Thanks very much, Bruce. Thanks for that introduction. So welcome everyone this evening, and thank you for logging in to listen on this beautiful sunny evening and joining us.

So I want to sort of spend the next hour or so looking at how we deal with toxin exposures in our patients, . And what we'll hopefully try and do is sort of focus on the top 5 commonly reported toxicities that we see in our canine patients, how they can cause a problem to our patients and the things that we need to be thinking about in terms of supporting these patients whilst they're in the clinic with us. So just to mention again, this webinar has obviously been kindly sponsored by JHP recruitment.

So if you happen to meet them or see them at an upcoming conference or meeting, then make sure you do pass on your regards and thanks. OK, so to sort of kick us off, I think toxicity cases are often really quite rewarding cases and in particularly cases that I actually really enjoy working with because often with prompt treatment and support, we can actually really improve the chances of the patient having a positive outcome and hopefully no sort of long lasting effects of whatever it is that they've become exposed to. So toxicology is the study of toxins and what people look at is how different poisons affect different organisms.

And so when we talk about a poison, what we're we're meaning is any thing which is either a solid, a liquid, or a gas, which can come into contact with our patient, which then can with homeostasis or with a life process of cells. And so if we think about things around the home and things around the garden, there's a huge amount of toxic things kicking around. So we've got plants, we've got things like household products, we've got drugs, we've got foods.

So a huge part of thinking about the management of the Cases is actually education for our clients and making sure that we are educating clients, you know, perhaps at the first stages when they're bringing their pets into the practise, so things like puppy parties, again, certain times of year thinking about Easter or Christmas time where we might see more of these toxin cases presented to the clinic, is thinking about sort of education for our clients. When we talk about exposure to toxins, there's different ways that we can think about how these toxins can come into contact with our, our patient. And so usually what we're going to be seeing for the majority of the cases that present is that they have an acute exposure, so something that happens within less than 24 hours, so they eat the thing they're not supposed to eat, and then they present to us with signs associated with that toxin exposure.

But we can also have cases where they have a sub-acute exposure, so maybe they've been exposed over a longer period of time, perhaps up to about a week. So maybe this is perhaps the patient where they're being looked after by family friends and they've inadvertently been given the wrong medication for several days before we realise that there's a problem. And we can also see chronic exposure as well.

And so usually this is an exposure which takes place over a more kind of a longer period, over 3 months or above. And so usually what we'll be thinking about with this type of cases is perhaps environmental things. So particularly sort of in large animals, we can think about things like lead toxicity, so things where animals might be exposed to these elements over a longer period of time.

What we find is that with most of these toxins, the toxic effects that we see in our patients are usually going to be dose dependent. But sometimes some of these toxins, we can see what's called an idiosyncratic. Reaction.

So with these group of toxins, what we find is that there there isn't a specific toxic dose range. It's just that some patients seem to be more susceptible, and we're not really sure why that happens. And so for example, grapes and raisins, these seem to come about with an idiosyncratic reactions.

So some dogs can eat one raisin and go into sort of a full blown acute kidney injury versus other dogs who can eat a whole bag of raisins and seemingly be OK. So these are all things that we need to factor in when we're thinking about these toxin exposures in our patients. Again, Thinking about the dose that that patient is exposed to, and sometimes they can have an undetectable problems, sometimes we find that they get effects can be at a sort of a therapeutic level, sometimes they're a toxic level and in really severe cases or cases where there's been a big toxin exposure, we can find that these are lethal.

And when we talk about a lethal dose, what we're referring to is the dose that was lethal to 50% of a test sample. And so sometimes we'll find that this data is available so it can help guide us with our therapy and perhaps how aggressive we need to be in the management of these cases if they've had a really, really, really big dose. Thinking about exposure as well, we can think about how our patient comes into contact with this toxin, and so usually what we find with our our canine patients is it's likely to be an oral exposure.

Cats seem to be a bit more clever really than dogs, I think, and don't tend to eat as many unusual things. But obviously we've also got sort of dermal skin contact, we've got inhalation, and we can have contact via the eye. And then thinking about patients perhaps more in the veterinary setting, then we can also have either an intravenous or a subcutaneous route as well, where patients perhaps can become exposed to something at a toxic level.

When we think about things that affect or influence toxicity, things that we're talking about here, so we can have exposure related factors, so obviously the dose and the duration, frequency of this exposure. Also whether the patients have this exposure if it's an oral exposure on an empty stomach or not. So sometimes if the patient has an empty stomach, they may be more prone to absorbing that toxin quicker and therefore we might have a tighter time frame to work in.

And they, they may be more likely to ingest and absorb a higher dose. We've also got biological factors that can affect toxicity, so, specific breeds, specific species, age-related factors, obviously the size, so, again, obviously our smaller patients are going to be at a higher risk of a perhaps a lethal or a fatal exposure, purely because they're a smaller patient. Also, if the thing that our patient has been exposed to undergoes enterohepatic recycling, so this is where these drugs are taken into the gut.

They go around to the liver to be processed and they are then excreted in the bile back into the gut. And so they tend to sort of go round and round for potentially up to a couple of days. And so again, this can factor how we treat these patients and the likelihood we're going to see signs develop.

