Hi, thanks for the introduction, Bruce. And welcome to tonight's webinar. So tonight we're going to talk about heat stroke and anaphylactic shock.

So obviously two different topics, but they tie in quite well together, and I think probably quite appropriate because we've had really nice weather the last couple of weeks in the UK. And I think as we get more towards summer, that's hopefully, fingers crossed it's going to get better. So we'll start with heat stroke.

And the path, pathophysiology. So heat strokes a really common problem, particularly in the hot summer months when it's humid. It's a life-threatening condition and it doesn't really discriminate against breed, age, gender, although we do see, we do see it frequently in brachycephalic breeds, just because of their inability to oxygenate sufficiently anyway.

So it's the most severe form of heat-related illness, and it can be defined as a non-pyrogenic increased body temperature above 40 °C, with a spectrum of systemic signs, as well as central nervous system abnormalities. In human medicine, they define heat stroke as a form of hypothermia, and that's associated with systemic inflammatory response, and that leads to a syndrome of multi organ dysfunction, in which encephalopathy predominates. So the maintenance of normal body temperature is a really important aspect of performing, preserving this homeostasis within the body, to prevent interruption of this normal metabolism.

So we know that homeostasis works by sending negative feedback, and either through to cool or to warm the patient, through the hypothalamus. So obviously with cooling we get this vaso constriction, shivering. Which causes this warming of the patient, and then heating in our patients and we get this vasodilation, and diaphoresis.

And this all works to keep the temperature normal. And, if this doesn't occur, then we get this blood shunting, from organs performing these normal metabolic functions. So, you know, your gastrointestinal system, your pancreas and things like that.

So the thermoregulatory centre in the anterior hypothalamus maintains his body temperature within this very narrow range, and We, we either then become hypothermic or hypothermic. So a pyrogenic hypothermia or a fever, is induced by an increase in the set point in response to a disease. So this is when we get pyrexia and this is often as a result of things like infection, or, a virus, whereas heat stroke, what we're looking at is, it's an external, change, to that temperature, so there's not a, a change in that hypothal hypothalamic thermoregulatory set point.

So there's multi-organ dysfunction can lead to disseminated intravascular coagulopathy, so DIC, acute respiratory distress syndrome, acute lung injury, acute kidney injury, and obviously death following those, . So it's really important that we treat this condition quite quickly because once we get over this set point of 40 degrees, We're gonna start to see these changes within the body. So we can split heat stroke into two groups, exertional and non-exertional.

So exertional heat stroke occurs, during exercise, and it's more common in dogs that have not been accli, acclimated to their environment. So, We may have seen some recently because I think especially with lockdown, we have seen an increase in people exercising their dogs, you know, because they want to get that hour outside that they've been allowed to have. And so you might see that these dogs aren't used to having an hour's worth of exercise and especially in a little bit warmer climate.

So it can occur in working dogs, but it's really less common because, typically handler is a, a bit more knowledgeable about, the effects of heat stroke. And then we have non-exertional heat stroke, which is what we most commonly see, and this results from exposure to increased environmental temperature, in the absence of adequate means of cooling. So it might be dogs that are left in parked cars, with the windows closed or cracked, left in the yard without any shade or water.

And even in some cases in brachycephalic breeds, you know, That they've been left in the house and there's been no windows open and it's got too warm in there as well. And there's no, you know, there's no cooling, environment. There might not be wooden floors and things like that that can buy .

So with the pathophysiology, . A minimum non-pyrogenic body temperature elevation of one degree. So it's not very much when you think about it, can activate these heat re receptors found in the periphery and they trigger the thermoregulatory centre, .

So the skin contains these thermally sensitive receptors which lead to, almost a pain sensitization, and these are known as thermal nose receptors. So when they're activated, they respond to harmful temperatures. And so when we get this increase in temperature externally, these nosey accepts will respond.

And this triggers, a constriction of renal and splenic vessels, With and generally vasoconstriction all over. So you get this tachycardia, and then cutaneous vasodilation and this vasodilation cutaneously is to allow the blood to cool at the surface. I The hypothalamus is also stimulated, so we get this tachypnia, and pantin and this is to again to assist with cooling because we know that dogs can't sweat, and they basically use evaporation from their panin to do this.

Other ways that the body works, within this heat stroke is that we get this decreased blood blood flow. And an increased epithelial membrane permeability, . And again, this decreased blood flow to the guts is just to redirect blood where it's needed, .

So we can get . Two types of heat stroke essentially so heat exhaustion, and this is going to include weakness, ataxia, and potentially these patients are going to faint and an inability to continue with normal function. So they're basically just concentrating on trying to stay cool, and you'll notice this with, you know, the dogs they, they, .

They're panting, but their jaws are really set back. They're almost smiling, you know, they're, they're not moving much. They're just really concentrating on trying to cool down.

