Good evening everyone. So again I just want to say thank you very much to the sponsors this evening, Tales.com, and JHP recruitment.

We are gonna spend the next hour or so, talking through heat stroke, and thinking about how we manage these patients and the important role that we play with these patients, as veterinary nurses. So I want you just to take a minute to just think back to the last heat stroke case you saw. Maybe it was recently as a result of this beautiful warm weather that we've been having, or maybe it was a little while ago and maybe think back to, you know, what, what was it about that case that sticks in your mind?

What did you learn from it, what was the outcome? And hopefully then as we talk over this topic of heat stroke over the next hour, we'll be able to come up with sort of some refresh some knowledge and think about how we can deliver nursing care to these patients when they end up being hospitalised with us in the practise. So in particular what we're gonna work through is we're gonna take a review of the physiology of heat stroke.

We're gonna talk about some of the risk factors that are associated because this is then becomes important for us when we need to think about educating our, our owners. We're gonna work through then which of the sort of major body systems can be affected and also outline then how we can then treat these patients and support them through their recovery, hopefully to get them to the stage where we can then get them back home. So first of all, if we think about what heat stroke is, there's a number of different definitions that are used in the literature, in both the human world and the veterinary world.

But the definition of hypothermia associated with a systemic inflammatory response syndrome, leading to multi-disorgan, multi-organ dysfunction syndrome in which encephalopathy predominates is a description which Seems to be used in both human and veterinary medicine, and this definition kind of encompasses this syndrome that we see where these patients have this massive inflammatory response to this heat that they're exposed to, which can then lead to them to go on to have multi-organ failure for which they are obviously central nervous system derangements are, are present. We'll come on to talk about this a little bit more, but there's different types of heat stroke, that our patients can experience, so either exertional, so exercise related, or also non-exertional. Obviously these patients can present to us, you know, at a variety of different stages.

So in some cases if they're severely affected, this can be a life threatening condition. But it's obviously really important for us to remember that this is a preventable disease or process often. And so again, this is where we as nurses play a really important role when we're educating our, our pet owners.

Usually we see that it's seasonal, so around about obviously this time of year, very topical subject for us to be talking about this evening. Seasonal with regards to the warm weather, particularly sometimes humid weather, but again, because there's a non-exertional aspect sometimes to this heat stroke, we can see that it does fall outside of those summer months too, so it's important for us to be mindful of that. And veterinary nurses just play such a role I feel in these cases.

As I said already with regards to owner education, but also, detecting when we may have patients which are at risk of developing heat stroke from the time when the clients may be called the practise through to these patients arriving, us helping to stabilise these patients and act quickly, and then obviously delivering any nursing care to these patients which are then hospitalised with us in the practise. Just quickly a little note on cats. So it's not common that we see heat stroke in cats.

I think I've seen it a couple of times in my time as an emergency and critical care nurse. I've seen it once as a toxin related thing, so in a cat which had some we thought had had amphetamines and so this cat had a non-exertional type of heat stroke, and then obviously also we can sometimes see it perhaps secondary to tumble dryer injury, so, where patients may be climb into the tumble dryer and end up then presenting to the clinic. Often kind of in a heat stroke type crisis and obviously then with the potential of added burns on top of that.

Generally speaking, the treatment is going to be exactly the same for cats. So, everything that we're going to talk about, we often see in cats as well as dogs, but obviously we just don't see cats generally don't tend to present very often. So thinking about what happens in humans, because there's a lot of evidence that's been published in the literature, we see that there is this sort of three syndromes of heat illness which form a continuum.

And so we see that again, we can, can translate this through to what we see in our veterinary patients. So usually this continuum will start when our, our patients or people first of all start to develop heat cramps. And so usually at this time, the people will experience muscle spasms, they'll have alterations to their sodium and chloride because these are lost.

So this is maybe often associated kind of with exercise in a warmer environment. And usually we see that kind of core body temperature doesn't tend to change too much at this stage. We then can move kind of along the continuum.

So if this kind of load of heat is, is continued and prolonged, patients then move towards a kind of state of heat exhaustion. And so then we start to see the added sort of signs of fatigue, weakness, and sometimes vomiting and diarrhoea. And if patients then continue to progress, we then move towards kind of that true presentation of, of heat strokes.

So as we said, where we kind of have this massive inflammation, we have this CNS disturbance, and we start to get other organ systems involved in what's going on. Usually what we find for the majority of our patients that present to the veterinary clinic, our owners are going to alert us at the point of heat exhaustion. So they start to see that something's not quite right at this point.

They, these patients are likely to have an alteration in their core body temperature. And so hopefully if we can catch them at this stage, we can kind of start our treatment, start our stabilisation and prevent these patients progressing to kind of that full blown heat stroke crisis. It's important just to also acknowledge at this point the sort of difference between hyperthermia and pyrexia.

So our body can gain heat from two different sources. So we've either got endogenous heat, so heat that's produced by cell and muscle cell and muscle activity, but then we can also gain heat from exogenous sources, such as our environmental factors as a warm, hot, humid day. The set point of our, our body's temperature is determined via our thermoregulatory centre, which is in our hypothalamus, and as our body temperature changes, there's a number of mechanisms that are deployed in order to keep that temperature within that set point so that everything's nice and happy.

With a pyrogenic hypothermia, so this is usually as a result of an infection or inflammation and is often referred to as either a fever or pyrexia. What we see happening during this time is that the body temperature increases above that set point. As a protective mechanism.

And so because that body temperature is now outside of what was a normal set point, the hypothalamus doesn't initiate any of these protective heat dissipating mechanisms. And so for that reason, we don't tend to actively cool patients that are pyreexic because it's the body's protective mechanism against that infection or inflammation. If we think about a non-pyrogenic hypothermia, in these cases that temperature rises above that set point again.