And also whether we've got concurrent disease. So perhaps maybe our older group of patients where they've got maybe some underlying renal disease, some underlying endocrinopathies, again, this can affect the level of toxicity. And also then there's some chemical factors.

So in particular lipid soluble drugs are very rapidly absorbed, whereas drugs where they've got an enteric coating or maybe a binding agent, they may have a delayed absorption and so again this will affect how we potentially treat this patient and think about decontaminating them if they've had an exposure. So to put things into context, we can take information from a couple of different resources that are available. So the VPIS is a veterinary poisons information service, so obviously based here in the UK and these are a great go to resource for our toxicology cases.

So last year they answered nearly 11,000 inquiries, and what they find usually is that there are a couple of peak times of year, so usually around about Easter time, obviously lots of inquiries about chocolate toxicity and also December time. So again, thinking about the things we've got lurking around in the home at Christmas time, we've got plants, so things like poets, we've got things like raisins, mince pies, Christmas puddings, and again, lots of chocolate. From their data last year, they took inquiries on 84% of dogs, 14% of cats, and 2% of other animals.

There's a pet poisons line, which is a line which has now been set up, again for owners to contact, so this is again a great resource which we can refer our owners to thinking about back to that education and and cluing our owners up. But this is a a a contact line for owners to phone in if they want more information about a possible toxin exposure. In America, they've got the American Poisons Control centre, and so obviously their inquiries, is their number of inquiries is huge compared to the VPIS and so last year they took nearly 200,000 inquiries.

So again, they've got a huge amount of data which is now available, which again can help us guide our therapy for our patients where they've come into contact with something toxic. So generally thinking about our advice to clients as we've said the key is prevention, so it's making sure our clients are aware and I think there's been a lot recently in the national newspapers in terms of certain things, so certainly now people are much more aware that chocolate, grapes, lilies, for example, are toxic to our pets. And so again, just making sure we're thinking about education our own is about keeping things out of our pet's way out of their pet's way, and also keeping an eye on their pet when they're at home or in the garden.

If we have a patient which has potentially come into contact with something, usually our advice for our owners at home is is not to attempt to make their pet vomit. I think this is sometimes a bit of a contentious issue, and I think there are times certainly when I think back to my time in mixed practise where it was something that we would perhaps suggest for owners to do, but I think the reality is it's very difficult to make a pet vomit at home. And I think it's often not very successful, and it's quite stressful for the owner and it's quite stressful for the pet.

So usually now what we try and recommend is we try and get that pet into the clinic if we're worried about an oral ingestion in order to make them vomit effectively. Again, educating clients not to treat and medicate pets themselves, so we always get those sort of cases that crop up and it's, you know, sometimes a simple case where the pets come in because it's lame, and then when you start talking to the owner, it turns out, well, they've tried some doses of ibuprofen or aspirin or things like that at home and actually suddenly you're now not only dealing with a lame dog but also a dog which has got a a potential toxin ingestion on top of it. Usually we advise clients to to go against a watch and wait approach.

So ideally they want to contact the vets immediately that they, as soon as they're aware of a potential toxin exposure so that we can obviously give them the best advice that we can and whether that then is to recommend coming down to the clinic or whether we actually then educate them as to what they would need to look out for at home if we're not worried about a toxic dose exposure. Then we can do that, but usually we want to sort of make sure that we are obviously addressing those cases where we know a toxic exposure has has been eaten or, or dermal contact so that we can get that pet in as soon as possible. Again, retaining any product information or any product packaging so that we know what we're working with.

And particularly with dermal dermal contact, we need to just make sure that the owner doesn't inadvertently contaminate themselves. So thinking sometimes about things like oils and crea soaps, things like that can be quite sensitive to the skin. Make sure that the owners put rubber gloves on and things or wrap their pet in a towel, bring them down to the clinic so they don't contaminate themselves.

So usually, as we said, these owners are going to call the clinic and they're going to usually speak probably to a nurse, be passed through from reception to speak to a nurse so that we can ascertain some more information and decide obviously whether we need to see that pet urgently. And so useful information is going to be what the species and breed of that pet is, and in particular their weight, so that we know then we can try and calculate potentially how much exposure they've had to what and work out what sort of dose range that falls in. Again, thinking about those risk factors that can affect toxicity, so does that pet have any underlying medical conditions?

Are they on any other medications that we need to be aware of that could then throw a little curveball in, just thinking about our treatment plan? Also sometimes we'll find that multiple animals are involved. So in particular I think about things here like perhaps their owners maybe have taken a couple of dogs down to the yard where they've got horses, and these dogs, several dogs could have come into contact with horse wormma and end up needing to come in for treatment for that.

And usually thinking about phone etiquette here which is thinking about, you know, for most of our clients this is a stressful time if they suspect that their pets come into contact with a toxin, owners can be quite stressed. We need to try and tease these key pieces of information out because what we do know is that time is of the essence if something has been exposed and so we need to get these patients, ideally into the clinic as quick as we can so that we can decontaminate them effectively. And usually, again trying to ascertain on the phone whether this is actually a witnessed exposure or just a suspect exposure and sort of the time frame that we're talking about.

