Hi, so we're gonna talk about tremogenic microtoxins. So all things about like what they are, how they come about, how they're gonna affect our patients, the kind of diagnostics and the treatment that we're gonna give to these patients that we suspect have tremogenic microtoxins. So chemogenic microtoxins is the ingestion of mouldy foods or compo compost that may cause a remogenic microtoxicosis, and it's a basically a poisoning.

And it's quite often, and I think as, as we become more into climate change and environmental changes, these homogenic microtoxins will become more prevalent, just because the prevalence of, you know, mould and things like that will become more prevalent, you know, in, in compost bins and, and normal bins as well. So it's deadly. I'm, and we need rapid treatment of this.

So we'll talk about that later in this webinar. So we're gonna look at the review and the causes of tremogenic microtoxins, as well as the discussion of pathophysiology of the toxin. We're gonna look at the presenting symptoms and the overview of the diagnostic testing as well that's available for these patients.

And then as well as that, we're gonna review our treatment, and kind of our considerations for these patients. So what are microtoxins? Microtoxins are a secondary, metabolites that are produced by several fungal species.

They're toxic to animals, plants, as well as other organisms as well, so not just limited to our patients. Their effects all differ, and that is based on their chemical structure. So tremogenic microtoxins generally will cause a neurologic, syndrome that includes tremors, hence the name.

These toxins are produced by moulds, and they present on foods, compost, and that mould grow grows under a range of conditions from about 20 to 30 °C. Different species have different oxygen requirements, but the optimal temperature range is at 20 to 30. So, as I said, unfortunately, I think as climate.

Change, environmental changes become more prevalent, that 20 to 30 degrees will be hit a lot, a lot sooner, than they would in the past. So there's been multiple mechanisms of action, suggested for tremogenic microtoxins. And as I said, because they differ, It differs for each toxin, and also for the species of animal involved with the exposure to that monro toxin.

So there's 2 reported, and we'll talk a little bit about them, but basically there's the microtoxins, that involve the neurotransmitters, and glycine and that gamma aminobueric acids that GAA. I'm So remogenic microtoxins in particular, are those fungi that cause neurotoxicosis. And so there's several, fungal metabolites that might cause this.

Most research and, and most things point to, these two, penicillium species, and that's that ROC 14C and penetram A. So that penetram A is the primary microtoxin that's involved. Although there are about 20 that have been identified as tremorogens.

So these two, this penetram AOC14C are produced by the penicillin, and they are detected, they can be detected in stomach contents. And we talk about diagnostics, and we can actually do, look at the vomit in, in our patients and the stomach contents, and identify if there's ROC 14C or penetram A, present. So identify, identifying the specific, microtoxins isn't always necessary, and we'll talk about that a little bit in our sort of diagnostics and treatment, because regardless of that, the treatment is similar, very similar, .

So that penicillin, that especially that penetrom A grows really well on meat, cereals, nuts, cheeses, eggs, fruits, processed, refrigerated food, refuse, and compost as well. So it's really important to take history from our patients and we'll talk a little bit about that is that's a main part of our diagnostics is that we really want to get that comprehensive history and to see if these patients. Are able to get into any bins if they have compost in the back garden, if they've been out on a walk, and maybe the owners have seen them, you know, snuffling and bushes and things like that.

So that production of those microtoxins and human food or animal feed, in that waste will depend on the, again, like you say that, species of mould, but that penicillium is that dominant trimogen producer. So how do these microtoxins work on our patients? I just mentioned a couple of slides ago about that gamma aminobuyric acid.

So this production of microtoxins in human food or animal feeds, like I said, will depend on that species of mould, but we get these penicillin. Species and that there's several mechanisms of action that are thought to be, and proposed, but there's still nothing definitive as to whether this is why these tremors happen. But this is sort of the proposed and what and what everyone goes along with.

And so. Basically get the neurotoxins reach these central nervous system synapses, and so that penetrium A crosses the blood brain barrier very easily, it's lipophilic, and causes an inhibition of calcium regulated potassium channels. So what we start to see is, these voltage, gate channels, are blocked, and as well as that.