And the body isn't able to compensate. And so this can happen for a number of different reasons. So if we perhaps got damage to the hypothalamus, to that thermoregulatory centre, so maybe as a result of a brain tumour or trauma, we can have a failure for the thermoregulatory centre to be able to respond.

So maybe sometimes we see this with particular medications. Are administered if the patients may been seizuring a lot. And again, we tend to see this non-pyrogenic hypothermia associated with extreme environmental factors, so heat, humidity or or exercise.

So this is kind of where we're thinking about this classic kind of heat stroke presentation. So when our patients are exposed to this this environmental heat or they're undergoing sort of high levels of exercise on on perhaps a warm day, as we said, that body temperature starts to increase and it starts to move outside of that set point, that happy kind of level. And as loads of heat increases, what we find is that that dissipation, mechanisms become overwhelmed.

And so this change in our body temperature is detected by, as we said, by these thermoreceptors in the hypothalamus and the first thing that our body does. Is we vasodilate, so we try to shift our blood to our periphery. Our cardiac output becomes increased.

We get reduced blood flow to our major organs. So we're trying to shift our blood flow to our periphery to try and shift some of that heat via vasodilation. What this then can lead to in these patients is they start to move towards a sort of a state of vasodilatory shock.

So they can develop a relative hypovolemia because their blood is now no longer within sort of their main blood circulation, it's moving out to the peripheries, and what we find then is that the patients start to develop hypo perfusion. In addition to this sort of vasodilatory response, we've also talked about this kind of systemic inflammatory response that happens. And so what we see here is that there's this sort of pathophysiologic sequence in heat stroke that begins with the production, the release of interleukin 1 and 6 from our muscles and we also get the release of kind of bacteria and endotoxins from our gastrointestinal tract, and these go then out into the circulation.

And they then lead to the activation of white blood cells, so we get leukocytes and endothelial cells become activated. These then in turn lead to the release of both pro-inflammatory and anti-inflammatory cytokines, which then have an effect on the endothelium cells which are involved in our coagulation cascade. And so we start to see in these patients as they go into this inflammatory status, they can start to have altered coagulation, and reduced fibrinolysis.

These patients that are having sort of this alter coagulation can either have bleeding tendencies or alternatively clotting tendencies and so as a result of these bleeding abnormalities, so perhaps we've got lots of little clots forming in these patients, this then leads to worse perfusion to certain areas which leads to obviously to cell death as a result of this hypo perfusion. And so what we see then is that these patients can end up with kind of then organ damage, and go into organ failure, as a result of this kind of severe inflammatory process. So as we've sort of mentioned already, we've got a few of these protective mechanisms which our body has.

So we do have a bit of an armoury for how we deal with what happens is that that body temperature starts to move outside that set point. And these three mechanisms play quite an important role then in these patients which are exposed to high environmental temperatures. So the first is our thermoregulation, so our heat dissipation mechanisms.

The second is an acute phase response, and then the third is our heat shock proteins. So when we think about our heat dissipating mechanisms, this sort of takes me back to my time at school when thinking about how we lose heat from our bodies. And so if we think about convection, this is where we lose our, our heat into the environment and it's a cool circulating air around us will help to transfer that heat away from the body.

In radiation, we find that heat moves naturally into the surrounding environment. We've got evaporation where we lose our patients lose heat via panting. So obviously this is something we see much more in our our canine patients than we do in obviously human patients which may experience heat stroke.

And then there's also conduction, so where the body comes into contact with a cool surface, we, they will lose heat via this mechanism as well. And it's quite important to remember these different heat dissipating mechanisms because again, these, if we can maximise these during our kind of way that we actively cool our patient, we're going to be much more effective in, in bringing that temperature back down to that set point. The acute phase response is that second sort of protective mechanism that the, the body has.

And so this involves these sort of inflammatory cytokines that we have, which lead to the release of white blood cells that are there to help kind of fight this sort of inflammation that's going on, this inflammatory response. And what we find is that these White blood cells act as part of this inflammatory process and eventually lead to the stimulation of our hypothalamic pituitary adrenal axis. So this is our neuroendocrine system which is involved in our kind of stress response and our, our release of cortisol.

The last mechanism then is our heat shock proteins and so these proteins are made in the liver and they kind of act as like a molecular guardian. So these proteins will go then out into circulation, when our, our body's temperature starts to move outside that that temperature range. And so these proteins work at the level of the cell and they.

Protect cells against the effects of hypothermia. So they'll help to maintain an intracellular function and they will also help with sort of the structural integrity of these cells to prevent them from denaturing and dying and hence our patients going into kind of that stage of, of, you know, end organ failure. So heat stroke essentially is, as we said, this continuum of heat-related illness and it's kind of that end point.

So when these patients are exposed to this heat either from an endogenous or an exogenous source, we get that phase. Of our thermoregulatory mechanism mechanisms, they can't they become overwhelmed, they can't compensate and cope any longer. We get this increased acute phase response and then alteration to these shock proteins.

These are the patients that then present at kind of this end of the spectrum where they're in a full blown crisis that we call heat stroke. So we kind of already mentioned the two different types with exertional heat stroke being more associated with dogs that are exercising and sometimes that might be perhaps in a climate that they're not acclimatised to, so. Again, kind of thinking about the kind of human medicine side of things, there's been a lot of work kind of done to look at acclimatisation, particularly for athletes.

So people who will train in kind of areas where there's quite intense heat or perhaps go and compete in different parts of the world and they're exposed to a different environmental factors to what they would be normally. And so usually it takes people. And evidence to suggest to our our canine counterparts, and it can take between 10 to 60 days to acclimatise.