So questions that we might want to ask, so what's the exact name of the, the toxin or the product, the active ingredient, that they're worried their pets come into contact with, and is there a strength or a concentration on the packaging, or the, the product information? If it's a plant, it can sometimes be useful to know what part of the plant was eaten, so is it the bulb or the flowers or the leaves, if it's medication perhaps, can they work, try own try and work out how many tablets is missing? And how long ago?

So you know, was it this morning maybe when the owner was at work, they've come home and realised, so actually maybe a whole day's gone by, or was it, you know, within the last 5 minutes, they dropped the tablets on the floor and the dog ate them, you know, because again, that's going to affect how we then think about decontaminating that patient. Also, is the pet showing any behavioural physical abnormalities at this time? So, again, thinking about what the pet's been exposed to as to what we might then see that pet go on to develop.

And again, thinking about access to the container and the packaging, is there any warning signs on there that we need to be aware of, because again, this information can really help us guide our advice and to the clients and our treatment plan for that pet. So once we've ascertained that this patient has come into exposure with something, ideally we want to advise that this pet comes down to the clinic. What we want to really think about on the phone is, have they had a potentially toxic dose if we can work out what's missing or what they've come into contact with versus the weight or size of that patient, versus have they had a lethal dose?

And so usually what we can do is get some information. We've got obviously a number of resources available to us, so, there's a lot of things like chocolate calculators online which can be really, really helpful, or in the form of apps. And again thinking about some of the books which you may have available to you in practise, it can be useful to have this information to hand.

Alternatively, what we'll usually do where I work is we'll get, get the key information from the owner. We'll usually then try and contact the VPIS straight away, so that we can get their recommendation, and then call the owner straight back in terms of to try and get them to come in if, if the VPIS is recommended that we need to crack on with fairly urgent treatment. What we want to do at this point then is get things ready, so making sure that we can make this process as smooth and quick as possible once these patients come into the clinic so that we can get that ball rolling quickly and we want to get our decontamination equipment ready.

There is an antidote and perhaps to the toxin that they've become exposed to. We want to make sure we've got that available, get any supportive therapies we might need ready, and then some monitoring equipment too. So when this patient arrives, we can crack on with our our treatment plan.

So usually it's down to the nurses when these patients arrive to carry out our triage, so we're thinking here about treating the patient and not the toxins. So we're gonna go back to our simple principles of triage, so thinking about ABC, so our alertness, our respiratory system, our breathing, and C for our cardiovascular system. So we're going to assess those three major body systems during triage, and then we're gonna go on and address any life threatening problems.

Usually at this point we're gonna want to get some owner consent for what we may need to then go ahead and do, so thinking then about decontaminating this pet, thinking about supportive therapies for this pet, and any baseline emergency minimum sort of database that we might want to do. It might be that we've not got the full information from the owner over the phone, so we may need to get a bit more information, maybe they've been able to bring the packaging with them with them so that we can get some more information perhaps about what this pet may have been exposed to. So when we think about decontamination, we said obviously there's a variety of ways that our pets can become exposed to these toxins and so just want to run through how we really can think about decontaminating an eye, and obviously skin, for dermal contact, and then the GI tract, and again with the sort of GI tract we've got a few different options of decontamination available.

So thinking about eye decontamination, so usually eyes are going to be coming into contact with things like cleaning products, perhaps, or acids or alkalis, the little dog bulldog cross in the picture on the screen. So sadly this was a case that was looked after by a grandparent. The dog was on optimmune eye drops for a long standing eye condition, and sadly, Granny put superglue in the dog's eyes.

So you can see that dog is presented with eyes which are actually stuck together. And so this is actually sadly, I think something that we do see every now and again. And so obviously what we want to do is try and act as quickly as we can to decontaminate that patient's eyes so that we can try and salvage salvage them without any further problems.

So we can recommend that owners do this at home. Again, I think the reality of being able to do this is quite tricky. If I think about my own pet cat and dog, my dog won't even let me look in his eye when I want to, let alone try and flush his eye out in a controlled manner.

So often these pets are going to benefit from coming down to the clinic, they may require sedation, either systemically or topical local anaesthetic into the eye if we can access the eye to try and help numb that area in order to give us the best chance of flushing that eye out. And the recommendation is to flush for 15 minutes, and so this can be done either with tap water or with sterile saline, if we're in the clinic. Obviously tap water if we were going to try at home.

And what we want to do is flush like we've got in the picture at the bottom. So we want to flush medially to laterally, ideally with the patient, so thinking if the patient was in lateral recumbency with the bottommost eye treated, and then we'd roll the patient over so that we're not going to contaminate, inadvertently contaminate the opposite eye if both eyes are affected or if one eye is affected. As we said, usually for about 15 minutes, so we need to get a good sort of pressure on there to flush anything out.

And as I said, usually these patients may require sedation in order to do this. If we said that we're gonna recommend for the owner to do it at home, ideally tap water, we want to avoid things like contact lens solution because sometimes these can be irritant to the eye and potentially could cause further problems depending what the toxin exposure to the eye actually is. Thinking about dermal dermal decontamination.