And then we come to heat stroke, which includes a dysfunction of the central nervous system. So at this point, these patients are going to be comatose or, you know, have depressed mentation. Often these patients will be hypovolemic, and they're going to have a, a cellular level, dysfunction there as well.

And at this point, the core body temperature is going to be elevated. So within this process, the acute phase response cascade is going to be activated, and this acute phase response is, is a coordinated cellular response, which is triggered in order to protect these tissues from this excessive heat and to try and promote repair. And so this is the body's way of trying to counteract this heat stroke.

So during this response, negative acute phase proteins, so things like albumin. Are gonna decrease, often by about 25%. And this is due to gastrointestinal or renal loss, or potentially just decrease production because we've got that shunting of the blood.

Whereas the positive acute, acute acute phase proteins, so, C-reactive protein and serum, serum amyloid A, are going to start to increase by 25% around that sort of figure. And these are really responsible for things like phagocyto cytosis, cytokine production, inflammation inhibition, and, chemotaxis, . And so these are all gonna try and counteract the effects that I'm That the heat strokes having, so we talked about that decreased blood flow and the endothelial cells and the gas are going to be more permeable in the gastrointestinal system, and, you know, that might promote inflammation, whereas these positive acute phase proteins are going to try and counteract that a little bit.

I also, they initiate the production of heat shock proteins, and these heat shock proteins protect against protein gene naturation and this endotoxin leakage across the intestines. And they're also going to work to reduce cerebral ischemia. So we talked about that there's going to be this central nervous system affected as well, because of this blood shunting, and these heat.

Shot proteins are basically a protective layer, to try and Prevent that from becoming more, you know, becoming a traumatic, almost like a a secondary injury to the brain. Other things I might do is, increase production of ACTH or cortisol, . And muscle breakdown.

So he, so we think clinical signs, diagnosis and treatment. So I, this table here is a basic summary of things that are going to be happening throughout the body, and then we'll come to the clinical signs that we tend to see in clinic, but we all know the heat stroke dogs, you know, they come in, they've got extremely brick red mucous membranes, they're panting, they're often tormentation. But this is basically what's happening within the body and we can start to think about this in terms of clinical signs.

So central nervous system, we may get cerebral edoema or haemorrhage, as well as necrosis. So this is where we're gonna get these central nervous system, depression. So that's where we get the dolementation.

We may have things like seizures as a result, . And as I said, you know, this opens up to secondary brain injury, which, as part of our recovery process or our treatment process, we need to be aware of. Coagulation, so it really affects the, because we've got this endothelial damage, and these patients are at risk of systemic infla inflammatory response syndrome, which is then going to lead to this disseminated intravascular coagulation.

So you're gonna lose your clotting factors and potentially. You're gonna lose platelets, and these patients are going to start to haemorrhage, so you may have petiation, you may have, quite a lot of bruising, ecchymosis, things like epistaxis, you know, you may have melena, . How much easier, hematemesis, hematuria, and this is, you start to think that this starts to get to the, worst stages of heat stroke, but frequently I've seen, I've seen the last couple of heat strokes that I've seen have all had, They've all had hemorrhagic diarrhoea, and they've all had hematuria.

So it's really important to look out for these signs. Cardiovascular wise, initially these patients can have a cardiac output, that's increased because it's trying, it's almost a response and you'll get this peripheral, vasodilation. But also the central basic constriction.

And then it's gonna lead to hypertension and shock. So think about, you know, there's blood pooling around the skin trying to cool and there's vaso constriction everywhere else, that blood's not getting around properly, the plumbing's not working, so we get this hypertension and so low blood pressure. And shock as a result, often we class it sort of hypovolemic, but it can also be distributive shock as well.

And then, again, we get electrolyte arrangements, and this may be because, the, you know, The blood shunted from from the kidneys so that that . Homeostasis there isn't working as well and we get a build up. Of hydrogen ions, we get an acidosis, .

And then as a result, we get myocardial damage, . And this causes ventricular arrhythmias quite often. So I'm pulmonary.

I'm Again, we're gonna get things like pulmonary edoema, because we get, leaking of capillary vessels, we may have increased pulmonary vascular resistance, and we talked about the central vasoconstriction. And then things like acute respiratory distress, distress syndrome. And the way we're gonna assess that, which we'll come to is, through the use of things like, blood gas analysis on, arterial samples.

Gastrointestinal, we mentioned that we're gonna have this compromised integrity of the GI tract. It becomes leaky, and, endotoxins can pass through. We get cellular hypoxia, increased permeability of this GI mucosa, which leads to endotoxins, bacterial translocation, which leads to bacteriaemia, endotoxemia and sepsis, and these patients are really high risk for sepsis.