And so I think there is an element of, of then we see kind of with our our pets and our patients that, you know, it's not every dog doesn't present to us on a hot day with heat stroke because many of them will be acclimatised and they become kind of accustomed to that weather. There's also non-exertional heat strokes, so, generally we find that this is then obviously associated, as we said, with alterations to the thermoregulatory system, or if we find that patients have an impairment in their ability to dissipate heat. So again, this is where we can kind of think about some of the risk factors that we might see for our patients developing a non-exertional heat stroke.

It's also possible that we can see patients that have a combination of both of them. So it might be that we have a patient that has, the inability to be able to dissipate their heat very well, and they've then gone out on a hot day and maybe slightly overdone it on their walk, and so they have a combination of both. So thinking about risk factors, there's a number again of both endogenous and exogenous risk factors which are associated with heat stroke.

And so we generally tend to see that patients which are obese, if we've got patients with cardiovascular cardiovascular disease or abnormal abnormalities, those perhaps with neurological and neuromuscular disease, so here perhaps thinking about patients with sort of muscle tremors and things like that, if we have patients with a super thick dense coat. And in particular, which we're gonna come to talk about a little bit later on in the talk, patients with their upper airway abnormalities. So we're thinking here about our kind of brachycephalic patients.

We find that these patients are not very good at being able to sometimes evaporate their heat. and, because of their, sort of, upper airway, compromise, we find that these patients again are are at higher risk of developing heat stroke, and hypothermia. Exogenous risk factors.

So if we've got those patients where there is a lack of acclimatisation, so probably not something we tend to see too much in the UK but may be something that we see in other areas of the world. Obviously confinement without ventilation or shade. So there we're thinking about those patients that are shut in a car on a hot day, if we've got patients with water deprivation.

And again, sometimes some medications, so things like ACP has been linked with hyperthermia, and some of the loop diuretics and beta blockers. So As nurses, it's important that we are aware of these risk factors so that we can then educate our clients, you know, to try, as we said, to try and prevent these patients from moving along that continuum, you know, from, from this kind of heat cramps to heat exhaustion to heat stroke. And we can try and hopefully .

You know, put some things in place, so that we can prevent these patients having to, to present to us at the clinic, you know, in a full blown heat heat crisis. Now luckily enough, I think most of our most clients will generally pick up the phone when they've got an emergency, but obviously we still do have clients who will just, you know, dash down to the clinic and present present their sick pet to us. But it's quite helpful, I think, if we can try and ascertain over the phone, if we are lucky enough to get a phone call, how likely do we think it is that this patient does have heat stroke.

So usually it's going to be the nurses that are perhaps fielding these phone calls. So again, thinking about, you know, do we know that this patient has any of those risk factors, for example, are they a bulldog? Is it a super hot day?

So is there a reason, you know, it has the owner left them shut in the car, for example, do we know that there's any other contributing health problems that might be adding to this situation? And it's also quite important, again, if we are lucky enough to get this phone call to say that this that the client is worried about their pet, it's also just to find out if they've started any cooling methods already, because again, if we can catch this patient in that heat exhaustion stage. We can get the owner at home to start actively cooling the pet before they bring them to the clinic.

We can maybe try and kind of turn things around before that patient gets to that kind of stage of having central nervous system dysfunction or organ failure. Once, once they arrive down at the clinic, obviously it's gonna be all hands on deck, so thinking about with the presentation of, of any emergency visit to the practise, we need to think about our triage. So thinking about our A, B's and C's, so triage is our major body systems assessment.

So I generally tend to have a for alertness. So here, thinking about my neurological system. So again, these patients can present anything from very sort of bright and and quite alert, all the way right through on that spectrum to kind of comatose and collapsed.

The be I would then have us thinking about breathing, thinking about this patient's respiratory system. So, again, thinking about some of these risk factors, it might be that these patients are panting, they might have a a respiratory tract abnormalities or noises that we can pick up kind of early on in this patient assessment. And then with regards to see, we're thinking about circulation.

So again, likely to see that these patients if they are, are heading towards that heat stroke end of the spectrum, they're likely to be vasodilated as we've already talked about. They're likely to be tachycardic, hyperdynamic pulses, and, quite sort of red injected mucous membranes. We're gonna want to get our temperature reading pretty early on in this initial patient assessment.

So again, depending on where these patients present, their temperature can either be high, it can be normal or it can be low. And so even if we don't document a hyperthermia, it doesn't still necessarily mean that that patient, . Hasn't been a heat stroke patient, it might just be that they've kind of gone the full circle and into kind of a decompensatory state of shock if they're presenting quite late to us, and actually their temperature, their body temperature started to drop back down again, and even drop lower than sort of normal.

Once we've done our initial triage assessment, we're gonna then look for any life-threatening injuries that this or concerns that we have with this patient, and we're then going to move on to this sort of secondary survey. So more of a kind of full clinical exam of the patient and nose to tail examination, and we're gonna focus this examination on our major body systems because we know that those patients with heat stroke are at risk of organ failure or organ damage. So we're gonna work our way through our body systems in a a nice logical fashion, as we said, from a sort of nose to tail exam and look for kind of signs that we might have things that are starting to show up on this clinical exam that would you know, maybe alert us to them how we need to support this patient with regards to our treatment plan and our nursing care.

So usually with regards to our cardiovascular system, as we've mentioned, we get this increased cardiac output, vasodilation. We also see that these patients are likely to have an alter fluid balance. So with regard to that vasodilation, they can have a relative hypovolemia because their blood is shunted to their periphery.

If they've had vomiting and diarrhoea associated with their kind of heat stroke, it might be that they're also kind of presenting dehydrated as well. So, we need to use our clinical exam to look at things like our heart rate and our, our blood pressure and pick up the key pieces that we can. And to look for hypovolemia and to look for dehydration.