So again, this is something we can recommend that the owner starts at home. And so really as we've sort of mentioned already, we don't want our owners to become exposed to whatever it is that's toxic, so making sure that owners put a pair of gloves on if they can, and again thinking about these pets when they arrive at the clinic, we might need to make sure we've got PPE on and in place. So usually warm water with a mild soap, so something like fairy liquid or a baby shampoo.

It's going to be the sort of go to first line dermal decontamination option, particularly sort of oily, greasy things, so things like car oil, creo soap, things like that, then we can use sort of degreaser or hand cleaner type products, so as you can see in the picture there, S forfiga is a really good option for these cases. In some cases it might be we actually have to try and clip some hair away. And so particularly for our feline patients, this little cat was incredibly tolerant who came and presented covered in oil.

Often these patients again might require some form of sedation in order for us to be able to give them a really, really, really thorough bath because it might be that we've got to do it over and over and over again several times to try and get rid of as much of the toxin that as we can. In particular with our sort of smaller patients, we want to be careful with hypothermia. So as we said, making sure we use our warm water and we dry these patients off.

And for any patients where they've got particularly got sort of sort of seizure in neurological patients, a very altered level of consciousness, then these are patients where we're probably going to want to try and treat the side effects that we're seeing of the toxin before we can go on to decontaminate them safely. One thing as well, just to point out, so making sure we've got buster collars on these patients because often little cats want to try and help us with our decontamination and we'll have a really good go at grooming, and then not only are we dealing with a dermal contamination, but we're also dealing with an oral ingestion as well. Thinking about our patients then which have eaten something, we need to think about how we're going to decontaminate the GI tract and so emesis inducing emesis is gonna be our first line treatment for these patients.

So usually we want to make sure it's done within 1 to 2 hours of ingestion. And our sort of first line treatment, so we've now got a product available to us which is licenced, so Emiog is a licenced version of apomorphine, . So we can give this either intravenously or subcutaneously, and this will induce emesis really quite quickly and it's usually pretty pretty effective within a matter of minutes.

We might find it's not very effective if the thing that our pet has eaten is actually an antiemetic. So sometimes, for example, patients that eat marijuana, and this has antiemetic properties, and so we might not be very effective at making them vomit. We also know when we make our patients vomit through inducedtemesis, that they'll only actually vomit up about 60% of the stomach contents.

So it might be that we actually don't manage to get rid of everything that's in there and it might be that actually, you know, if there's a few tablets missing that actually we don't find those tablets because they're not in the, the stomach contents that have come back up. When we think about our feline patients, they're a little bit more tricky because cats never like to play by the rules. So apomorphine is not very effective in cats, and so we've got a couple of options that we have available for those.

So we've either got Xylazine or metomidine. The good thing about meatomidine obviously is it can be reversed, and so, often we can use that to make our feline patients sick and then reverse it so that we don't see the side effects of sedation. Ideally, we don't want to be using things like soda crystals, things like mustard, hydrogen peroxide.

These can go on to cause a lot of GI irritation, and they work, that's the way they work in order to make our patients sick. And also obviously things like soda crystals, salt crystals, we actually can cause quite a nasty hyponatremia in our patients. So really we need to be sticking with the morphine in our dogs and thinking about xylazine or medoomidine, whichever we've got handy for our feline patients.

I'm also quite a big advocate of once we've actually made these patients sick, and they do seem to have sort of emptied most of their stomach contents out. A good old dose of an antiemetic after can make them feel a bit perkier. So obviously with these patients, they are quite nauseous for some time after the administration of pomorphine.

So times when we might want to hold back on making our patients vomit is if they've already vomited and there's going to be little point in making them vomit more because there's probably not much left in their stomach. Again, if they're neurologically inappropriate, if they've got a reduced cough reflex or they're unable to protect their airway, then there's going to be a concern that they could go on and aspirate. So thinking about this little patient here, this is a tremologenic mycotoxin patient, so as you can see, he's sort of quite neurological, he's very tremory, he's got a little muzzle on there because he was a bit nervous about being there in the veterinary clinic, and so he's a patient that we wouldn't make vomit.

We also don't want to make our patient vomit if the substance that they have ingested contains either oil, it's a volatile substance, or it's got detergent compounds, it's a strong acid or alkali because again thinking this substance going down has probably caused a lot of irritation to the mouth and the oesophagus. And so if we then end up making that patient vomit and bringing it back up, it's going to do double the damage. And cause double the irritation and inflammation to that that area.

So we don't tend to make those patients vomit. Gastric lavage is the step that we're gonna think about using if we've got a contraindication to inducing emesis. And again it's something that we could consider if we know there's been a fatal dose ingested, because as we said, only 60% of our stomach contents come back up.

With MSys, and so actually if we know we need to rid everything from the stomach, then we can consider doing gastric lavage. Again, particularly certain things which are ingested. So for example, iron tablets, the way that these work, .

These work is that they stick to the wall of the stomach, and so, often, for example, gastric lavage for those is not going to be efficient at removing them, so we'd have to take it a step further and consider a gastrotomy, which is quite a, quite a big step in terms of decontamination. If we're going down the gastric lava route, usually what we're going to need to do is anaesthetize these patients so we can actually pass an ET tube and protect their airway, and then we're going to pass that stomach tube down and we're going to lavage their stomach, often with sort of warm tap water in order to get rid of, so a little bit like we would do with a GDV patient in order to get rid of everything that's in the stomach. Whole bowel irrigation is something which is not really done over here in the UK as much.

