Then you get, you know, the cell death, and at this point, you're not gonna be able to regenerate those cells, and Basically regenerate and renew that brains store and at this point, these patients, they have a grave outcome.

So when we go through patient assessment, It's really important from the beginning. To still think about your ABC, so your airways, your breathing, and your circulation, because all these things are gonna affect your cerebral blood flow, you know, your oxygenation, of the brain. And obviously we need patent airways in these patients.

So when these patients come in, often they come in, they're rushed in, after a road traffic accident or they come in as emergencies. It's not very often that they come in as, you know, as a, an outpatient that's made an appointment later in the day. So always go through your ABC.

And I just checked, . Snout to tail, all the way down, but in particular focusing on the airways, the breathing rate, is it erratic, you know, is that patient, does it have any crackles, wheezes, any stutter? Is there any damage to the airways, so any physical trauma?

For example, you know, tracheal tears that you can see, or, is there any punctures to the chest, chest wall, is that all intact? Again, looking at the pattern, erratic patterns, can be quite common with Traumatic brain injuries, and looking at the effort as well, is this patient putting a lot of effort into breathing, they got paradoxical breathing, You know, have they got any other strokes, so, you know, is there potential that there's gonna be a diaphragmatic hernia in these patients as well. And as I said, having to listen to that, the whole thorax, listening to each area, you know, ventrally dorsally, and splitting them into four quadrants, and again, with the heart as well, listening for any murmurs.

You know, any muffled heart sounds, you know, these patients have the potential for, pericardial effusion or pleural effusion that may be, masking the heart sounds. And with the heart rate, I'm just checking, is it synchronous to the pulses? Again, is this heart rate regular?

Is it synchronous to the breathing patterns, You know, and if there is any abnormalities, you know, noting whether they're regular, a regular or a regular regular, and And if so, obviously putting a But I'm An ECG on And again, with the pulse quality and rate, I like to feel, multiple pulses. I often will, go for the metatars or pulse first, and just seeing whether these pulses, what the quality of them are, you know, are they smooth, are they weak and bounding, are they thready? You know, a pulse will tell you a lot about, you, Volume dynamic of the patient, and whether these patients potentially are hypovolemic.

And to follow that up, you know, doing a blood pressure, and doing a blood pressure in these patients, ideally before we get these patients on fluids, so we can see that the response to, fluids, whether we're giving them shock rate bolus, and the response to those. And On a small note with this one as well, I often look for dehydration signs as well. So I've seen, tacky mucous membranes, decreased skin to, and just, I'm assessing that as well because we'll come to the significance of, you know, ensuring these patients are, evolemic, and just making sure that these patients aren't dehydrated before we give them, medications such as, Osmatic diuretics.

And then temperature, again, this will tell you about your perfusion status, and, often these patients with traumatic brain injury, they may often, be hypothermic, and will come to warming them in a little while in the, in the treatment section. So when we're looking at these patients, often these patients aren't walking in, they may walk in, and in which case, we might look at the gait, you know, whether they're a toxic, you know, if they are toxic, is it just the front limbs? Is it all for imbs, just the hind limbs, and the way that they're walking, you know, are these patients circling?

If so, are they circling to the left or the right? I You know, these patients have any head tilts on nystagmus, and often, you know, vertical nystagmus, or rotational nystagmus is a, is a sign of head trauma. And when we're looking at the nystagmus, whether we've got, a fast phase and a slow phase, so often the fast phase will run away from the brain lesion, and then slow phase back.

And so we often see this in long term, neurological patients, but it's good to get into practise, especially with head trauma, and to look for these signs, . Because it may indicate a haemorrhage, that we're not aware of, or prior to imaging that we may, suspect. So when we're talking about, decereb rigidity, these patients, are often stuporous or comatose, and all four limbs are rigid, and they have and they'll have epistoonis as well.

And this is an indication that the lesion or a haemorrhage is in the rostral brain stem, Whereas, in contrast, we have the decerebellar rigidity on the right, and these will have, rigid front limbs, epistotonous, flexion of the hind limbs, but they are often with it mentally, you know, they're conscious, they're able to respond, to, to sound, and, and potentially, vision as well. . And this is an indication of a rostral cerebellum, problem.