Again, we can sometimes see that we get sort of myocardial issues if we've got poor perfusion to the heart muscle, these patients can develop arrhythmias. So again, that might be something we pick up on that secondary survey when we start to take a closer look at the patient. We might think about them with the respiratory system.

Can we identify any of these upper respiratory tract abnormalities? Is it that the patient has got a mass in its larynx? Have they got a collapse in trachea?

So again, we've had a patient this weekend, a Pomeranian, that's presented to the hospital in a heat stroke crisis because of a secondary to tracheal collapse. We might see that these patients, again, if they're at the far end of that heat stroke spectrum, they can go on to develop kind of leaky lungs, so they get vasculitis, which can then kind of lead to, an acute respiratory distress syndrome. If these patients have got coagulation issues, again we might detect that as more lower airway issues with regards to pulmonary haemorrhage, if they've sort of developed some bleeding tendencies.

And again, if these patients are kind of in a state of semi collapse and they've also been vomiting, we might need to have in the back of our mind that they, they may be a a patient which goes on to develop an aspiration pneumonia. So these are all things we're gonna be looking for in that kind of clinical exam. So here we have a bulldog.

So this is an unusual presentation for us, and this bulldog actually presented to us with. So you'll see he's kind of got that wrinkled forehead, as he is a pinched back on the top of his head. And they talk about these patients having a sort of a sardonic grin.

So we really struggled with this patient because he would cycle into these episodes of having this sort of respiratory crisis which would tip him into a heat stroke crisis within probably a matter of 10 to 15 minutes. So you can see that this patient here has already got some of these risk factors. He's got a neurological disease, he's brachycephalic, so he's got upper airway respiratory tract compromise already, and he was a chunky chap, so probably not obese, but certainly could have done with losing a few pounds.

So, he obviously presented to us and we managed him for several days in the hospital with regards to treatment of his tetanus, but heat stroke was a huge concern because he kept cycling into these sort of respiratory crises fairly frequently. The other sort of group of patients again that we sort of might see as we talk about upper airway compromises laryngeal paralysis. So this is an olderable massive cross that presented to us.

You can see here this patient is really struggling to breathe. He's quite orthoonic with his elbows that sort of abducted, his neck and head stretched out. He looks absolutely terrified, bless him, and he's a horrible colour.

Usually with these laryngeal paralysis patients again on this clinical exam, we might be able to detect that noise that we sometimes hear with the laryngeal paralysis dogs. So again, thinking, I think particularly here, I've got an old Labrador as a pet, and I think we generally tend to see Labradors and bigger breed dogs that suffer with laryngeal paralysis. We've already mentioned how the central nervous system derangements play kind of an important role in kind of this definition of heat stroke, so.

And we find that the central nervous system, we can get direct thermal damage. We can have haemorrhage within the central nervous system, which is obviously secondary to these coagulation issues. We can get metabolic abnormalities so if patients become very acedemic or if they become hypoglycemic, that can again alter their neurological status, or again if their liver, they sort of tend to get kind of a liver injury, they can.

Go into kind of a state of hepatoencephalopathy. And so all of these things can then lead to essentially reduce cerebral perfusion. If we get things like haemorrhage, we can be at risk of these patients developing a raised intracranial pressure or again, even the development of cerebral edoema.

So we need to make sure that when we've done this kind of full survey and assessment of these patients that we do. Pay attention to our neurological exams, so keeping an eye on that patient's mentation and kind of getting a baseline for where we are when this patient presents to us, looking out for any signs of, you know, ataxia or seizure activity, keeping an eye on their cranial nerves, because again, we're going to then use this baseline information to then help us monitor this patient when we keep them in for delivery of our nursing care. The renal system, again, is, is one that can be affected with patients with heat strokes.

So again, the kidneys can be affected either through thermal injuries sort of directly, but probably more commonly through an ischemic injury. So either as a result of vaso constriction from the major organs. Due to, hypovolemia, leading to hypotension and then poor perfusion of the kidneys.

Again, if these patients have got perhaps an exercise element, so an exertional element of heat stroke, they can kind of go into a state of rhabdomyolysis and so these patients will then sometimes release myoglobin which when filtered through the kidney can again have it cause an injury to the kidney. So, you know, thinking about these patients again, we're gonna be having a little look at our kind of, parameters that we can in terms of our diagnosis and getting a baseline to try and establish where we're at. The gastrointestinal system can also then be affected and so on our clinical exam and our history, we might find that, as we said, this patient's been vomiting or having diarrhoea.

They are likely to get sort of gastrointestinal mucosal injury again, secondary to hypo perfusion. If they do end up with hypo perfusion to the gut, we see that these patients can then go on and develop this bacterial translocation leading. In very, very severe cases, you know, an endotoxemia or bacteremia, which leads on to sepsis.

So again, thinking about those really sick, collapsed heat stroke patients, that's going to be kind of something we want to have in the back of our mind and on our radar. With regards to then the coagulation system, so we think about what happens when we get damage to the wall of the blood vessel, and what we see is first of all, our platelets move to plug that injured area area of the vessel wall. Once our platelets have have moved to that area, we then see our red blood cells move to help start to form this kind of platelet plug.

And then, over time this platelet plug is strengthened with our clotting factors. So they come and they strengthen that plug, so that we, the body can work to then try and kind of repair that area of, damaged vessel. So when we think about our coagulation system, we have got our primary coagulation, which is related to our platelets, and we've also got our secondary coagulation, which is related to our clotting factors.