It's carried out more in the states, and this is where our patients are administered and osmotically balanced polyethylene glycol solution. So the idea is that these patients are administered this and it kind of just flushes them all the way through, a bit like a clean prep, for example, prior to an endoscope. So it's usually something, as I said, we don't tend to do in this country.

And activated charcoal is also another important part of our decontamination of our GI tract, and, sort of, in particular, it's going to help us reduce the absorption and bind and remove toxins that have perhaps made it through into the gut and . Things that we haven't been able to get rid of during our induced emesis. Usually what we'll do with this is administer it sort of 4 to 8 hourly for the 1st 24 hours at a dose of about 2 to 8 grammes per kilo.

If we have a product that the patients ingested, which undergoes enterohepatic recirculation, as we mentioned already, as we said, this is where these elements can go round and round between the gut and the liver. Usually we'll find that we need to administer activated charcoal for a prolonged period of time, so maybe 2 to 3 days in these patients so that we can keep catching that product in the gut and binding it and and ridding that toxin before it goes back around to the to the liver and back round to the gut again. Ideally we want to give this within about 2 hours of ingestion and we need to be very, very careful if we've got suspicion of the GI perforation.

Most of the time, we can try and tempt our patients to eat with food, and we want to try and avoid syringe feeding them again because of the risk of aspiration. And it's also just noting worth noting it's not good for certain things such as Xylitol, it doesn't seem to really help us in those cases, in patients where they've got acid or alkaline ingestion. And particularly things like ethylene glycol or ethanol ingestion, usually these are very, very rapidly absorbed, so activated charcoal doesn't help as much in these cases either.

It's also worth thinking about if we do need to give an oral antidote, then maybe we should give this first and then wait a few hours before we administer the activated charcoal just so it doesn't bind with that antidote. So thinking about the common toxins that we've got, as we said, lots of things around the house, so foods, things like chocolate, xylitol, mycotoxins, we've got insecticides, things like pyrethrin or oxidectin, human medications, so in particular on non-steroidal anti-inflammatory drugs, things like paracetamol, aspirin, antidepressants, some illicit drugs, things like marijuana or MDMA. Household cleaners, bleach, detergents, disinfectants, washing powders, again, plants that particularly we see linked to to toxicosis, so things like lilies and tulips and daffodils, and then there's also sort of other things which I guess come in sort of ebbs and flows depending on what's sort of big, big at the moment.

So there's been A big rise in e-cigarettes, patients becoming exposed to those. Again, sort of more stuff in the press and newspapers about essential oils and exposure to perhaps cats, and things like batteries and blow sticks as well. So looking at the chart quickly just gives a bit of a rough breakdown.

This was PE plan did a rough breakdown of common poisons claims over in America. So as you can see, food or additives comes out highest with a miscellaneous, so illegal drug poisoning ethylene glycol, lead poisoning, second highest, and then prescription drugs, most commonly non-steroidals as the 3rd highest. When we look back at the top 5 common poisons last year, from the VPIS data, what we found in our canine patients is that #1 was non-steroidals, number 2 was paracetamol, #3 anticoagulant rodenticides, number 4, grapes, and number 5 chocolate.

In cats that came out slightly differently. So number 1 for cats was lilies, number 2 was permethrin, number 3 was paracetamol, number 4 was ethylene gcol, and number 5 was actually a big group of things so which underwent the heading of unknown toxic toxicology exposure. So I want to just run through these top 5 in terms of how they cause a problem to our patients, how we're going to treat our patients and support them if they have had a toxic dose exposure.

So number one, non-steroidals, obviously this could include veterinary and human products and thinking about what we have in the household, most of us will have over the counter products which contain non-steroidals. So here we're thinking about things like ibuprofen, and thinking about things like aspirin, and baclofen, thinking about our veterinary preparations, so this might be things like Metaam or Carrofen, Rimidil, things like this, . So again, thinking about this exposure, it might be that actually it's an inadvertent exposure that owner's been given 10 times overdose by accident and then they realise there's a problem a few days later, or it might be that that patient has, you know, got into the the store where you keep your medicines in your house and they've helped themselves.

So the way that nonsteroidals cause a problem to our patients is that they produce both central and local anti-inflammatory effects by inhibiting both COX1 and COX2 enzymes. And our COX 1 and our COX2 enzymes are responsible for the production of prostaglandins, and prostaglandins basically work at 3 different levels in the body, so they work on the gastrointestinal tracts. They work on the kidneys and they work on the platelets.

And so the role of the prostaglandins is to keep these three areas ticking along and unhappy. So what we see if our patients are exposed to a high dose of nonsteroidals, and is that COP 1 and 2 become inhibited. We have less prostaglandins, so therefore we see gastrointestinal, renal, and platelet problems.