And so whether it's a lesion, whether it's a, a contusion or, or edoema in that area. And then there's just a third one that I'm, I'll go through. I haven't got a picture of, is Shift Sherrington.

So I think a lot of people know this one. So it's a thoracic limb, extension, and pelvic limb paralysis, and this is an indication of an acute severe lesion of the thorac thorac lumbar, spine. So you may see this if this patient has been in a, a polysystemic trauma, for example, in a road traffic accident, they may have, fractured the spine, in this area, and they'll come in and shift Sherrington.

So it's just important to remember these postures, and looking for your patients because it may be your patient comes in, Normal or I'm, you know, I'm with one and then becomes a deer but rigidity or of Sherrington, if the edoema or haemorrhage spreads. So we're talking about people size and symmetry as well. So this is, in response to the parasympathetic and sympathetic responses that we see.

So we're looking at whether these pupil sizes are equal, you know, if there is any myodrosis, or meiosis, and In reaction to a pupillary light response as well. So the sympathetic sympathetic neurons are in the thalamus, is the first arrow, and then the non-sympathetics and the medulla logo, so the second arrow, and the, sympathetic neurons, . Are responsible for, the people's constricting in the dark, sorry, in the light, and the non-sympathetic non-sympathetic would be, parasympathetic would be.

The pupils constriction in the light. Sorry, I'm Parasympathetic, is constricting, in the light and then, sympathetic is, expanding in the dark. And often what we'll do is a test, is to cover 11 eye, and shine the light in, the uncovered eye, and just measure the response in the covered eye.

So does that, concurrently, Contract, or in, in light, in response to the other uncovered IB . Shone with a light. So we come to testing the cranial nerves, .

And so I am, there's a lot of rude, Anagrams out there, but I just remember, 000, to touch and feel, a very good velvet, such heaven. It's a less rude one than I originally learned, and I'm sure many of you, have different ones. But we just want to go through, all the different cranial nerves, just to see if there's any affected, And just to, make sure that none of these are affected, and it's a good, objective test to continue doing throughout that patient's stay, you know, to monitor improvement or, Make sure that it's all continuing to be the same.

So obviously we have the Pupillary light reflex, and this is the cranial nerve too. And we've just talked about that, and like I said about the, covering, of one eye and measuring its response to the uncovered eye, and making sure they match. And then so we have a physiological and nystagmus.

And so to, test for this, we want to move the animal's head quickly from side to side, while we look into this, into the animal's eyes. So it's characterised by a quick, eye movement phase in the direction of the head movement and then a slow phase in the opposite direction. And so with cats, it's easier to hold them under their forelimbs, and then you just sort of turn with the cat facing you, and so you turn both ways.

And so any lesions, or haemorrhage or edoema in the ocular motor nerve, region will cause a fixed, ventrilateral strabismus, along with a lack of, conjugate the stagmus. I'm So then we have Protosis, which cranial nerve three, that's drooping of the eyelid. And we would evaluate this by, the menace reaction and then the PLR, .

And this menace reaction, it doesn't only evaluate the second cranial nerve, and but also looks at the ocular components and. And, the visual pathway. So it's good to test that as well, to test, ocular and vision and function as well, because, some patients, I've seen a lot of cats, especially, that, can become blind either in one or both eyes.

I'm And then so the palpibr reflex, so you just gently touch the medial canthus, the lateral canthus, so this will measure the ophthalmic branch and the maxillary branch, as well as the base of the ear, and of the jaw so the mandibular branch. So the effron part of the reflex is sort of mediated by the facial nerve, and it will result in the eyelid closure. And then we have nasal sensation as well.

So we, you can use a piece of cotton wool, and, or we can touch the upper lobe and the nasal septum, and then basically you just want a reaction from your patient, you know, often these patients will move away from, away from the touch, . And then in addition to this, you might, have an eyelid closure, . So you often get your early closure plus your Push your movement away.

And then we have our He tilt pathological nystagma. So I talked about this already. About the moving, but this path like I said, this pathological, agnosis can be, present all the time, or just when these patients, are being moved, in lateral flexion or full extension, .

And So usually when you've got the head in full extension, it's usually in cases of less severe involvement, . And it may mean that there's some involvement of the vestibular system, I'm And then we have the gag reflex, so again, we just would. Open the mouth, and test the gag reflex by, you can use a tongue depressor and tongue depressor or, you know, if you're looking at the tongue, It might elicit a gag reflex from them, and again, a movement away.