We also get a, an, an effect on this, a secretion of the neurotransmitters, glutamate, aspartate, and that gamma aminobuyric acids that gather in the cerebral cortical sy synapses. So it stops all those making those messages, . So, what we also see is there's a metabolite, and a verruculagen that's made by penicillium.

It reduces the concentrations of that GABA as well. So basically, the, the overall, suspicion of the, the pathophysiology of it is that we it stops these synapses and that's why we see these tremors and we see inappropriate . Amounts of gamma, gamma aminoretric acid and glutamate aspartic.

We have inhibition of those calcium channels, so they're either held open or they're closed, and then therefore is inappropriate messaging through those synapses. So when we start to come onto our clinical symptoms, what we start to see, and then the, the main name of this, disease is, this pathophysiology tremorogenic microtoxins. So we see these muscle tremors, and we get these fascillations, twitching, and often these patients are hypostatic as well.

And this can lead, into things like lero spasm. Often, they get these, like I said, these s vasculations, the tremors, and again, this can lead into seizures. It can lead into This hyperesthesia, nystagmus, vomiting as well, diarrhoea sometimes is a, a secondary clinical symptom as well.

And, With this vomiting, we now have these patients are a massive risk of aspiration pneumonia, and that's because they're unable to control themselves. They're vomiting. They're also, they're having these massive muscle tremors.

They often have hyper salivation as well. And so really important. To, to recognise these signs in our patients, and these signs can sometimes, coincide with other, intoxications as well.

So again, I kind of important to look at the smaller things like the hyperesthesia, the muscle, the muscle tremors in particular. We can get tachycardia as well. And often the clinical signs will be an onset of about 1 to 2 hours, but we can actually for several hours with this.

And as I said, that aspiration pneumonia can actually complicate that clinical prognosis, just because that vomiting, and, and the need for gastric age as well. So, the higher stress of putting them under anaesthetic to do that. So, hyperextension of the extremities is another one that we can see with these, and often these patients will be, potentially hyperexcitable, tachypneic, as well as that might have vocalisation and eventually weakness from those muscles.

So I'm gonna show you a video. This is like a very typical tremogenic microtoxin patient. So as you can see lots of muscle tremors.

This patient was hyperstatic, it was tachypneic, it was tachycardic, but you can really sort of see the muscle tremors and the whole body is kind of shaking as well. And this patient didn't have the stagmus, but was attaxic when it was walking. You can kind of see as well actually, when you're, when you watch it, it, you know, it's quite wobbly and just because those, those massive muscle tremors actually just make them really attaxic.

But also thinking about the fact that, you know, this is a, a neur a neurotoxic, intoxication. So just to add on that as well, so memory, many tremogen exposures of dogs are non-lethal, particularly because we pick them up and we give, we give our, antidotes and supportive treatment, but with some dogs, that end up having severe seizures, they might be euthanized, and so something that was found in postmortem. Euthanized patients that had seizures from remogenic microtoxins, actually had something called ischemic neuronal necrosis in the cerebellum.

And they think that that potentially develops from cytotoxic neurotransmitters, such as that glutamate and aspartic acid. So what they have is these multifocal haemorrhages in the cerebellum. In the stomach, in the liver, and, and as well as I lung as well.

So I'm kidney as well so these like haemorrhages everywhere and they get these I'm. That, that penetrim A and ROP14C in those postmortem patients were actually found in those lesions, in the stomach, liver, and kidney, and the only penetrain A was found in the brain. So potentially because that's got that crossing of the blood brain barrier.

So potentially when we are thinking about diagnostics, if we feel like it's just the case that maybe looking at stomach contents and seeing which ones we have and, and therefore being more cautious with these. So the liver and the kidney damage could be due to the remogenic toxins or because of the therapy that we give them the antidote which you'll talk about a little bit. So again, just a complication that we might see, so just something to be wary of, it's not something that we're gonna discuss a little bit further.

We might, you know, but what we might start to do is in those patients that we see with severe symptoms, obviously, given a, a guarded to grave prognosis and also looking at things like our coagulopathy, parameters as well for diagnostics. So we're doing our diagnosis, we're looking at our baseline lab tests, so we might do a complete blood count, couple of complete blood counts or haematology, as well as our serum biochemistry, electrolytes and urinalysis. So what we might see in our serum biochemistry is elevations in liver and kidney values.