We can have certain risk factors that we know about, so, an increased dose, if we've got patients where they're dehydrated, hypovolemic or hypertensive, and they're exposed then to non-steroidals, if they've got underlying GI or renal disease. Or perhaps if they're on other medications, concurrently, so perhaps steroids or they're on non-steroidals and then have a further overdose of non-steroidals. Obviously, the toxic dose very much depends on the drug that they're exposed to, but what we do know is that many non-steroidal drugs do undergo inhepatic recirculation, so we have to bear this in mind in our treatment plan.

So things that we need to watch for, so usually if these patients receive a toxic dose, they can then present vomiting with blood. So, sad case in the picture was a Labrador where sadly he'd been receiving a 10 times overdose of Metacam for a week. He'd gone on to develop vomiting and diarrhoea, and he presented to us at the University of Bristol when I worked there.

And he probably vomited that much blood about 8 times and tragically, we could not stabilise this dog, and we lost him. And that was really, really, really sad because it, it was purely a miscommunication and the owner had sadly overdosed several days in a row and this patient had actually gone in and actually had a gastric perforation. So we can see a lot of this sort of fresh blood in the vomit.

We obviously can see hemorrhagic diarrhoea as well, fresh blood or digestive blood. These patients are often gonna be inappetent, lethargic, have abdominal pain, and potentially PUPD. So if these patients are asymptomatic, we're gonna decontaminate them, induce emesis, and we're gonna give activated charcoal for up to 3 days to catch that enteropathic recirculation.

If they're symptomatic, then we're gonna need to address their fluid balance because if they've had a bleed, they're likely to be hypovolemic. So we're gonna do that by administering fluid therapy, potentially blood products or plasma products to patients who are actively bleeding. We need to be very, very careful with gastric lavage in these cases, so we know that they're going to have GI upset and so again, these might be at risk like that patient on the previous slide of gastric perforation.

If there is perforation of the gastrointestinal tract, then really these patients are going to need to have surgical intervention, so surgical intervention and management of septic belly. For those which haven't had perforation, then we're going to be thinking about administering gastroprotectants. So misoprostol is a drug which works a little bit like an antidote, I guess, in a sense that it's a synthetic prostaglandin.

So we can administer misoprostol to these patients, and that misoprostol will then act on the level of the kidney and the gut and platelets and will again hopefully kind of keep all of those areas a bit happier at the times of toxic exposure. Also drugs such as H2 receptor antagonists, so things like omeprazole antiemetics, so that we can try and control any vomiting and nausea in these patients, making sure that we get on to nutrition so that we can try and feed that gut and keep it happy. And in cases where these patients go on to develop an acute kidney injury, then we may need to think about more aggressive therapy.

So, managing these patients as an acute kidney injury patient and potentially thinking about dialysis. If it's been a very, very high dose exposure. The second thing, toxicology is paracetamol, so also known as acetaminophen.

And so usually again, this is an over the counter analgesia. So thinking about this in particular, it's very rapidly absorbed. So if we think about when we take paracetamol for a headache, usually within about 20 minutes, half an hour, you'll feel that hopefully kicking in.

So this, these patients with paracetamol ingestion, we really need to see really, really quite quickly down down at the clinic. Obviously it comes in a number of forms, so tablet versus liquid, and again, just thinking that it can be combined with other drugs, so it can be combined with Xylitol you know sort of sugar free solutions sometimes or it might be a cold and flu type remedy and so it's combined with things like a decongestant. So the normal dose, because we can obviously can give paracetamol safely to canine patients and the normal dose that we would think about with these is usually about 10 to 20 mg per kg, every sort of 6 to 12 hours.

And actually we can use paracetamol very effectively as an analgesia, but obviously we see it cause problems when we exceed that dose, and particularly in cats. And so the way that paracetamol is usually metabolised is via the liver and 3 different pathways. So we've got glucuronidation and sulfation in the liver and so the these roots then lead to the excretion of paracetamol in the urine.

And then we've also got oxidation by cytochrome P450. And so what happens here is, cytochrome P450 is oxidised, which leads to the formation of a product called Nacqui. And what NAI does is it's Naqui that then leads to red blood cell erythrocyte oxidation and also liver damage.

And so what we find in our canine patients is that canine patients have glutathione naturally sort of floating around, and so this can binds to a neutralised Naqui which Which is why canine patients can deal with paracetamol. Sadly, cats don't seem to have very much glutathione around, so they have an inability to be able to bind and neutralise an aqui, which is why we see that cats can develop quite an adverse reaction to paracetamol toxicity in comparison with our canine patients. The toxic dose we usually see, so for dogs, as we said, usual dose is 10 to 20 mg per kg as a therapeutic dose.

Toxic dose starts at around about 100 mg per kick, so 10 times the therapeutic dose. And in cats, what we would class as a therapeutic dose for a dog is actually a toxic dose to a cat, so they really don't need to have much before we can see problems. Common signs we see, so you.

Lethargy, swelling of the face or pores, difficulty breathing. Patients can go on to develop methane glo anaemia, so we can see a blue or brown tinge to the gums. And again, GI signs, so vomiting, inapetants, anorexia, they can develop GI bleeding, so black tarry stools and obviously if we get the liver involvement as well, then these patients can become quite jaundice.