Less important, in, these patients because, muscle wastage on their shoulders and neck, which is the cranial nerve 11, this is often just going to be in long term, neurological patients. But it may be an indication of deterioration in these patients that we've had him for a little while, But it's just one to remember. And then Tongue symmetry, again, this is one that we'll see in long-term neurological patients.

Just again, it's a, because of the muscle, it's just the way the muscle wastage, due to use, that's cranial nerve 12. So we have a little lab in our lab. And, so when we talk about diagnostics, I think the most important A is blood pressure, and then B, for me would be the arterial blood gas, because these are two, so your blood pressure is gonna tell you mean arterial pressure.

And whether you do this non-invasively or invasively, you know, you can get a, a figure, that's gonna help you to decide, . Where these patients being properly profused, and, you know, give you a, a good idea of, of that, you know, ICP, and cerebral perfusion pressure as well. The ECG, as I mentioned, this is if your patient has got any, Cardiac abnormalities, it's good to put these patients on multi-parameter monitors while they're in hospital.

Because with traumatic brain injury patients, we're going to be with them constantly, and we want to make sure that these patients, And monitored at all times and it's very difficult to do that sometimes in a hospital setting, and particularly with staffing numbers, you know, other emergencies coming in. So having that multiparometer, with, markers for the ECG and blood pressure for alarms to go off, will assist in identifying abnormalities, if there's not someone with that patient 24/7. So arterial blood gas, it's really important because you have you Your partial pressure of oxygen, partial pressure of carbon dioxide, along with glucose and blood pressure, and the blood volume all assist in this auto regulation of the cerebral blood flow.

So we go back to that cerebral blood flow being directly linked to cerebral perfusion pressure, and again, that mealter blood pressure, the difference between that with ICP. So, We talk about lactate because the buildup of lactate is gonna cause changes to the metabolism and those ATP depletion. So it's good to have those little lactate monitors.

We can do quick lactates. Again, lactate is a really good, objective, . Monitor of how well you're perfusing these patients, and how well they're responding to those fluids.

I know it's adding there as well, sort of . PCV, and is really good as well. PCV in particular, because if we're looking at PCVs of less than 20%, and potentially total proteins of less than 50 grammes per litre, then we want to be looking at blood products because, the best practise is always like for like.

So if we've not got blood products available, or, you know, there's concurrent issues going on with these patients, then oxyglobin as well is a good alternative for 2.5 mL per kilo, to increase the oxygen carrying capacity. So we're talking about blood pressure.

We want to be making sure that I mean arterial blood pressure is in between 8 to 100 millimetres of mercury, you know, or potentially just a systolic of 120, . If you I'm doing a manual, you know, Rather than asymmetric or an invasive method, you know, if you're using a sigmometer, A systolic of 120, should ensure that you're, reaching that correct immune arterial blood pressure. And then we come to radiography and MRI .

So, in these patients, Obviously, an MRI would be the most beneficial, because it gives the best image, For diagnostic, . Quality, and to be able to identify bleeds, and edoema, and any fractures. But we can do, radiography in-house, before we refer, if we need to refer for MRI, if we think this patient may need surgery.

So with radiography, we want to be, making sure that we, take, lateral views as well as, DV or VD views, and making sure that we get, Involvement of the, cervical area as well as into the thoracic, thoracic lumbar and spine. In particular, you know, these patients look like they're in shift Sherrington, as we've talked about. And with that arterial blood gas, we want to be making sure that that Partial arterial, carbon dioxide.

If you're unable to get an arterial sample, you can do a venous sample and we can make sure that that partial arterial, yeah, partial pressure of carbon dioxide is, above 50 millimetres of mercury, sorry, below, and if it's above 50, we want to maybe be thinking about putting these patients on mechanical ventilation, taking over for them. Reducing that, partial pressure of carbon dioxide. So another sort of diagnostic tool that we can use, both in, the beginning and also, as a, a continuous, scale is the same modified Glasgow coma score.

So basically assesses the level of consciousness, and it does through, does this through, the, brain stem, reflexes. Looking at abnormal posture and motor activity. It also looks at, that pupil size and symmetry.