And again, renal because we get this blood shunting, you're at risk of tubular necrosis. So we've done a basic look at each body system and the kind of clinical signs, but we'll go quickly through again. So again, we get collapsed patients, the tachynic, and they're quite shocky, so the tachycardic with weak absent pulses, especially metatarsal pulses are often absent, and we may have a weak femoral pulse.

These patients are hyperemics, they're gonna have these brick red mucous membranes. So you think about that, peripheral vasodilation, that blood's pooling and trying to cool down. At the mucous membranes, we, we get these dull comatose patients, signs of coagulopathy, petiation, haemorrhage.

We talked about this diarrhoea, often hemorrhagic and it may be menemic, depending on whether there's a bleed. And obviously these patients are going to be hypothermic. I know that goes a little bit without saying, but it's got to be on there, .

And history is the key thing for these patients as well, because we'll talk about an anaphylactic shock, but there's a lot of other conditions that, you know, have a very similar clinical signs list. And so history of recent exercise confinement in an area, and no access to water or shade, obviously the breed, if it's a brachyhylic breed, and bearing that in mind, and when we're taking the history, I still thinking about, you know, if those patients have been Walked for half an hour as opposed to 15 minutes that they're not, you know, they're normally used to, I'm thinking that it could be, heat stroke. So our diagnostics are gonna include urinalysis.

Again, we're looking for hematuria, we may be looking to see whether that patient is is is uric, you know, to see whether they're dehydrated, whether they're appropriately concentrating the urine or not, and more importantly, a blood gas, blood analysis. So we're gonna do a serum biochemical profile, . Which can include, we might do a full blood count, so haematology, specifically, we're looking at biochemistry.

ALKP is often increased, due to hepatic injury as well as, creatinine, is increased often to ren because of renal damage, either because of a direct thermal cause or because of pre-renal isoenmia, so dehydration, and that hypovolemia that we see. I Blood glucose we'll be looking at because these patients potentially going to be hypoglycemic and this is because of an increased demand of ATP and therefore an increased use of ATP as well as these patients being septic risk, so often we get a decrease in Glucose when we see septic patients, as well as lactate, we're gonna see hyperlactemia, and again this is because it's hypovolemia and tissue hypoxia. Electrolytes will often have electrolyte, derangements, you know, it could be that these patients are hyperkalemic, or hypo, and maybe some sodium deficits as well.

. When we're looking at our complete blood count, we may see some signs of thrombocytopenia, and this is secondary to platelet consumption, often because of gastrointestinal haemorrhage, as well as things like platelet aggravation. So that happens in, DIC. So we're going just checking that with a smear.

For those platelets, as well as looking at the PCV and solid, so often we'll see an increase in PCB and this due to, dehydration. And then we start to look at our coagulation panels. So we're looking at prothrombin time, and activated partial thromboplastin, times APTT, and both of these often are going to be increased, in this scenario.

So when we come to treatment, obviously cooling is gonna be our mainstay of treatment, because we want to try and bring this temperature down. It is the most important aspect of the treatment, but it might, it, it's not gonna prevent, like the, the worst effects of the heat stroke, so we need to treat those as well, . Often what we'll tell them is while they're on the phone before they come down to the clinic is to start trying to actively cool, their patients.

So this might be, this might include if they, if they have the ability to, is to soak the patient thoroughly in cool water. So not cold, you know, not freezing cold water, not ice, we shouldn't be using, towels, with, you know, wet towels because although we are wetting the patient, because of the heat coming off those, they dry pretty quickly and then we're adding another layer to those patients, that's gonna effect if the heat these patients up further. So if they have the ability to, they've got a tap or they've got, you know, buckets.

Then by all means, you know, you start to cool that patient down really starting to try and wet as much as possible because obviously a lot of dogs in particular things like collies and you know, have these double coats, so we need to try and soak all the way through. Things like using fans if they've got the ability to put a fan in, if they're in the car, putting, you know, putting their air conditioning on as, you know, as cool as possible. And then once they get to the clinic, we're going to be giving these patients room temperature fluid therapy.

So again, we don't want to put in ice around the lines. We don't want to be putting, you know, dousing these bags in ice baths because we think about the room temperature in comparison to say a dog with a temperature of 41 degrees. That's still quite a big difference.

So we're still going to be actively cooling those patients by giving them room temperature fluids. And in human medicine, they've suggested things like massage in extremities, and this is just to try and actively, you know, get this, . Cooling and circulation back to what it would be so we'll come to it in a second but ice packs and cold water and as a contraindicated .

And then basically when we think about our cooling, we should cease to actively cool our patients when they get a temperature of 39.5. If we carry on cooling these patients past the point and we try and get them to normal, to say we stop doing it at 38, often what we'll see is a refractory hypothermia because we've, you know, we've cooled them too much.