So usually if they're presenting asymptomatic, we're gonna make them vomit, but as quickly as we can because of that that quick absorption, we're gonna want to deliver activated charcoal and usually we'll do this for 24 hours. We have then got a couple of things we can do in terms of helping support our symptomatic patients. So an acetylcysteine is actually a glutathione precursor and so if we can administer an acetylcysteine, it will convert into glutathione and that will then help, as we said, bind bind to the Naqui to the product that's causing this liver damage and also causing this red blood cell, destruction.

Vitamin C, so ascorbic acid, will help convert methemoglobinemia into haemoglobin, and cimetidine has been proven to inhibit P450 pathway and therefore reduce the amount of Napqui that's actually produced. So we've got kind of a bit of a triple pronged attack there really, which we can use on our patients. We can also think about then supportive care in terms of hepatot protective and antioxidant therapy, .

Along with the usual sort of GI protectant. So again thinking similar to nonsteroidal toxicity, so things like omeprazole antiemetics, these patients, if they've had a severe red blood cell destruction, mainly blood transfusions and potentially oxygen therapy support whilst we're supporting them and getting on top of things. The third common toxicity is anticoagulant rodenticides, and so usually we're going to be thinking here about rat rattle mice poison, and there's 3 main groups.

So there's the ramethyin group, there's a cholycalcifeol group, but it's the warfarin toxicity group which are the most common. And so again, what we find with this is that warfarin is very rapidly absorbed from the gastrointestinal tract, and what warfarin does is warfarin interacts with our vitamin K. When we think about our clotting cascade, there are a number of clotting factors, so 279, and 10 in particular, which are vitamin K dependent.

So our patients can have these clotting factors floating around, but without vitamin K, they can't activate these clotting factors to make them work. So in these patients that have a warfarin toxicity, their vitamin K is no longer active, which means their clotting factors are not activated. So we therefore see that these patients develop coagulation issues.

What we can find with these patients is that 2nd generation reddenticides usually can take a longer time to kick in and develop a problem and signs in our patients and we can also sometimes see a secondary toxicity. So perhaps if a patient eats a mouse or a rat which has been killed by a rat poison, they can then go on to also develop toxic signs. As we said, dose depends on active ingredients, and usually with these patients, what we're going to want to do pretty early on is check out a haematology and a coagulation profile.

So in particular, a PT a prothrombin or an activated partial thromboplastin time, an APTT. And science we want to look for external haemorrhage, so bleeding from injection sites, bleeding from the nose, internal haemorrhage, so hemothorax, hemo abdomen, these patients, if they have had a bleed, will present shocky, so they might be weak and lethargic, tachycardic weak pulses. Patients can present with a lameness if they've bled into a joint cavity.

And they can have respiratory distress if they've bled into their thorax, which is compromising their, their lungs, or alternatively if they've had a big bleed and they're now really anaemic acutely. We can see patients bleed into their spinal cord or into their brains, so they can present with quite sort of significant neurological changes. And again, usual GI upset as a result of of ingestion of that product.

So treatment usually for asymptomatic patients again thinking about decontamination of the the guts so emesis and activated charcoal, usually once we've had that baseline coagulation profile, if we're happy, it's normal at that point, we still want to recheck it 48 hours to make sure that the patient hasn't gone on to develop coagulation issues. So the symptomatic patient, then we're gonna want to administer vitamin K, so we can administer vitamin K either subcutaneously or orally. And we need to do that with caution again, so we're not obviously causing further bleeding to that patient.

Patients who have bled might need blood therapy in addition to fluid therapy, and we can think about replacing those clotting factors by administering fresh frozen plasma. These patients may need oxygen therapy if they have got respiratory compromise. And sometimes what we will consider once we stabilise these patients a little bit is a therapeutic centesis.

So what we tend to do with these patients is, is then think about maybe tapping their chest if we need to, otherwise we'll try and really sit tight, if we, if we can because we don't want to cause further bleeding by sticking sharp needles, catheters, etc. Into our patients. We're going to want to recheck this coagulation profile at 72 hours at 3 days.

So again, then might need to consider administering vitamin K. Orally to these patients once we get them home and out of the hospital. The next most common one then is grapes and raisins.

So, as we said, some of these exposures that we get with our patients are idiosyncratic. So, as we said, there's not a specific dose that we know. And when we think about grapes and raisins, this includes things such as wines, grapes and raisins in their form sort of in other products as well, and We don't really know the mechanism of toxicity and so there has been some speculation, so there's different suggestions have been bounced around.

So there's a thought that grapes and raisins are nephrotoxic to the kidney level of the kidney. It could be to do with either fungicide, herbicide, or pesticide contamination. It could be To do with heavy metal contamination, high concentrations of vitamin D, or fungus or mould contamination of the fruit.

So we've got some more work to do. What is now clear is that some animals really cannot tolerate any raisins and grapes, whereas some seem to be OK and less sensitive if they have exposure. What we usually see is these patients go on to develop an acute kidney injury and so what we find is that the sort of histologic findings include renal tubular necrosis.

So these patients have a real sort of insult and injury at the level of the kidney. They can get metastatic mineralization. And they get renal tubular epithelial regeneration.

So we can support these patients and get them over this often, but we, often might need them in the clinic so that we can support them on fluids for a few days. So we usually see, so these patients might have vomiting or diarrhoea, they can be lethargic, anorexic, again, have some sort of kidney pain, abdominal pain. They might be dehydrated if they've got themselves a bit behind with vomiting and diarrhoea, and if they've also been polyuric.