And so in order for our patients to have a full working coagulation system, they have to have both of those components working well and as we know with these heat stroke patients. They can go on and develop sort of weird coagulation abnormalities. So as we said, they can either fall sort of on the spectrum of of throwing clots, so they throw lots of microthrom little clots which get lodged in the blood vessels, which then cause reduced perfusion either to that area or to that organ.

They then start to get, develop a thrombocytopenia. So with these sort of primary coagulopathies, we'll often see thrombocytopenia show up on our clinical exam as sort of bruising of the skin. So like in that picture, that's a patient that had bruising as a result of clipping to place an IV catheter.

And so, we tend to see surface bleeds, gastrointestinal bleeds, bleeding perhaps into the eyes, whereas if we've got secondary coagulation abnormalities, we generally tend to see that more as as a cavity bleeds, so, so bigger bleeds either into the thorax or into the abdomen. It's more sort of common I think for these patients that we tend to see more of the microthrombi being created and, and sort of shot off into the perfusion and so that's where we would kind of think about saying that these patients are, are developing a disseminated intravascular coagulopathy, so, DIC. So typically, as we've mentioned with these patients that develop full-blown heat stroke, we get this element of kind of multi-organ dysfunction syndrome or certainly injury to multiple organ systems.

And so really these patients are the ones that will tend to have a poor prognosis. They're going to need much more intensive care, much more supportive care and treatment. And so we need to make sure with these patients that we've you know got full .

Investment from the owners that we've got owners on board because these patients can carry a much worse prognosis. So usually with these patients, as we said, we're going to start to see a combination of any, any of the things listed here. So that kind of cardiovascular system with circulatory collapse, our neurological system with our our our.

CNS abnormalities, we get the coagulation abnormalities, the lung injury, acute kidney injuries, muscle breakdown, we can get more cardiovascular issues with regards to this myocardial kind of hypo perfusion, and gastrointestinal injury. So, you know, these patients can be hugely challenging. They can take a huge amount of time and resources.

And so, again, we then kind of need to think about how do we treat all these things to best support these patients that are presenting to us in this super sick state. So with regards to diagnosis, there's a few things that we can think about. We're usually gonna want to get an emergency database from these patients, so when they arrive, once we've kind of done our, got our history, we've done our triage assessment and got our more information from our secondary survey, we're gonna want to think about what information we can help to.

Again, guide us as to where we are with the baseline for these patients and sort of flag up any concerns that we've got at this point. So usually what we're going to see is that our PCV and total solids might be elevated or increased, suggesting our hemo concentration because these patients are dehydrated. On blood gas, we potentially can see that these patients have a metabolic acidosis, so as a result of a lactic acid, because they've kind of gone into that kind of state of shock.

Their glucose can be abnormal, along with some of their other. Electrolytes, so we often see that sodium can be altered. So if they patients have had a free water loss, then they tend to have an increased sodium, whereas if they've had quite a bit of vomiting and diarrhoea, and they may have a low sodium.

We can see that if they've started to enter that stage of cellular death and organ failure, that they can have a high potassium. Other things that we can think about with regards to our blood work, so on a haematology, we can see sometimes that these patients can have either a leukocytosis or a leukopenia. If they've had some bleeding, it might be that they've had a GI bleed, and that they've then got become anaemic.

They can be thrombocytopenic, so we're gonna want to either have a little look at a smear in-house or, or, or pull blood for a, a complete blood count. One thing that's quite interesting that we might see on our haematology, so just in the picture here on the top right, is that we sometimes see nucleated red blood cells. So this is a finding which is unique to dogs and we don't see that it occurs in people, but I think there's a page.

In 2009 that found that 90% of dogs with heat stroke have nucleated red blood cells. So if you do a blood smear and you see those on there, then it's pretty likely that your patient has has experienced heat stroke. Serum biochemistry can be helpful just to kind of look for any evidence of organ damage, so looking at things like our liver parameters, looking to see if we've got acute kidney injury linked with an azotemia, and again coagulation profiles.

So we've talked about the use of looking at both our platelets and our clotting factors again to look for any evidence of that. Urinalysis may help us a little bit again with regards to sort of monitoring and establishing our patient's hydration status, but obviously if this patient has bleeding tendencies and we're worried about coagulation issues, it may be a bit more tricky to get a urine sample because we won't want to do something like cystocentesis, and we probably may need to be cautious about placing a urinary catheter, for example. So what do we know so far?

We kind of have a better understanding hopefully now of you know, what causes heat stroke, the two different types, exertional versus non-exertional, some of those predisposing risk factors. We hopefully kind of understand that this is this continuum of heat related illness, where patients progress. From kind of heat cramps through to heat exhaustion to finally that sort of global state of heat stroke, which is this complex process that involves the activation of our inflammatory cascade and leads on to obviously many of our body organ systems becoming affected.

We also hopefully understand then the role that some of the blood work we can do as our baseline can help us also then diagnose heat stroke, obviously along with our history and our clinical exam findings. So first things first, when these patients present, we wanna make sure that we are getting that temperature, body temperature down in those patients which truly are hypothermic, and getting that body temperature down to nearer to that set level so that it's safer for the patient. And there's a number of different ways that we can actively cool our patients.

So the ones on the left, so the use of tepid water with a fan, ice packing over major vessels, so either in the armpits or the groyne area and the administration of cool IV fluids generally tend to be the most effective methods that we can use. So again, thinking back to our conduction, convection, radiation and evaporation, hopefully here by the use of these sort of three methods, we're going to be maximising on those heat dissipating mechanisms. Other things that some people do tend to do, but they generally are less effective, so ice water, that's a bit of a no no because if we use water that's super cold, actually we're going to cause those patients to vaso vasoconstrict.