So once you get to 39.5, and often by this point, the patients then start to slowly decrease by themselves. So in addition to active cooling, we're going to be evaluating obviously the airway for patency because, you know, sometimes these patients, they, they get this exertion, this heat stroke from their inability to breathe and particularly in brachycephalic breeds, or maybe patients that have been stung by a wasp or they've got an obstruction in the airways, and this might cause them to get a heat stroke and so we want to.

Potentially we may need to intubate our our patient or perform an emergency tracheostomy in order to help call them. And then we want to be providing them supplemental oxygen. And this is either by a mask or flow by, and we just want to make sure that these patients aren't stressing out with this as well.

So I'm thinking about oxygen cages, you know, the heat that comes off in them, and we will probably want to be avoiding them. Fluid therapy, so intravenous fluids are considered a, the cornerstone again of, heat stroke treatment. So that coupled with, cooling, and this is, room temperature we want balanced and buffered crystalloid solutions.

So for example, Hartmann's, and this is going to increase our intravascular volume, and have a cooling effect. In patients that we know have got cardiac, conditions, hypertonic sale might be beneficial because we use lower amounts. But we basically we're gonna be using shock, shock rates.

So, you know, 10 to 20 mL per kilo over 20 minutes and then just monitoring our response to that. Obviously, considering any ongoing losses of these patients got large amounts of hemorrhagic diarrhoea, adding that into the patient as well. And thinking about if these patients have increased PT or APTT, times these patients are going to be candidates for fresh frozen plasma or frozen plasma.

Other things include an indwelling urinary catheter and this is to check for hematuria as well as the ins and outs because we're thinking about this these patients may have renal damage as well. Things like antibiotics, so broad spectrum antibiotics because of this bacterial translocation in the GI, GI damage that may be occurring. Maybe a consideration as well as GI tract support basically.

So things like antiemetics, particularly when we've got CNS abnormalities because these can cause nausea as well. You know, we want to prevent gastric ulceration, so we can use, proton pump inhibitors, as well as histamine to receptor antagonists. We may give them acralfate.

Orally, and this hopefully will, help our oesophagus. And then things like CNS support. So we can use Manitol in these patients, as an osmotic diuretic, if they've got neurologic signs, but only if they don't have dehydration or things like pulmonary edoema or aura, .

In these sort of contraindicated patients, again, apart from dehydrated patients, we may pick hypertonic saline to try and improve that cerebral, coronary and micro microvascular blood flow as well. . Obviously, nursing management for these patients may be, you know, we avoid jugular samples, avoid compression of the jugular veins, elevation of the head and neck.

And then cardiac support. So again, we talked about that these cardiac cells are susceptible to thermal injury and ischemia, and the damage to the myocardium, is going to cause defects this conduction. So we treat these with lidocaine often because it's ventricular rhythms, but obviously checking your ECG first.

So contraindications, so over cooling we talked about, we need to stop cooling at 39.5 °C. But basically, we don't want to use ice, .

You know, cool water is fine for them to drink, you know, water with, you know, you get these things on Facebook with, the ice water. They're fine to drink that, but if we're actively cooling our patient, throwing ice or ice cold water on them is only going to cause peripheral vasoconstriction. And this is gonna prevent the cooling of the blood, and it's all gonna be shunted, you know, because it's being shunted the periphery.

And it may also cause damage to the skin and be painful for our patients as well. We talked about those thermal nose receptors. Gastric lavage and cold water enemas.

I think this used to be quite quite a popular thing a long time ago. I think it's more less and less people are doing it now. And it's just because there's a risk of aspiration, and also the cold water is potentially going to damage the already compromised GI tract.

We want to try and avoid shivering. And we talked about that that homeostasis and that shivering is basically a mechanism to warm up the body. So we're going to be basically counteracting what we're doing.

Although there have been some human studies that sort of suggests this is minimal, and it's better to avoid it and because we know that it's a a a warming mechanism of the body. As well as corticosteroids. So now we come to anaphylaxis and anaphylactic shock.

So heat stroke often, can be a big trigger for, anaphylaxis, . And so anaphylaxis is, an acute allergic reaction to an antigen. So things like a bee sting, you know, it could be a snake bite, which I think at this time of year we're seeing a lot of, things like food allergies, maybe injections, and like I say, heat stroke, to which the body's become hypersensitive.

I'm Another definition is that anaphylaxis is a severe life threatening, a generalised or systemic hypersensitivity reaction, or a severe potentially fatal systemic immediate hypersensitive hypersensitivity reaction. Which is most commonly caused by immunoglobulin Emediated immunologic release of mediators from mast cells and basophils, So anaphylactic shock is most commonly seen within seconds to minutes of the exposure to the cause. And anaphylactic shock results from massive haodilation secondary to the mass cell degranulation that we see with this anaphylaxis.

As well as a histamine release, and a rapid release of inflammatory and vasoactive mediators. So this vasodilation in turn is gonna, decreases the relative circulatory volume, decreases perfusion, and thus, oxygen delivery to tissues. So we're gonna get splenic contraction, tachycardia, as well as myocardial and cerebral hypoxemia, and cardiovascular collapse and death.