And so this is generally just for dogs. It's not very well adapted for cats. And I have found in using it.

That there are some, hindrances to it. So I think it's good to use, as a tool, but I think a good physical, and neurological assessment and exam of these patients is key, and not just relying on this, modified Glasgow Croma score. So the higher the score, the better the prognosis is the opposite to things like your pain scores, and that the lower the score, the better for those.

And with these, the higher the score they get, the better, prognosis, better outcome for these patients, . And, so it's important that we have the continuity of care as well with these. So if you are going to use these scoring systems, Making sure that when you do a handover of staff, that you go through your decisions on the last, score that you did or do a score together, so that that subjectiveness is reduced, because in particularly with these patients, to one person, they may seem like they, you know, maybe turn in a corner, and to another person, they may be deteriorating.

So it's good to, on handovers, of staff to be on the same page, essentially. So look at treatment now. So I'm gonna go back to this ABC survey.

So we have this, airways breathing pattern, abnormal sounds and auscitation. So these all relate to, do these patients need oxygenation? Do these patients need pain management to, you know, is that breathing pattern because these patients are in pain, and in Turn, obviously, that pain relief is gonna settle that respiration rate.

It's gonna help these patients to oxygenate better. It's gonna help them to ventilate, and, you know, because of these patients hyperventilating, are they going to be hypercapnia or hypocapneic depending on, you know, whether they're hyperventilating or hyperventilating. And then we have, blood gas, arterial, blood pressure, heart rate, ECGs, lactate and body temperature, and these all relate to the treatment that we're gonna come to.

So do these patients need fluid therapy? Are they under perfused? Are they hypovolemic?

Do they have systemic hypertension that needs correcting? Do these patients eventually need osmotic diuretics to increase, that's. Cerebral perfusion pressure, all these patients adequately thermoregulating, you know, is that thalamus been affected, and we need to take over that, thermoregulation for these patients, to maintain a good temperature, for homeostasis.

So tier one to me is the ones that you would give, to all traumatic brain injury patients. And this one in particular is the most important. If you suspect your patient has got traumatic brain injury, if these patients are breathing erratically, or if these patients are you know, if these patients have some respiratory involvement, then give them oxygen.

Oxygen is a wonderful drug and that I think is very underused, and I realise it can be quite difficult to provide these patients with oxygen. And we have a couple of these . Sort of tents, they're buster tents, but you can get incubators that are sealed, and you can get oxygen cages, you can makeshift, short term, you can makeshift the bus collars by covering 75% of the bust collar at the bottom and with Cling film and putting oxygen into that and letting the oxygen flow up.

The one thing that is, contraindicated in these patients is to place nasal prongs on nasal catheters, nasal oxygen catheters in these patients, because we're gonna potentially add an, increased pressure, . To the head area and we don't want to be putting any more pressure there. So we want to be maintaining again, maintaining the ICP, .

So we talked about the oxygen carrying capacity, . And So The best thing that I like to do is just get these cages set up, you know, or even cling film in a cage if you don't have these cages, . Just doing the best you can to try and create an oxygenated environment for these patients, especially just in the triage and assessment phases, just getting as much oxygen to that patient as possible, And then, so potentially long term thinking about ventilation, you know, often these oxygen tents will get hot, or, you know, you can't keep these patients with a bust collar and the cling film on.

And maybe these patients aren't adequately oxygenating even after you've provided them with this, sort of oxygen environment. So this is when we're thinking about mechanical ventilation. And so we can ventilate them in-house, if you, Don't have a ventilator, you can use, you know, IPPV, but realistically, if we're thinking about ventilating these patients, we want to get them onto, mechanical ventilator that is has the ability to be, to have a percentage of less than 100% oxygen, because whilst oxygen is a great drug, it can also, there can also be toxicity, .

And so the maximum really you can have a patient on 100% oxygen, which we have in anaesthetic machines, is, is 24 hours. And these patients are on ventilators required 24, they need someone with them at all times, and 24/7 care. .

And so at this point, I'm, you know, you may be starting to think about whether you want to refer these patients. If you've got this ability to do this in-house, then great, you know, the sooner the better I'm taking over these oxygen, oxygenation, is going to be more beneficial for these patients when we think about that degeneration of the DNA, and we want to prevent that. Second injury from happening.