As well as creatinine, increase, we might see that because of, either because of those kidney changes that we just talked about those lesions, or because of like pre-renal azotemia from from hypovolemia, and if our patient's been vomiting or also had diarrhoea as well. So said that Pennetrim A has been previously isolated from the liver and the kidney and an intoxicated dog. But we don't know the role that it actually plays in the liver and kidneys.

So we, we may get potential liver and kidney elevations, and as well as because we've got a significant muscle activity, we're gonna see changes like our increased lactate as well. And, because of muscle activity, and as well as looking at the changes for our, adverse effects of drugs that we use to control these clinical signs. Again, glucose may be low just because of the increased muscle activity for prolonged periods of time.

So monitoring that and making sure that we are keeping that at a good level. I'm And that urinalysis again is gonna show us if there's any kidney issues, whether there's pre-renal enmia, whether they're diluting or concentrating the urine, effectively, so looking for eyes and in your ear as well. Again, things that we're looking for when we are looking at our diagnostics, we're not necessarily looking at whether it's a, that penetram A or Rockfortin C.

What we're looking for is the changes that we can then support, do supportive treatment for, and so these patients might develop dehydration, and electrolyte changes secondary to that vomiting and diarrhoea that I mentioned. And so doing our electrolytes, doing things like our blood gases as well. So again, we might see changes to our pH and we might have a metallic acidosis again because of that increase in lactate, lactic acid.

We may see severe, changes, so, metabolic acidosis that potentially is compensated. By respiratory alkalosis or a concurrent, respiratory acidosis. So you can see that patient pain, that was achyneic and potentially might have concurrent, metabolic and respiratory acidosis and therefore that needs addressing, and we'll talk about that with, you know, with things like fluid therapy.

Obviously stopping those muscle tremors. Our complete blood count might shows that we might have an infection. Obviously looking at, levels of our dehydration, so looking at, PCV versus total solids.

So if we have an increased total solids in normal PCV, we might have dehydration, you know, points to dehydration again. Looking at our dehydration parameters as well, so, looking for dry mucous membranes, like dry tacky mucous membranes, decreased skinteria, sunken eyes. And as well as I like looking at I'll wait as well.

And again, dehydration, if we have excessive gruelling, if we have that hyper salivation, for prolonged periods of time again, that's something that, is a fluid loss over that time. In addition to that, like I just mentioned with the With the lesions, disseminated intravascular coagulopathy, might occur, and that's either because of the lesions, but also likely because of the severe hypothermia. So often these patients get, are extremely hypothermic because they've got those massive muscle tremors, because of that increased muscle activity and therefore, the hypothermia untreated, can lead to that trigger system that goes into that DIC.

So that diagnosis of tragic, remogenic microtoxin exposure is based on the clinical signs that we just talked about that, that the, clear central nervous system stimulation, that include like the vomiting and the tremors, things that like the tremors, if they're intensified by handling or sound, which often they are, so as I said, they're hyperstatic, they are intoxic. If they have, like I say, hyper seizure, tachycardia, and then, worst cases, seizures, and as I said earlier, there are other toxins, that actually, pro provides differential diagnosis for these patients as well. So it's like toxins, and pesticides, metaldehydes, soloate, poisoning, ethyl glycol.

And as well as illicit drugs can also cause this. So, important we kind of get a really, really good history with these patients. So, like I say, asking the owners if they have recent access to mouldy foods, any free ranging behaviour, and access to compost, you know, if they live on a farm, and what kind of access they have on that farm as well.

So as I said, you can, send off the vomit test for, a diagnostic, to diagnostic labs and do a mass spectrometry, chemical testing to see what is in that material, and as well as that, you can also also send off serum and urine as well. So obviously, with the differential diagnosis as well, like we would look at our treatment and when we are doing our gastric lava, we might be able to see like metaldehyde poisoning. We might be able to see certain drugs or we might have other symptoms that fit better with illicit drugs.