I'm so nice cherry. I'm things for the dogs. So When we think of the path of physiology.

And the types, they can be an immunoglobulin E mediated or non-immunoglobulin E mediated. Or non-immunologic, so basically histamine, is primarily released from the gastrointestinal tract into the portal vein, which leads to a hepatic arterial vasodilation, and an increase in hepatic blood flow. I'm And this happens in dogs, and which will come to in a second.

So basically you get this antigen and . It causes hypersensitive reaction in the mast cells and basophils. You get these release of, things like histamines, C-reactive proteins in which these little Stars that I've put here, and you get this vasodilation and vascular permeability as well that will come to.

So we have these mediators of . Of anaphylaxis, I'm So we get histamine, which causes smooth muscle contract contraction, vasodilation, this increased vascular permeability, and decreased venous return and hypertension. You get heparin which inhibits clot formation.

You get decreased clotting factors and a hypercoagulable state. So again, you're gonna get haemorrhage in these patients. You may see petiation in these patients as well.

So very similar signs to heat stroke and that we've just talked through. Cytokines, so. They cause an increased cellular responsiveness to inflammatory mediators.

So you can get what effectively is the cytokine storm. And these patients, potentially they are gonna go into systemic inflammatory response syndrome or potentially disseminated intravascular coagulation and . And this is, you know, bad for our patients.

So prostaglandins as well, these are released, and as a result of this, we get bronchoconstriction. Pulmonary, coronary, vasoconstriction, and peripheral vasodilation. So again, very similar to the mechanisms of heat stroke in that the blood is trying to be conserved and sent to, Vital organs, but then we get this peripheral vasodilution as well.

So, as a result of this, we get this anaphylactic shock or which is in the classification of distributive shock, where we have just very differing blood pressures all around the body, and nothing's really been pumped around properly. And then we get platelet activating factor as well, which is going to decrease our coronary blood flow, and myocardial contractility. It's going to increase pulmonary resistance.

It's gonna cause vasodilation and this profound hypertension that we'll often see with these patients. And we talked about that myocardial and cerebral hypoxemia, and then cardiovascular collapse, and at this point, these patients are in trouble. So often, the early signs are dermal, so as you can see in this picture of this dog, you know, you might get Androedema, you may get erythema, utarus, you might get hives, you may get a swelling of one area, you may get, you know, swelling of a few areas, .

And other earlier signs might include vomiting, diarrhoea, weakness, lachrymation and pruritus, . You know, these patients can be potentially going to be itchy depending on the cause as well. And so this is where good history taking comes into play.

I mean, if they, if they've been fine up until 15 minutes ago, they went out in the garden, you know, we can potentially narrow it down to a sting, or a snake bite. But again, like I say, heat stroke may be a mediator of anaphylaxis as well. And then as we get more as we move through the severity of the condition.

We'll get cardiorespiratory signs, so we may get dyspnea, tachypnea, tachycardia, hypertension, dysrhythmia, as I said, because of that, cardiac collapse, and lack of oxygen, as well as strider. If we have involvement of the upper respiratory tract. And we talk about these late signs, so seizures.

In patients that we've got the cerebral hypoxia hypoxia. I'm So I think it's really important, to take history of these patients. Again, the same with heat stroke and that these conditions can manifest, similarly to things like, acute haemorrhage, Things like severe hemorrhagic gastroenteritis, .

Addisonian crisis, you know, we often see these patients with hemorrhagic diarrhoea, or like, you know, severe vomiting, heat stroke, airway disease or respiratory distress, and pericardial effusion as well, you know, we get these collapse, we get arrhythmias, . You know, it may have weak thready pulses. I'm So this is where history taking comes into place.

So we have, if you have no known antigen exposure, but you have huge car angioedemia, plus at least one of the following, so respiratory signs, a decreased blood pressure or collapse or urinary incontinence, then it's likely we have a patient in anaphylaxis, or we may have a patient that has a likely antigen exposure that we know of. Plus 2 or more, so skin signs, respiratory signs, low blood pressure, or gastrointestinal signs, they might have diarrhoea or hemorrhagic diarrhoea. Then again, we may be suspicious of anaphylaxis and that we may be high up on our differential list.

Or we may have a known allergen exposure with a low blood pressure, the patient could be an anaphylaxis and potentially anaphylactic shock. So I've mentioned, anaphylactic shock comes under this distributive shock because of this, because you get this peripheral vasodilation, and peripheral and and central vasoconstriction. And we think about distributive shock, it's just that The plumbing's all there.