And obviously they've started to vasodilate as part of that kind of heat loss process. And so actually that it can take them much longer to, to cool down with using ice water, which is why we tend to choose tepid water. Wet towels are fine if we want to lie the patient on them, but we don't want to be draping wet towels over patients because that will trap hot air between the towel and the patient, and obviously we lose out on that convection element.

Some people will put alcohol on the feet of patients, or douse them in sort of areas of their body and alcohol to try and help with kind of evaporation of, of heat loss. I don't tend to like this. I think that alcohol surgical spirit smells pretty gross.

I don't feel like it, it necessarily helps cool patients down any quicker than, than the, the, the things on the left-hand side. In severe cases, if it's documented again in literature, so we, we can do more invasive methods of active cooling, so gastric lavage, cold water enemas, and abdominal lavage. Obviously, all of these are kind of a more intensive way of cooling patients and so again, generally we tend to stay away from those because we, we do find that just some good old tepid water dousing that patient down with a fan on them, some ice packs and cool fluids does the job.

What the aim is is to cool that patient to 39.4 degrees over about 30 to 60 minutes. We don't want to go any cooler because what we worry about is a rebound hypothermia for these patients.

May then actually have to actively warm them to get them back up. With regards then to the sort of supportive care and nursing, as we said, really we're gonna be monitoring each of these body systems and you know, keep keeping going back to that kind of monitoring of trends, reassessing these patients. Looking for any evidence that we have involvement from any of these body systems and and you know, trying to offer our supportive care as best we can whilst we have these, these patients that are are needing treatment.

So usually as we said, we'll be ongoing management now of hypovolemia so thinking here about our shock rate fluids and addressing then any deficits, so any dehydration deficit that that patient has with a slightly longer term fluid therapy plan over probably about 12 to 24 hours. So again, keep coming back to our clinical . Examination of these patients, so thinking about assessing our perfusion status, we can use things like body weight to help us, we can use things like urine output to help us, and again, thinking about, you know, our, our simple parameters such as our heart rate, our, our mucous membrane colour, capillary refill time, again, they're all gonna help us to establish what that patient's perfusion status is doing.

Keeping our blood pressure can be helpful. So again, if these patients are vasodilated, sometimes we'll see that they have this sort of hypotension, and again some sort of relative hyperbulimia. So monitoring blood pressure can help us to, to keep an eye on that and obviously if these patients are experiencing hypotension, and we need to act.

And again think about whether it's hypovolemia associated, so we will give fluid bolus for those patients and if it's more of a vasodilatory effect, then it may be that these patients would sort of benefit from some of our sort of vasopressor agents, so things like noradrenaline or dibutamine. Again, keeping an eye on ECGs because we know these patients can go on to develop arrhythmias, so it's not uncommon to see that these patients can have ventricular rhythms. So, on the left hand side at the bottom, this would be what we call an accelerated idioventricular rhythms.

So, kind of a ventricular tachycardia but not fast enough. Generally, we would say a ventricular tachycardia, so what we're seeing in the right-hand ECG is a ventricular rhythm but over a rate of about 180. So the, if we see the ECG on the left-hand side, the AIVR, generally we wouldn't jump in to treat that with medication, but we would monitor the patient closely, we would monitor their blood pressure and their perfusion parameters, whereas the ECG on the right hand side, the ventricular tachycardia, we would think about treating that patient perhaps with a lidocaine bolus or a lidocaine CRI.

With regards to that respiratory system, we're gonna keep coming back to monitoring our respiratory rate, our effort, our pattern, we're gonna think about that auscultation. Have we got any changes that we can detect? And we can assess how well that patient's breathing via either an arterial blood gas sample if we've got access to be able to measure that.

Or alternatively, we can check an SPO2 on that patient. And again, if we've got any concerns about either the way the patient's oxygenating or the way that they're breathing, . Then we're gonna want to think about, starting some oxygen therapy.

There's a variety of different ways we can think about doing that. So in the non-invasive sort of short term options, so thinking particularly here about where we've got this patients sort of in the clinic in the emergency situation and we're stabilising them, we'll think about flow by oxygen, maybe oxygen with a mask. If we've got nasal prongs, so a little bit like we've got in this patient here.

They can be really useful or for smaller patients, maybe an oxygen cage. Just need to be a little bit mindful with oxygen cages and our hypothermic patients because obviously we know putting them in a confined environment, actually we can end up heating them up even more, so we need to use that option quite cautiously. Some of our longer term options, so if these patients need longer term oxygen therapy might then be the placement of nasal cannulae.

Some practises have high flow nasal oxygen now available. In severe cases, so thinking back to this Pomeranium we've seen at the weekend with the tracheal collapse, we ended up having to intubate this patient and actually start mechanical ventilation because this patient not only has his tracheal collapse and also a heat stroke crisis, but he had also aspirated secondary to everything that was going on. And so this patient progressed to the mechanical ventilation to support his respiratory system.

We saw this video earlier of this laryngeal paralysis patient, so as we said, signs here of respiratory distress, elbows abducted, neck outstretched, and one thing that these patients that do present in this respiratory crisis, particularly our brachycephalic. Patients or these patients with laryngeal paralysis, for example, one thing that we can trial in these patients is a low level of sedation. So what we've got here is this patient was just given a 0.2 mg dose of the tool.

And we can see it's actually that alone has improved this patient's breathing, no end. So this patient has no longer got their neck stretched out in this awful position. They no longer look totally panicked by life.

And so again, you know, thinking about these patients. Particularly if there is a stress element to the hypothermia, sedation can be our friend certainly in the sort of immediate instance of getting them in to the clinic and stabilised or or also if we have them in the hospital and we're worried about the management of their stress. With regards to our central nervous system, again, we're gonna make sure we keep coming back to monitoring that patient's mentation every time we interact with them.