We might do urine testing or serum testing with those illicit drugs. So kind of with femogenic microtoxins often it's . You know, all the central nervous system signs are quite obvious, but then we just have to kind of do a process of elimination sometimes as well.

And so as I said earlier with the COAGs, that's sort of as we start to suspect, if, and particularly if we have prolonged hypothermia, we might start to, perform on coags just to see if we have normal . Activated partial thrombin time and and and and partial thrombin time as well. So APPT APTT and PT.

Just to make sure our, coagulation cascade is, still working and that we've not got, risk of this patient starting to throw clots or, bleed out. And so other things that we might be looking for as well in these patients in later stages, we suspect that these patients might start to go down the road of DIC is to look for petiation, bruising, you know, ecchymosis, hematuria, . Hemasia and Melina, you know, any sign that that patient is bleeding.

So now we're gonna talk about treatment. And so, as I said a couple of times, there is an antidote. Or, it's, it's not a specifically, specific antidote for this, but it's thought to actually treat these patients really well because of that leophilic, penetram A.

So what we're aiming to do mainly with our treatment is to support these patients and And all the signs that come with this tremologenic microtoxin. So not just, you know, not just giving the antidote and that's, that's it, we're supporting this patient, we're stopping those muscle tremors. We are on seizure watch, so treating this patient as if they, are likely or or in partial seizure, .

We're supporting those blood results, so supporting the kidneys, if they're pre-realisoemic, with fluids, if we have electrolyte changes, cha, you know, correcting those electrolyte changes, so we'll talk about that now. So the management of those signs must be prioritised as well, so any signs of acute central nervous system stimulation, they should really be addressed first, so controlling the tremors and seizures. So one way that we can do this and it's really effective, at least with the tremors is to use methocarbonyl, so Rebaxin's also known as.

And this is a essentially acting muscle relaxant. So you give it a dose of around 55 to 220 makes a cake. You can give it that IV at a rate of normal than 2 mL a minute.

You can also give the tablets, and, and I find this most effective, especially if you've not been able to get an IV in yet in these patients, is to give the methcarboyl rectally. And so, you get your dosage, you crush those tablets up into a 10 ml syringe with water, place a urinary catheter. of the rectum and give the methcarbonyl rectin.

It actually works really well. And, and that's anecdotally, but I've used that for years and, and that's worked, just as well as getting an IV to effect. So that tremor and seizure control might also be achieved by giving diazepam, but there are case reports that, diazepam alone isn't effective.

So barbiturates such as, phenobarbital, have also been shown to be effective in controlling the tremors and seizures in those dogs exposed to tremorogenic microtoxins. However, because phenobarbitals come with that risk of heavy sedation, it does place that pet at risk for aspiration, so. Just care with that patient.

But because these patients are hypothetic, attaxic, what we want is a nice dark area, quiet area, so we can have them in an ICU or if we're able to put them in a kennel that again. Padding so if they're they're not bumping up against walls and, and injuring themselves, but nice quiet as we would with seizure management for these patients. So maybe you have a sign that you put on your kennel door, maybe you have a sign that you put in your hospital for people to be quiet.

And if we know that these patients are coming down, just getting everything ready for that, getting, if we hear tremors on the phone or shaking, you know, preparing the clinic by, preparing diazepamorphineobarbital, ready for that patient to arrive, and to get an IV into, and again, mecarbony and really effective. Because of that rapid absorption of penetum A, and, and because of that rapid onset of clinical neurological signs, that window of opportunity to induce a meus is quite short, and as well as that, you know, the, the opportunity to administer activated charcoal when we've got that stomach tube and is quite a short window. We may use radiographs to assess how much materials in the stomach before we do the X-ray before we induce a mess.

But it just depends on the timing and also how bad those tremors are as well. So, ideally, in a, you know, in an ideal world, we want to get rid of all the stomach contents so that we avoid as much as possible the penetrain or the rock potency being absorbed and, and again, that, that penetrain A crossing the blood brain barrier. But ideally, we do want to do this, so we can induce mess by, giving our ouretics such as, apomorphine.