Nothing's really broken, but because we have these leaky vessels, there's, you know, there's potentially we're losing fluid through that. So we have an element of hypovolemic shock, but just nothing's really been pumped to the heart and the heart's not, I'm sending blood out to that plumbing properly, . And distributive shock occurs when the body is unable to maintain the vaso constrictions that leads to the systemic vasodilation eventually.

So I talked about in dogs, the liver, is a shock organ, and this is where the histamine is primarily released from, into the portal vein. So we get this hepatic, this vascular resistance, that increases, and a result, as a result, we get this, decreased venous return to the heart, and a reduced hepatic venous return, to the heart decreases the cardiac output. So we're going to contribute to hyperbulimia, decreased oxygen delivery to the tissues, and then coupled with the shock, means that these patients are going to often be collapsed.

They may have an acute onset of gastroenteritis that is hemorrhagic. So often patients are dogs that come in, will have this hemorrhagic diarrhoea, they'll be collapsed. Whereas cats, obviously, cats are different always, their shock organ, What we class the shock organ is the lungs.

So typically they respond to, allergens with this profound bron constriction. So we're gonna have, decreased, blood oxygen levels, increased, carbon, carbon dioxide levels, decreased cardiac output, so you get acute hypoxemia, which causes an increased Sympathetic tone, which may cause splenic contractions and then hemo concentration. So often these patients, these cats are going to present dysneic, they may be coughing because of this bronchial constriction.

They may have weak peripheral pulses, a low blood pressure, and these patients may be collapsed as well, but often, we see this profound dyspnea, and coughing, and that goes along with it. I'm so Particularly in the dog, and we talked about that the liver is the shock organ. So diagnostic changes is if we pop the, we pop a FAT scan on and we're doing a FAT scan looking for, any free abdominal fluid or free, thoracic fluid, we may see this gallbladder halo, so.

It might not be particularly, it's not the best picture of one, but you can see a thickening here and then like the slight black line here. So this is known as the gallbladder halo. So it's almost an edoema of that gallbladder and can be suggestive of, Of, anaphylaxis, we should take care that it's not the only, It's not the only marker for anaphylaxis.

It also can be, we can get this gallbladder halo in, cardiac disease, and when these patients, patients are in congestive heart failure, so obviously ruling out other, causes, but if we're suspicious of anaphylaxis and we have this gallbladder halo, then it can, you know, it's almost a tick off the, checklist. And as well in dogs, we're going to get this biochemistry, so we're gonna get this raised ALT because this ALT is a marker of, Of liver damage. And in cats, we may see pulmonary edoema, we may see lung rockets if we're doing a FAT scan, and so these bee lines, as a result of, this anaphylaxis.

So when we think about the treatment of these patients, we talked about that they're gonna have this profound hypertension, decreased myocardial contractility. So they're always inevitably going to have this decreased circulating, oxygen. Therefore, the demand's always going to be increased and they're always going to benefit from our oxygen.

I say this with most patients, and if in doubt, stick it on oxygen, you know, there's very few conditions that you're going to do more harm than good and especially if they're coming in and they're in shock, and all shock patients really should receive oxygen. You know, consider the airways as well, in these patients and for those in severe respiratory distress, so cats, and obviously with cats, we need to be careful that we don't want to stress them and cause further exacerbation of that condition. So often getting an oxygen kennel set up for these patients and may be beneficial.

You know, preparing in the tracheal tubes if we think that this patient, needs to be intubated and mechanically ventilated, as well as things like tracheal tracheostomy tubes, just in case, because we may have, it depends on obviously where, this, this, event has happened, it may be that these patients have got an inflammation of the airways and we need to basically open up those airways for them. And then we want to try and assess oxygenation and ventilation using the blood gases if available. So obviously, in an ideal world, we'd be doing arterial blood gas samples.

To assess the oxygenation as well as ventilation, but if, we're unable to take arterial samples for whatever reason, whether it's, you know, a patient is stressed or, we're not able to get them because of, you know, this, vasodilation. Then, you know, we can use venous samples to assess the ventilation and these patients aren't ventilating appropriately, thinking about, you know, taking over that ventilation for them, and so intubating them and sedating them all and General anaesthetic, to put to mechanically ventilate them, put them on a ventilator, in most serious cases. And then we come to fluid therapy, so the treatment for shock and profound hypertension usually warrants an aggressive fluid therapy, so we want to tailor to our patients.

But a good place that we usually start with is a balanced, buffer solution such as as Hartman's, a crystalloid, and we're gonna get bolus rather than a huge shot dose of 90 mL per kilo. We're gonna break it up into smaller ones. So 10 to 20 mL per kilo over 15 to 20 minutes, and then reassess using, using your measurable parameters.

So your blood pressure, your heart rate, . You know, feeling for peripheral pulses as well, the quality of them, and potentially temperature as well, you know, is that temperature increasing with, you know, if they were hypothermic, which they often are when they're in shock. And then Pharmacology wise, so, I'm, we may, administer antihistamines, as a first line treatment to down regulate the release of more mediators, .