We can implement the use of coma scales so we can again think about using a coma scale to assign a score to the patient. Usually we'll find that a lower score is associated with a worse prognosis and this score again can can kind of help us trend what this patient is doing. Again thinking back to metabolic causes for alterations to these patients' neurological status, we might just need to have in the back of the mind that again it might be a metabolic thing such as a hypoglycemia, hypocalcemia.

So again, just ruling out if we have a change in our patient's mentation, ruling out a metabolic cause can be helpful because obviously if they are hypoglycemic, we can supplement that and hopefully improve their neurological status. If these patients do go on to have kind of a true, we have a true concern of raised intracranial pressure as a result of maybe cerebral edoema or a bleed, then these patients may benefit from the administration of hyper osmolar agents such as Manitol. We can look to keep some simple things like keeping these patients.

So elevated here, this patients propped up on a board, so a little bit of gravity to help out with blood flow and improving sort of flow away from the brain, so preventing kind of restraint around the jugulars, things, you know, rolled up towels, etc. Underneath the neck that might compress the jugular. Thinking about oxygen administration, and in particular if we're worried about raised intracranial pressure, we can monitor blood pressure and heart rate to look for signs of a Cushing's reflex in these patients.

With regards to these patients' renal systems, so again we need to make sure we are are kind of really on the ball with keeping an eye on urine output. So whether that is that we just monitor these patients and how frequently they're urinating or whether actually there is a concern, maybe we've documented an azotemia, and we're worried that we've now kind of worked at hydrating this patient and getting their blood pressure. Good and maybe this patient is not really producing much urine as we would expect them to, then it may be beneficial to place a urinary catheter with a closed collection system so that we can be super accurate in calculating what this patient's urine output is doing and use a urine specific gravity again to guide our fluid balance.

If that's not an option, if the patient's perhaps got a coagulopathy and we don't want to place the urinary catheter, there's other things we can. Do we can perhaps just try and catch our urine if the patient is mobile and they're going out and about. We can perhaps encourage patients to urinate on an incontinence pad and then weigh incontinence pads.

So usually 1 gramme of urine is the equivalent to about 1 mL of urine. So there's other things we can do again to kind of monitor our urine output and keep a close eye on that to make sure that we're, we're happy our kidneys are functioning OK. We might want to just have a little look at ongoing urinalysis.

So again, thinking about those patients where they are excreting myoglobin or if we worry we've had a sort of a severe acute kidney injury, it might be that we can see things like casts sort of on our urine analysis. So if we have got a super concern over an acute kidney injury, it can be beneficial to kind of keep an eye on what the urinalysis is doing. If there is, I guess a severe acute kidney injury, then there is a potential and that patient may be a candidate for dialysis, but I think that because these patients, if they have got multi-organ dysfunction syndrome, that they're, they're probably less likely a dialysis candidate than just a pure acute kidney injury patient.

Because of the added elements of the other organ injury that they have. So obviously if they've got a coagulopathy, that would make dialysis incredibly tricky because we wouldn't be able to probably you know, get a jugular catheter into that patient in order to do it and it would mean that the prognosis of those patients is really, really guarded. Again, thinking about how we can support patients if their gastrointestinal system has been affected.

So simple things here like management of vomiting and diarrhoea, so thinking about the administration of gastroprotectants, antiemetics, there's a number of different drugs that we've got again in our armoury that we can use to try and make these patients feel better. whilst they're in the hospital. And again, keeping a close eye out for GI bleeding, so either as, Melina, like we've got in the picture, or patients that are kind of vomiting up blood, and it may be that they're passing fresh blood or digested blood.

So being really on the ball with monitoring for signs of GI bleeding. If we do see that, I guess the question is, is do we want to give antibiotics or not? Generally, where we work, we tend to reserve antibiotics, and we would only administer those in the patients where we're concerned that they're heading towards that sort of septic state.

So if we see that that patient has. Other indicators of sepsis, so such as hypoglycemia, increased white blood cell count, or they're becoming neutropenic, then we would then probably add maybe antibiotics, broad spectrum antibiotics into our treatment plan, but we wouldn't necessarily reach for them straight away. And thinking with our coagulation system and how we can support and nurse these patients that develop those bleeding abnormalities.

So we sort of mentioned the monitoring of our, our signs of bleeding, so in particular our thrombocytopenia, those surface bleeds and bruising. Generally if patients have bleeding tendencies and, and they have a big GI bleed, then they may benefit from some blood products. But if it's more kind of the coagulation side of things with the clotting factors that we're seeing that are prolonged, so either an activate a long, APTT or PT, these patients may benefit from the administration of some fresh frozen plasma.

And so if we do administer plasma to these patients, it might be that if they're a big patient, they need a couple of bags or a smaller patient, a bag, and again we can then recheck where we're at with our clotting factors and hopefully we'll have made an improvement. Again, little things we can do with our nursing care, so making sure we're careful when handling these patients because we don't want them if they, they are thrombocytopenic at risk of, of spontaneous bleeds. Higher education, as we've mentioned, is really, really important.

So, you know, we can use many occasions, so things like our our nurse clinics, our puppy parties, we can try and educate our owners because as we said, this condition often can be prevented. And again, making sure that our again, understand the risk factors and understand if actually their patient does have one or two of those risk factors. Is there anything we can do to try and minimise or eliminate that those risk factors?

And again, simple things coming, you know, making sure, you know, pets have access to free water and shade at all times. Quickly just want to touch on this sort of non-exertional hypothermia just before we tie things up this evening. And so as we said, this is kind of often something we see more with our brachycephalic patients and so, particularly I sort of think about this when I think about how we manage these BOAS patients when they're with us in the hospital.