So if we try and minimise that hypoxic injury, we're going in turn, decrease the chances of the second brain pathophysiology occurring. So we have to one still and we have fluid therapy. So there's usually a concern about, sort of giving aggressive, fluid therapy in these hypertensive patients, that have traumatic brain injury.

And this was all, it used to be sort of based on, the fact that it could worsen cerebral edoema, . But it's sort of been, looked into quite extensively and, it, it's sort of now thought that the use of the third fluid therapy in these patients with brain injury is really quite beneficial, on the dermatous brain. And even if high volumes of crystalloids are used, there's a study by Dean Fletcher, In 2015, that sort of looked at that.

And so we want to consider the blood pressure. We want to think about shock, whether these patients are hypovolemic. Why are they hypovolemic?

Is it, a systemic hypertension, you know, have they got a blood loss from somewhere else, especially if there's been a polysystemic trauma, you know, potentially it's gonna be brain bleeds, so you'll have some blood loss from there, . Is a disturbative shock, . You know, just thinking about the type of shock.

And then again, like I said, this dehydration, because we want to replace initially this, we want to correct the hypovolemia. But then we also would, ideally like to correct that dehydration, especially if we're going to go on to give, tier two treatment. So initial resuscitation, is performed with the use of hypertonic saline, or we can use, crystalloid bolus as well.

So when we consider hypertensive patients, they're gonna have a mean arterial blood pressure of 40 to 50, or again, like I say, if we just have the ability to get the systolic blood pressure, anything less than 90, you know, these patients come in looking like they've got, systemic hypertension. So if they got, either absent or weak and thready metatarsal pulses, you know, the collapse, that are hypothermic, . And, they've got, you know, desynchronized pulses to heart rate, then we want to be thinking about giving these patients bolus.

So what we'll do is we'll give a couple of crystalline boluss, you know, these patients are tachycardic, as well, . Then often this will help. But it may be that once you've done these crystalline bolus, they may not be sufficient enough, and hypertonic saline in these patients is, really good.

So, It's 10 to 20 mL per kg over 10 to 20 minutes. So in cats were, you know, it might, you might go 5 to 10, mL per kilo over 10 to 20 minutes, and dogs again, often we'll start with. Lower one first just to see how they respond to that.

And then I potentially go higher, and depending on the varying, assessments of, you know, blood pressure and things like that. If you got a really low blood pressure, then we'll often just go for 20 mL per kilo. And again, so if they're dehydrated, giving them crystallo bolus is gonna be good.

We want to give them that, and then the hypertonic, well then, help with the, shock with the hypertension. So it's gonna, short term increase that, circulating blood volume, and against the cerebral blood volume and in turn, cerebral perfusion pressure and cerebral blood flow will be, increased. So, Again, thinking about these patients if they're severely anaemic, so we talked about those patients that have the PCV of less than 20.

I'm trying to replace like for like, but in this case, you know, do we want to be given huge amounts of crystalline bolus, repeatedly, and basically diluting that blood even more, or do we want to be given hypertonic saline, that's going to restore that blood volume quite quickly and then obviously we'll over long term, we then, replace the crystalloid bolus, crystallo fluids. I'm And just thinking about that glycocaly in terms of these as well. You know, colloids are advised against, being used, because of the glycocalys and the damage it causes.

But even with large amounts of crystalloid bolus, it can sort of, It can cause damage to that. So just considering, you know, what we're giving and why we're giving it. So we're looking for these patients to be evollimic.

So I mean after a blood pressure of 8 to 100 or a systemic blood pressure of 120. And then at this point, we want to put them on a crystalloid. And we'll often just keep these on maintenance, so 2 to 3 mL per kg per hour, or you can use, 60 to 70 mL per kg per day.

And remembering just that dehydration plan as well. So if you were assessed that that your patients were dehydrated before those crystalloid or hypersonic saline bolus, you know, working out your dehydration deficit. And minusing those bonuses that you've given, from, from that end end volume and then, you know, either spreading that over 16 or 24 hours.

But with these patients, we want to try and keep the blood volume at the same. So once we've restored that blood volume, we don't want to be, you know, increasing it even more, or dropping back down again. So just keeping these patients on maintenance is important.