During the treatment. So often what we'll give is histamine one, and Antihistamines, and These are most effective in treating localised allergic reactions. So, you know, you bee stings, use, snake bites, so we'll think of them less if we're thinking of heat stroke, but you may, these include chlorophetamine.

Histamine 2 antihistamines include things like ranitidine and famotidine as well, . So maybe using these as gastrointestinal support system anyway, the histamine 2 ones. So when we think about anaphylactic shock, and anaphylaxis, epinephrine is essential to these patients and is the gold standard, and this is because epinephrine works to accelerate heart rate, it's gonna increase these cardiac contractions, and decrease mass cell degranulation.

And improve oxygenation through this bronchodilation. So we talked about these patients potentially gonna have bronchial constriction as well. So you can give it via, the endotracheal tube, you can give it subcu or IM, but most effectively in these patients in the way that we need to get it in as quickly as possible as IB, so they really benefit from a continuous rate infusion, .

Especially because we can then titrate these dose rates as the, as we continually monitor these blood pressure. So I would suggest having these patients on a monitoring device if you can do, or taking the blood pressure, at least every 10 to 20 minutes, especially when you first start this treatment. And often what is recommended is that you touch a dose rate of 0.05 mcg per kilogramme per minute, on your CRI.

And like I said, this is your gold standard, and a lot of these patients respond really well to this epinephrine, treatment along with their fluid therapy, and their blood pressure sort of normalises within about sort of 12 hours, . Other things that you can use are bronchodilators, so things like albuterol, or tebutyle, because it's an inhaled adrenic agonist, and this helps with bronchospasm, but it doesn't replace this need for, this epinephrine because bronchodilators don't have this alpha ad adrenic effect. So our patients, .

Still have . Bradycardia or they still have severe hypertension. There's unresponsive you fluid resuscitates these patients, you know, they're normal bulimic now as or they should be, you know, you've given them lots of shot bolus and you've accounted for any losses that they're having, and they've had the epinephrine treatment, at least for a couple of hours.

Then these patients then should move on to the next line of treatment, which is vasopressors, with or without anticholinergics depending on whether these patients are bradycardia as well. So vasopressors, are going to increase the myocardial contractility. So you get things like no epinephrine and dopamine and vasopressin.

So I would say the first line of treatment are going to be norepinephrine, and vasopressin. Dopamine, I would use as the last, . Last ditch almost, just because this can have beta effects as well.

And we want to try and minimise the amount of counteractivity as well. And then anticline cholinergics, these are going to be used in patients with persistent bradycardia. So, you know, the patients that we've, reperfused, and the heart rates come down, but they've still got this severe hypertension.

and the epinephrine hasn't helped for things like bronchospasm, so we may use atropine to resolve this persistent, bradycardia. And with these patients, it's just really key to monitor them constantly, especially in the first couple of hours. These patients are really high risk for SERS and sepsis and DRC, and, you know, making sure that you're looking at your blood gas analysis, your electrolyte derangements, .

As well as things like your clotting factors, you know, replacing it, like for like, you know, if you've got, increased parameters on your PT and your APTT, making sure that they get fresh frozen plasma or frozen plasma, in line with their treatment as well, because we want to try and, counteract any, any other side effects of this, anaphylaxis. Thank you very much for listening. I don't know if there's any questions, I'll hand over to Bruce.

Chloe, thank you very much. That was absolutely amazing information and really, really worthwhile to, to be listening and, and just, you know, kind of getting it all put together. And I like the way you tied the heat stroke and anaphylaxis together.

That was really good. So thank you for your time. We have a couple of interesting questions coming through.

The first one, which is a bit of a hot potato, so I'm sorry for it, but how, how high does the temperature have to go before you decide treatment is not feasible? Oh, I guess it depends on the owner commitment, the state of the patient, obviously, your blood results. I think the highest I've seen that we continued with treatment, it was like 4 to 2.3.

I think. They, they start to go over that and you start to get seizures. These patients, while you can attempt treatment, they have a very, very low success rate, and even those that you potentially, you know, that one that I said the 42.3, we resuscitate it quite well.

And it seemed to stabilise and then all of a sudden it started to haemorrhage. It started to have epistaxis, you know, it's pouring blood from its back end, it had matora, and then it started seizuring and it died. So I think they had, it's a pretty grave prognosis when they start to get quite high, and you know, even, even the lower temperatures, I think you have to have honest conversations with owners about, the success of treatment, .

Just because I think once you start to get that cascade happening within the body, and that hypoxemia and, you know, potentially anaphylaxis is on top of that as well, that the body just starts to. Deteriorate within. So, I think, I think it's a case of owner commitment, being realistic about, clinical signs, and, you know, your diagnostic tests, your results from your diagnostic tests and seeing whether they respond well to treatment, yeah.