But again, the risk of aspiration is quite high with these patients because of their tremors, because of their neurologic status, and therefore inducing, anaesthesia and there and, and doing a full, gastric lava with the stomach tube is, is better, so that decontamination. And so the size of the patient is gonna determine the size of the tube that you use them, so again, we, we're often these patients have just eaten, so think about how that we want to have the widest tube possible for that patient because it's gonna be kind of undigested food at this point. I'm So if possible, we want to try and stabilise these patients as much as possible, .

You know, because we, we, we want to reduce the amount of, risk to that patient by inducing anaesthesia. We want to risk, you know, reduce the risk of aspiration pneumonia. So trying to get those tremors under control, either with a bottle or with .

With, methcarbonyl, and what we want to try and do is as soon as we are reducing immune system to, to gain an airway as quickly as possible. So, if our patients have signs of vomiting before we anaesthetize them, then this is a much higher risk and then something that we need to consider, whether we give them antiemetics or whether we don't, do a decontamination at this point while they're still vomiting. So, if that animal hasn't previously vomited spontaneously, then that ingested that substance is likely to stop eating that stomach, so, .

Doing the decontamination with gastric lavage and so cough endotracheal tubes, and, and then just body temperature, water, and so warmed fluids in the. In the gastric tunes. So you do about 10 mL per kilo of body weight.

So obviously using gravity, as we would do when we normally do gastric lavage, . So you can put two tubes in like we have in this picture, this is actually for a metaldehyde one, or you can just do one tube and use the gravity, to, to get the water in and then, gravity again pull the tube down to get the, the food out. Once we've done that, we can then use, so we do that until our lavage fluid runs clear, so we've got everything out.

Again, we can repeat X-rays, to see if we have anything else left in there or perform ultrasound just to see how empty the stomach is, . And then often what we try and do is an activated charcoal lava and so again, . And we would install this through the gastric tube before it's removed.

So before we remove our gastric tube as well, just making sure that we kink our gastric tube and pull it out just so we don't get any kind of spill back to create potential for aspiration pneumonia. The activated charcoal is affected absorbing organic compounds. You can use things like cathartics like, sorbitol, magnesium sulphate, and they can help expedite the elimination, of that toxic, that remogenic microtoxin through the gastrointestinal tract, but often activated charcoal is enough.

So, Giving activated charcoal actually can affect electrolyte balances as well. So just monitor these closely, making sure that those electrolyte, electrolytes are as stable as possible. And again, the acid-based balance in our patients are as stable as possible before we go into.

So correcting that lactate, correcting our electrolytes before we start doing general anaesthetic. So that I'm gut decontamination, I'm With via our gastric stomach tube, can be considered, but it should just be weighed against if these patients are at high risk of aspiration. So, if we think these patients are gonna be at high risk of aspiration, we're filling their stomach full of activated charcoal, waking them up, and we think that we might, they might start vomiting and aspirating that that's a much higher risk than just leaving it and then waiting that, waiting until that patient is recovered from that general anaesthetic and then give them repeated doses of activated charcoal.

So, microtoxic undergo an enterohepatic recirculation, and, and therefore repeated doses of that charcoal are appropriate. So unfortunately, some patients like these patients, they end up a different colour. So this patient was actually quite creamy white when they first came in, and Ended up with, you know, it's just completely covered in charcoal.

So here is our kind of antidote is intravenous lipid emulsion therapy. So it was initially designed to treat local anaesthetic overdoses in humans, but it has been expanded to, to include a variety of lipophilic drug overdoses in both humans and batterary patients. So, again, the mechanism of this, so just like in remogenic microtoxins, the mechanism isn't exactly known.

The mechanism of action of intravenous lipid motion therapy isn't also known very well either. But it is thought that it's a lipid sync or a lipid shuttle, so it. Lipid soluble drug drugs, are transiently sequestered in intravenous lipsomes.

So, during the infusion of this emulsion therapy. It has like this, Aqueous portion, this water portion in the blood and it acts as a sink for lipophilic drugs. So it basically holds the lipophilic drugs out of the, out of the blood, and keeps them out as well, of the tissues.

It also has a direct myocardial effect as well and basically provides a source of energy for myocardial cells. So, the use of actually of this someul therapy is increasing. And .