And so as we sort of saw in that video of that patient where they were brachycephalic and they had tetanus, these patients can spiral very quickly into kind of a heat stroke type crisis within, you know, a matter of 10 to 15 minutes and sometimes actually the that can be. Life threatening for these patients and actually they, they can die whilst they're in the hospital under our care, even despite our best efforts. So it's really important that the whole team is kind of aware of that with these patients, they are at risk even when they're they're with us in the hospital.

Again, as we said, the management of these patients is going to be exactly the same as our kind of classic heat stroke patients. And so usually what we tend to do, so these two cheeky chaps came in last week. Obviously the weather was very warm, they'd had a long journey in the car.

They were very, very hot when they arrived, and they were coming both in for the surgery, and so these Two patients we ended up having to have together. They had terrible separation anxiety. They both had a respiratory crisis very shortly after arriving in the hospital, so we had to start activating cooling.

Both ended up having some sedation to try and keep them cool. They went and had the surgery as planned that day, and then we housed them overnight together in the intensive care unit in a kennel as a pair because they were much more relaxed and settled than when they were housed separately. And so that that was for us the best way of dealing with that situation.

And you can see on the floor there, they've got a little fan on them just to try and have a little bit of air circulation in that walking kennel to keep them cool. We also make use of a brachycephalic checklist, so here if we have any concerns about a patient that's a brachycephalic that they are becoming hot or overheating, they're becoming a bit stressed, we'll start with a basic assessment, we get a TPR on that patient. We'll try and reduce their stress at that point, so that's where we would think about reaching for some sedation potentially.

If they, we've documented a high temperature, we will then consider actively cooling those patients. We make sure we communicate and if that patient is still not doing very well and we're still concerned, then that patient would be moved from their ward area to the intensive care unit. Where we start to sort of think about other therapies that we can instigate with that patient and what other things we can do to try and prevent them ramping up into this full-blown crisis.

As we mentioned, communication is super important. It's super important for us as nurses in our nurse handovers. We know these patients can be affected and have multiple organ systems affected, so we need to be really on the ball with how we're supporting and nursing these patients and what we're monitoring for and looking out for.

Team communication is going to be important from the moment this patient arrives, so making sure that we're, we're good at communicating as a team, when these patients present as an emergency, it can be quite busy, it can be stressful, again, especially if you have more than one pet from the same household present at the same time. And again, client communication, we've already laed the point about client education, but again, Thinking about this owner bringing their pets to the hospital in an emergency situation is stressful, it, it can be an emotional time as well. So making sure that we clearly communicate with our clients and they're on board with what we're doing.

And I think the key to this really is just making sure that all parties, so, you know, nurses, vets, clients, the rest of the team, everybody understands what that goal is and we know the plan on how we tend to intend to get there. With regards to prognosis, there's a paper in 2006 in Jan that sort of, says that sort of roughly about 50% of dogs, will, make a full recovery, and generally I think it's sort of documented that we see worse outcomes associated, so if we have a prolonged time between the heat stroke crisis and treatment at the veterinary clinic. If we have documented increased clotting time, so those are the patients that then go on to develop potential bleeding abnormalities, the patients that go on to have sort of an azotemia or an acute kidney injury, those that are hypoglycemic and that's I think probably because those patients are more likely to be the ones that develop a sepsis, and those patients which are obese, so it's sort of, those are the things that are generally associated with a worse outcome.

So as we said, we play such an important role as nurses with regards to the management and nursing of these cases, right through from when that phone call arrives and all the, from when the patient arrives at the clinic and we do our triage assessment, thinking about getting the pieces of the puzzle and the history so that we can. Start our stabilisation and treatment promptly. It's gonna usually be us that's gonna be placing the IV catheters, getting that emergency database of bloods to help us with our diagnosis.

We're gonna be going back to that kind of clinical examination, monitoring our perfusion and our mentation parameters, administering a real variety of things to support that patient from fluids to blood products to oxygen. To, medications, we're gonna be thinking about, you know, maximising our cooling methods to get that temperature back down to the set point, placement and management of urinary catheters, in addition to our, our communication. So quickly just to tie up our our talk this evening with regards to our learning outcomes, hopefully now we kind of understand the physiology behind heat stroke.

So it is this state of hyperthermia which is associated with this systemic inflammatory response syndrome, which can then go on to lead to a multi-organ dysfunction syndrome. We're able to identify in our patients some of the risk factors, so this plays an important role in our client education, and we need to just remember those brachycephalic patients in the hospital because it's not just about the dogs that get shut in a car on a hot day. Obviously we've now got an understanding of the major body systems that are affected and, you know, hopefully, it's clear that really anything, anything goes with heat stroke, it can be any, any body system which is, is, can take a hit and be affected.

And again then thinking about, you know, specific treatments for these patients, active cooling is that first thing that we do, and then really it comes down to monitoring and looking out for any other problems that arise along the way and making sure that we're offering up supportive therapy to try and get these patients home. So that ties us up. So I want to just say thanks again to our sponsors, Tails.com and JHP recruitment.

Does anyone have any questions? Ellie, that was absolutely amazing and I loved your last statement on the previous slide, saying that nurses are integral parts of getting these patients home. I, I think that is so, so important.

It really is. There is No successful practise that doesn't survive and thrive because of the nurses, so that's really great. Couldn't agree more.

I, I think you've done such a good job that you've answered everybody's, because we haven't had any questions come through. Our numbers have been stable all the way through, everybody has just been sitting spellbound as I was listening to you. So thank you so much for your time.

That's OK. And I'd like to echo what you said to Tails.com and JHP recruitment.

Thank you for your support and remember support those that support us in industry. That's how we make the world go around and that's how we can bring these free webinars to everybody. Ellie, I really look forward to having you back on the webinar vet at some stage and thank you for your time tonight.