So you talked about thermal regulation a little bit. So the hypothalamus, is responsible for the temperature control. And there's been quite a lot of human studies that have looked into, induced hypothermia, and therapeutic normalmothermia, in traumatic brain injury patients, and their effectiveness in reducing, increasing intracranial pressure or cerebral blood flow.

So in humans, they actually do, induce hypothermia because they, It, it, it does help them, but it's not really recommended in, veterinary patients. I suspect that, you know, potentially in a couple of years' time, it may be different, once you've looked into it, but, the advisement is to avoid temperatures over 39 degrees, and then, we want to try and avoid anything under 37 degrees in these patients. So just keeping them normal thermic.

Because, you know, if you, I think the thinking is that if you decrease his patience, Temperature, . Then, you know, potentially it's going to trigger, a temperature control, and an increase, it's gonna be harder to get down. So 37 to 38 should be sort of your targeted temperature management.

So pain management is extremely important. And then before we give any medications and do any neurological assessment, We should do a neurological assessment before, because once we give this pain medication, it can affect your neurological exam. And it's just important to remember that when you're taking in consequential neurological exams, that your, your pain management option may have been changed this, for you.

I'm So it's, I would say, I would assume all these patients are painful. If we, I've got these patients, And they've they've had an injury to the head, and you just think about having a headache, you know, we even take paracetamol or ibuprofen for that, so. Assume these patients are painful, and often will opt for a pure or opiate, but just remembering that the effects that it has on, respiratory function, so you may get, you know, decreased respiratory rate, and in turn, sort of, a build up a hypercapnia.

So just monitoring that, on your blood gases, you know, potentially these patients are ventilated, then monitoring that, on, capnography as well. Sometimes these patients, they, May be intubated, . And not be ventilated, and you can have a, you know, side stream catnography on that as well.

. And often lidocaine is a good, adjunct to reducing the ICP, in some studies that they've shown that, I quite like a multimodal approach, and we come to contraindications, but non-steroidals, a contraindicated in these patients due to, changes in, in blood flow, and often haemorrhage, so any haemorrhage, contraindicates, non-steroidals, . So we come to tier two, so osmotic diuretics. So these, work by the osmotic radiant, so they move water from extracellular and intracellular compartments, into the vessels.

And this in turn reduces ICP, and it reduces it by, reducing that into cranial volume, to improve that, compliancy. Sorry for complacency there, but I meant compliancy. And so Manitol is the main one that we think of, of these osmotic diuretics.

And so it's main mechanism of action, is to promote the vasoconstriction reflex, and this is it through a reduction of blood viscosity. And it's also there as well to decrease, CSF, and to reduce edoema. So often we're given a 0.5 to 2 grammes per kilogramme bolus over 15 to 20 minutes.

So a maximum of 3 bolus in 24 hours, can be given to these patients. You can get these 3 to 6 hourly. I often find if you need more than 3 bolus in these patients, then, they've got a very grave, prognosis, and, you know, at this point, you may be thinking about, speaking to these patients about, sort of end of life, and, euthanasia.

So with these though, I, I think I'm in traumatic brain injury, and we reach Manitol quite regularly and quite frequently because, that's, you know, we were taught that Manitol is the thing, that helps these patients, but as I go back to tier one, fluid. Therapy, so hypertonic saline in these patients, is really the first front line, for these patients. As Manitol's got, such big complications that it can cause renal neurological impairment.

So it may do more damage than good in these patients. So I would say it's, A backup really if your fluids and oxygenation aren't working. So it'll increase your diuresis which will lead to dehydration, as well as systemic hypertension.

Ischemia and hyperkalemia. So we need to make sure that we're doing constant electrolyte on these patients to monitor that these, you know, that they're not becoming hyperkalemic. And as I said, with the dehydration, really correcting that beforehand and the systemic hypertension.

So not reaching for the man at all as soon as these patients come in. We want these patients to be stabilised before we attempt to give these osmatic diuretics. Otherwise, like I said, we're gonna do more harm than good.

And so again, storing these storing these at room temperature, and to avoid crystals in the solution, you know, making sure that they're well mixed before giving, and we'll use the hemanate flip philtres that you can get, for blood, transfusion, to philtre any small crystals, that may have or sediment that might be in those, In those bags. And again, just never warming these, fluids up because you can change the, chemical balance of them. So tier 3, after these, is a considerate hyperventilation.