That's because I'm, it works really well and, and particularly in this one, but as I said, penetram is a lipid-soluble compound, so it's a great candidate for this lipid emulsion therapy. There is limited evidence, although this is a really good, kind of study. It's a retrospective study, but 53 dogs met the criteria's kind of small, but actually, the results of the study showed that the median time of clinical clinical improvement, for dogs treated with suspected, remogenic microtoxicosis, with that lipid therapy is about 4 hours.

So this is much more favourable in the previous reports, that was about 24 to 96 hours, so much quicker. And again, anecdotally, knowing, seeing patients that have been treated with this in intravenous lipid emulsion therapy, there is a much quicker recovery from at least from those tremors and from the central nervous system signs, so that it attacks see the hyperesthesia, and then it's just a case of supporting them. Therapeutically, with these patients.

So, there are, you know, there's, it's not without adverse risks, and something that we need to, monitor is the liver, again, because it's a lipid emulsion, pancreas and kidney functions as well. And we also need to monitor electrolyte abnormalities. And so abnormalities with the electrolytes or any evaluate, any kidney elevations and liver elevations kind of need to be addressed before giving, the intravenous lipid emulsion therapy if possible.

So the adverse effects of this therapy can include, Because that lipid emulsion in the bloodstream can cause inability or decreased ability to clear lipids, on the bloodstream. A volume overload, and pancreatitis and hemolysis, anaphylaxis as well, . And, as well as that.

It can cause interference with other things. It can cause interference with our lab testing. So again, making sure that our live, you know, we've checked our liver values, our pancreat pancreatic, values before giving this because this can kind of skew the results afterwards the same your kidneys as well.

So, . Interference with other treatment modalities, so that lipid sync isn't just selected for our penetro A might also affect lip drugs that we give to our patients. So again, thinking about if we're gonna do gastric lavage and we're gonna anaesthetize this patient with like propofol, if we're given intralipid intralipid emulsion therapy.

And that propofol will be lipid sunk as well. So waiting until after we've done our gastric lava and our anaesthetic before doing that. And again, phenobarbital, is a lipophilic drug, that could be sunk by this, so just kind of being selective with what we're using.

A reoccurrence of clinical signs as well, so if that lipid emulsion is eliminated prior to the toxin being, absorbed. So sometimes we can give, several doses. So I think you can go up to, 2 or 3 doses within 24 hours, of this lipid, emulsion therapy, but just, yeah, being wary that like your signs might, .

For a little while after your first one, but if there's still if there's still some of that penetrama in the blood system, then you may see return of clinical signs or recurrence of clinical signs if they're not completely, been lipids sign. So supportive treatment I mentioned a couple of times, so that's symptomatic and supportive care, is indicated in these patients. As I mentioned earlier, that body temperature, often these patients can be hypothermic because of the massive muscle tremors, and that massive muscle activity.

And so it should be monitored and regulated because that hypothermia, at present, can cause seizures, can cause things like DIC. And as well as that, we just want to monitor it because once we kind of control those seizures and the tremors, and we might swing and get hypothermia. So important that we monitor those appropriately.

So try and manage the muscle tremors as a management, part of the management of the temperature, but also potentially looking at other cooling measures. So, we in the patient plans, IV fluids, in some patients obviously it's gonna bring the temperature down. I So cooling measures and discontinue those ones to get to 37.2 degrees and that's just prevent that rebound hypothermia as well.

If the patient is in shock, so again, because of, potentially because of distributive shock, because of, hyperpole shock from vomiting, I, then we need to sort of support that and give symptomatic treatment. So that's IV fluids. So, All IV fluid should be administered to all the patients that obviously don't have any contraindications to heart disease or chronic renal disease, but even those, we can kind of tailor our plan to them so that we're giving them some fluids, and monitoring, you know, monitoring any side effects.

So the benefits of those IV fluids include correction of electrolyte abnormalities, and any fluid loss that's secondary to comital diarrhoea, cooling, as I just said for those hypothermic patients, and also minimising that risk of. You know, supporting those kidneys, so there's a risk of, reduced risk of acute kidney injury and from the myoglobin myoglobin urea and secondary to the rhabdomyolysis that sometimes we can see with these romogenic microtoxins. Gastrointestinal supports that includes antiemetics.