Yeah, much more a multifactorial decision rather than just simply having a cut off on temperature, I think. Yeah, I think so. Yeah.

Jen says fantastic webinar. Thank you very much. And goes on to ask, do you use steroids in anaphylactic patients?

No, I think again, this is another contentious topic potentially. I think. Corticosteroids, I'm, I think.

A contraindicated as well as non-steroidals in these patients, unless you get into the end point and you're sort of thinking of, you know, Never give anything, you know, that's dying, try and give it steroids once. I, but I'm typically within our practise and personally with anaphylaxis that I've seen, I'm We, we don't give steroids. It depends on the severity, I guess.

I think the type of anaphylaxis that I've been talking about and that like anaphylactic shock, you wouldn't give, steroids, but potentially in patients that you see that the bee sting, I know there has been, you know, some Some evidence or some topics that discuss, you know, the use of antihistamines along with steroids, but I personally, no, I wouldn't use steroids. Excellent. Another question we've got, is how often would you redo blood tests with animals in anaphylaxis, anaphylactic shock?

So, Typically, I think again it's monitoring the patient and the and the physiological responses, and obviously if you're not getting those physiological responses that you want from your fluid resuscitation, and your epinephrine, you know, you're not getting that increase in blood pressure or you're still getting this tachycardia, and then you may want to repeat sooner, but often we'll do the first couple of hours we'll maybe do. Every half an hour to an hour, and then increase it to maybe every 2 to 4 hours and within that 1st 12 hours and then You know, then maybe you can repeat. Or to monitor changes, and in particular the first couple of hours when you're starting to implement that treatment, because, because they're so fragile, I think any, any, you know, any changes are gonna, affect these patients quite, drastically.

And so it's important to, to look at them. I think particularly if you've got access to a, a blood gas machine like an epoch or an ISA, it's really handy to, to be able to use those, because they You know, quick and easy to use rather than taking large blood samples constantly for biochemistry. Yeah, it's, it's, I mean, it, it, it also helps a lot with monitoring response to treatment, but it's also a prognostic indicator to help you have that difficult conversation with the client, if it's, if you're not getting the response, despite throwing everything at it.

Yeah, exactly. I think that's what I, yeah, I think going back to that first question is that if you If you've got those figures in front of you, it's an extra thing to basically come with the owner to say, OK, well, you know, it's not really responding the way that we wanted it to. So, so yeah, I think it's important the first couple of hours at least to be taken, you know, even hourly, you know, depending on the patient, you may be doing it every half an hour.

But yeah, just keeping a really close eye on those values to see how they respond. Yeah, and I think another thing to, to bear in mind with, especially with, with the severe cases of heat stroke and, and anaphylactic shock is that these are not cheap conditions. So, you know, you don't want to be, worrying about money, and therefore not doing your blood tests.

And you know that, you know, if they have got any chance of pulling through and being OK, you've got to throw bucket loads of money at them and tests and, and, personnel, nursing. Yeah, it's a lot of work. I think a lot of, a lot of monitoring and definitely, let's say, a lot of money.

Yeah. Yeah, and I think that's an important point to make when you've got one of these cases to that right up front with the client. You know, it's, it's part of the The sort of prognosis of it, you know, we've got a question coming from an anonymous, person.

They've said, would it be beneficial to give sedation in a stressed cat, even if it's breathing is OK on arrival. I think, again, case by case, but I think if you've got a really stressed cat, you know, using something like burophenol, often is enough to sort of calm them, at least to get things like, you know, intravenous lines and and things like that, because I think the risk obviously that we know that there's going to be some element of, bronchial constriction, whether they're showing severe dysneic signs or not. And I think with cats, they are so fragile, no matter what situation they're in, that, you know, if they are stressed, making the hospital scenario for them, a more pleasant experience is always beneficial, you know, in any condition.

So I think, I think, you know, the use of things like butrophenol, I wouldn't necessarily jump straight to heavy sedation, but yeah, you know, just to take the edge off, and just using, you know, cat friendly handling techniques, and you know, trying to minimise handling of that patient when they first come in, is, is beneficial to these patients. Yeah, I heard a, a, a term once that was used in a, a cat CPD where they said, blunt the stress factors. Yeah.

And I think that was a great term. Yeah. Yeah, they're not quite as bad as rabbits, but definitely, they're definitely very responsive to stress.

So any, any way that you can minimise that stress for them in the hospital scenario is beneficial. Yeah. Folks, I'm afraid that's it.

We've run out of time. Chloe, thank you so much for your input and sharing with us. I did promise our attendees a great webinar and you've lived up to that.

So thank you for not making me a liar. No worries. Thank you for having me.

We look forward to having you again and to Dawn, my controller in the background, thank you for making everything seamless as always. And to all of our members for attending. Thank you very much from myself, Bruce Stevenson.

It's good night.