So, we talked about how that, partial pressure of carbon dioxide, can, change the ICP and so intracranial basal dilation can cause increased, ICP and, this hypercapnia, so anything over 45 to 50, will cause an intracranial vasodilation. So hyperventilation, so less than 25 millimetres of mercury of this PCO2. Will cause a vasoconstriction and a reduction of brain volume.

So we want to keep it in normal. So anywhere between 25 to 45, ideally 30 to 45 millimetres of mercury. So again, like I said, with these patients, if we're thinking that they're hyperventilating and we're doing either venous blood gases because often the figures in PCO2 will be similar to an arterial sample, and reliable.

So in these, we, you know, if we're getting values, either above 45 or less than 25 on the blood gases, Then, then we would start to think about . Mechanically ventilating these patients and taking over and to make sure that we're correct in this. Mm And tier 3, and we'll touch on this a little bit, but again, this is, this will come after, an MRI, and often we're not doing this tier 3, as a, and as emergency procedure, unless these patients have an acute, extra axial hematoma, so an obvious bleed.

A depressed fracture, which again would be obvious, especially in patients with shorter hair. You know, maybe these patients like Chihuahuas or even cats, and you may feel this depressed fracture. Cerebrospinal fluid leak, this would be more, diagnostic from an MRI, But with all three of these, there is a high risk.

So with decompression cra craniectomy, it can cause further edoema. And a decrease, in reactivity of cerebral vascular pressure, and neurological impairment. .

Additional therapies that we really must think about as well as glucose control. So as I talked about with, earlier, the oxygen and glucose is responsible for the ICP homeostasis and so making sure that these patients, you know, have an adequate glucose level, often they become hypoglycemic, . Often because they're not eating, and they're critically ill.

So whether we think about placing feeding tubes, often these patients may need a PEG tube because esophageal tube placement, is another potential, but obviously nasogastric tubes are contraindicated. And just wait until we've got, these patients stable enough for anaesthetic, if we're going to do this. Otherwise, we may want to put them on, glucose drips, .

Seizure control, so making sure that these patients, are not having any seizures, not likely to have any seizures, because this is gonna cause change to the blood flow and may cause more direct damage, and, may cause hypoxia again, so may lead to further second injury. Elevating the head and neck at 20 to 30 degrees. So, What we often do is we use, like a plastic board or a wooden, like a almost like a cupboard door, and we'll put the, the front of the body down to sort of the chest area.

On, on the board, and sort of elevate it with wedges and towels underneath, so that they're elevated at that, 20 to 30 degree angle. And long term therapy for this patient of these patients of physical therapy. You know, we often think about turning them, so they don't get it like this, in the lungs or keeping them internal, but these patients are often going to be recumbent for, you know, potentially weeks, and they're going to get muscle wastage.

So making sure that we're massaging, you know, that we're doing passive range of movement, to ensure that these patients don't have a significant loss of muscle mass, if they recover. Lubrication of the eyes and mouth, so making sure that we're frequently lubricating the eyes and mouth as well. Maybe we put wet swabs in there to keep it, wet, and moist, and then, urinary and faecal catheters, or nappies, A for ease of use and be again because these patients are going to be recumbent.

Placing a urinary catheter allows us to monitor urine output, which again, allows us to monitor, adequate fusion, and faecal catheters. It may be quite difficult if these patients don't have diarrhoea. So again, nappies might be good or, frequent enemas, so they do manual, evacuation.

So these patients are comfortable, so they're not getting faecal scolds, urinary scolds, or any ulcers. And then again, nutrition supplementations we talked about is glucose control, and whether we use partial parental nutritional form parental nutrition, or if, you know, later on down the line with place, feeding tubes, and to make sure that these patients, get an adequate nutrition, so it's really important for the recovery of these patients, and, you know, so that these guts, Going to be mobile, if they do recover. I'm thinking about, you know, promotility, drugs, so metoclopramide, and, You know, making sure that these, you may want to do frequent ultrasounds to see whether these guts of parasols in, and whether you need to intervene.

So finally, we've come through to contraindications. So we've got some non-steroidals, as I've said before. So with haemorrhage, These are contraindicated, so often we'll hold off on non-steroidals until these patients have recovered, .