So once we've done our gastric lava or we've, you know, we, we've got rid of the gastric contents, we want to, now, stop the vomiting to reduce that risk of aspiration, to reduce the risk of dehydration or any further electrolyte abnormalities, . So gastrointestinal support is like I say, antiemetics, potentially these patients might later on might get . Pancreatitis because of that as a side effect of our.

In intravenous lipid therapy for supporting our gastrointestinal system, making sure that we have good nutrition in these patients as soon as they can eat. You know, potentially with these patients having, hand feeding them bowls of food, because often they're quite a toxic, soft food, just so they get used to kind of eating again. I'm, as well as that, I'm Potentially given things like you know, our proton pump inhibitors, and if we do know that there's regurgitation, and again, watching out for signs of aspiration pneumonia of lung crackles, increased respiratory effort.

And bee lines on our ultrasound, increased temperature. So other things we might give orally in these patients list, we might continue an oral treatment of methcarbonol. And particularly sometimes these patients can go home with that and be discharged from the hospital with it.

So I'm just making sure that we are repeating and. Haematology, serum, biochemistries, and just to make sure these are within reference ranges, because of that increased muscle enzyme activity that we've seen from the, from the tremors, potentially we might, have to monitor these for them to come down. So, recovery can be, you know, within hours, days, potentially over a couple of weeks.

And so some dogs, with tremologenic, toxicosis. Have reported ataxia in dogs for months to years after the exposure, so I'm very unlikely, but definitely a possibility still. So we're, you know, we're doing our supported treatment, we're doing our supportive nurses, so part of that supported nursing includes physiotherapy when they're in the hospital, so.

Padded bedding, making sure that we are sling walking them if necessary, because I think they're potentially still a toxic, doing passive range of movement, just that they, so again, you know, when we think about, that buildup of lactic acid, that we're doing massage, to, to break that down, and to. As well as obviously giving supportive treatment with our fluids to bring that, lactate down, you know, it's the same as if we like run a marathon for a very long time. Our muscles are going to be very sore, very stiff.

And therefore, physiotherapy is really important in these patients. You know, as part of our cool, as part of our cooling, active cooling, we might do, ice packs. We may, like I say, do massage, with fans and things like that.

So, I'm really supportive treatment of these patients. It's very important, you know, we're stopping the tremors primarily, and getting rid of that gastric content. But all the other things that go with it.

So our IV fluids bring on our things are looking at our temperature, monitoring our temperature, monitoring tachycardia. So obviously if we're getting And severe tachycardia monitoring on our ECGs to make sure that we're not having any arrhythmias, and making sure that we have, we don't have any pulse deficits, and treating that symptomatically as well. So if we get, profound tachycardia or we start to see ventricular premature contract contractions as a result, which is quite possible, looking at the criteria that's needed and to give our antiarrhythmics such as lidocaine.

And so yeah, this is just a picture of, that dog that we saw earlier, and you can see it sat down. I don't actually have a video of it, which is a shame. This dog was hypothermic, so we had it on the cool floor, you know, with a little bit of bedding, and, you know, someone can monitor it constantly.

So, It started having its, this, this dog had vomited, was not a candidate for gastric lava. So we started our intravenous, lipid therapy, lipid emulsion therapy. And within about 30, 40 minutes, this patient, as well as obviously having methcarbonny rectally, the tremors had stopped, was less hyperesthetic, and, we gave antiemetics to stop the vomiting.

And they went to do a repeated dose of our emotion therapy in this dog, but actually did really well, went home, I think the next morning. So I, you know, proof, proof in the pudding that actually it's very effective. You know, we did all that supportive treatment.

It went on fluids after its emulsion therapy. We had it on antiemetics. Nutrition was very important for this patient, so we started hand feeding it, and we'd hold the bottle up to the patients that could drink water rather than leaving it once it went into the kennel.

We didn't eat water in the kennel, in case, you know, still that sort of neurological signs. So we offered it water frequently, and held it up to the patients that it was able to drink properly. Thank you very much for listening.

If you've got any questions, please feel free to email me. My email is Chloefay [email protected].