Corticosteroids, I'm They, you can give them in some cases, but it's often, ill advised, and I think the only ones that we would go for is, The sort of last chance saloon sort of type of things, nasal cannulas I've talked about, so nasal prongs, nasal cannulas, and raising the head by itself. So we want to elevate the whole, that whole upper body rather than just lifting the head up. So you don't want to compress that spinal cord, in the neck.

And so that's the same with jugular compression and sampling, . A, because we're going to be raising that head up, but B, if we're going to be compressing that jugular, we're going to cause an increased, Pressure, and decreased blood flow to that and changes to the ICP. So that goes to putting central lines in these patients.

Often these patients would be better suited to, PICC lines, for, you know, if we want multiple, things on there and and the ability to, frequent blood sample. And zamide in these patients as well, is contraindicated, . So again, I'm dehydration, I may cause hyperkalemia, because of the, I'm Modality of use.

And just a quick one on considerations for your comorbidities. So we talked a lot about these patients, having polysystemic trauma. So when we think about these and we go back to that triage assessment, we'll do a neurological assessment, but thinking about what we're going to do to try and prevent that hypovolemia or hypoxia.

So you might want to stem bleedings, we may want to put tourniquets on, we may want to do, you know, we may want to go into surgery, which is obviously, gonna be quite difficult in these patients, anaesthetizing them, you know, whether we can, do local nerve blocks to, Quickly ligate arteries or ligate vessels, and then go back to at a later date. So sort of managing short term, So that the patient can last for long-term injuries. Pain management, long term for their injuries.

So, and maybe these patients may need long term, Pain relief and whether we think about multimodal, so thinking about stuff like gabapentin, tramadol, fentanyl patches, things that this patient might be able to go home with, and positioning a patient if there's other injuries. So, you know, if there's thoracic trauma, if there's fractured limbs, is it going to be comfortable for this patient to be in sternal position or we're going to have to put these patients in, Lateral and just, turn them every couple of hours. And again, thinking about that shock stabilisation, we've mentioned that before.

Thank you very much for listening. I'm I'll hand back over to Sophie. Brilliant.

Thank you very much, Chloe. Really interesting talk and so many useful tips that we can use in practise. So we do have time for just one question tonight, and we have one through already from Terry.

He said, you said to aim for a mean arterial pressure of 10, 100 millimetres of mercury if the animal has poly trauma and a hemoabdomen, would you aim for lower because of the risk of setting off a rebleed or displacing a clot? Yeah, so I'm, I guess that's a bit of a contentious issue that I'm, you, I'm, but, so I'm, you would aim, I guess, so I'm, I just say 80 to 100, so probably would aim for a lower end of that, so 80, . Just because, again, you don't want to increase the pressure there, but you don't want to lose that mean arterial pressure, in terms of that, cerebral perfusion pressure equation.

And like I said, trying to replace like for like, if you know there's an abdominal bleed, restoring that blood volume with, pack, pack red cells if you can, and as I just said, thinking about, You know, potentially, you're gonna have to either stabilise this patient, and you may be able to do that by keeping the mean arterial pressure at 80, and replacing with red blood cells, and then going in at a later date, to do that, you know, to stem any, or section of the abdomen and have a look what, you know, if there's anything bleeding, . Or you may need to go into surgery and in which case, you need to think about anesthetical, anaesthetic considerations and for these patients, you know, so induction methods, you know, using benzodiazepines to, induce these patients, . Yeah.

Lovely, thank you very much. We do only have one more question that's come through, so I think we should be able to just squeeze this one in. So the other one is, if hypertonic saline is not available, do you think isotonic saline is an alternative and preferable to other crystalloids?

I would use, . Crystalloid solutions over isotonic, . Yeah, isotonic ones.

I think at that point, I think if you can give a couple of bolus of the crystalloid, and if your patient isn't responding to those, and then potentially you may be able to, but you may be able to at that point start to be thinking about using, you know, asthmatic diuretics if your patient's not been responsive to, several bolus of, crystalloid solutions. Excellent. Thank you very much, Chloe.

And if anybody does have any more questions, I've put the email address in the chat box so you can email webinar vet if you do have any others. And please take just a couple of minutes to fill in the feedback form that should pop up in your browser when you close the webinar. And I'd just like to thank everybody for logging in tonight and a massive thank you to you, Chloe, for taking the time for educating us this evening.