And, obviously sometimes if they go into in a state of acute kidney injury, then these are the patients where we need to watch their urine output very closely because it might be that their kidneys start to shut down and they go into an oliguric or anuric stage. Treatment for these patients, so usually if they're asymptomatic, we will err on the side of caution and we will keep these patients in the hospital so that we can administer fluids if the client can finance that. If we are in a situation where we can't do that, then we will administer activated charcoal after we've made these patients sick, and we'll try and get a baseline urea and creatinine and then just recheck that 48 hours later.

If we are able to keep patients in the hospital, really we want to give them aggressive fluid diuresis for a couple of days. So you usually put these patients on about 6 mL per kg per hour of fluids just to try and flush them out, keep their kidney perfusion up. Keep a close eye on our renal functions, so monitoring our urin and creatinine, potentially placing a urinary catheter in these patients to monitor our urine output.

And again, thinking about the management of these patients that go into an oliguric or auric state, these are the patients where we may consider hemodialysis and whether that's appropriate. And the last toxin sort of just to cover this evening is chocolate, so again, a pretty common one that we all see in practise. And so chocolate contains products called methyl xanthine, and so.

Again, thinking about chocolate, it can also contain a whole heap of other stuff, so things like nuts, raisins, and xylitol, so it's quite important just to quiz the owner on that, because they may not be aware that these other things are toxic as well as the chocolate. So we worry about theobromine and caffeine in chocolate. And severe chocolate toxicities can be potentially life threatening.

So what we see is it's actually quite slowly absorbed from the gut and it goes through the enterohepatic recycling. So we need to think about this in terms of treatment for these patients. But what we end up with is a release of our fight and flight hormones, so a release of adrenaline and no adrenaline, and we also get changes to our calcium channels.

And so this Goes on to lead to increased muscular contractility and also both neurological and cardiac stimulation. So these patients can present often very hyper excitable, very restless. They can have an increased heart rate and some abnormal heart rhythms, often hypertensive.

In severe cases, they can be really, really tremory and seizurey, even present collapsed, and as we said, it can be life threatening. In 2014, the VPIS reviewed a large number of cases, so I think it's about 700 or 800 cases, and they made new toxic dose recommendations. So the recommendation now is that we should treat patients that have an exposure of 3.5 grammes per kilo for dark chocolate or above, and 14 grammes per kilo or above for milk chocolate ingestion.

Treatment for these patients, as we said, if they're asymptomatic is usually gonna be to make them vomit and usually we've got a bit of a wider window with this because it's slowly absorbed. We want to administer activated charcoal because of the entopathic recycling, and we want to do that then for 3 days. We're gonna make sure we educate our owners on signs to look for whilst they're at home.

Symptomatic treatment will involve keeping an eye on these patients in terms of their abnormal heart rhythms, so keeping monitoring with an ECG perhaps and treating things like ventricular arrhythmias perhaps, whilst the patient's in the hospital with things like the lidocaine CRI. We might need to implement a seizure control plan, so if the patient is very, very trembly, they can be at risk of hypothermia. So we might need to think about with these patients management of lots of muscle tremors.

It might be if they've had a huge dose, so a fatal dose that we consider gastric lavage in order to try and get rid of as much as we can. And then in the meantime, we're going to support these patients with intravenous fluid therapy. Meanthes interestingly can be reabsorbed from the bladder, so there is a rationale to place a urinary catheter.

It's not something we tend to do with our patients. We just tend to schedule them for really frequent walks. So we'll try and take these patients out every 2 hours for the opportunity to urinate and void their bladder.

Other general supportive therapies that we'll think about with these toxin exposures, as we said, this list of the five we've talked about just the common ones that we tend to see, but once we've decontaminated that patient, it might be we need to consider fluid therapy to support them, gastroprotectant, so things as we said like omeprazole, antiemetics, it might be that patients require analgesia or some mild sedation, and again, thinking about nutrition and nutrition. And while these patients are in the hospital, we want to keep a close eye on monitoring their cardiovascular parameters, and again potentially using blood parameters of particularly renal parameters, some of our blood red blood cell parameters, as a baseline and a guide for our, our therapy. So just sort of to tie up, there's a couple of newer treatment options available.

So intravenous lipid emulsion therapy is probably something which you guys are are now using. And so there's evidence to support the use of intravenous lipids for intoxication with lipophilic drugs. And so we don't really understand truly how the lipid emulsion therapy works, but what we think is that it creates this sort of lipid sync and will bind the lipid lipophilic drugs to the intravenous lipid emulsion.

So that they can then be excreted. And so you can actually find really amazing results. We've had some really amazing results with mycotoxin cases in the administration of this.

It's generally fairly benign. You can get a 20% solution of intralipids now on the veterinary market and usually what we do is we give a small bowlless dose to these patients and then we'll continue a CRI for about an hour. There's still more work to be done in this area of toxicology, so optimum products and optimum dose rates are still being investigated and researched, but it's certainly, a, a, a cheap, fairly cheap, fairly, easy to get hold of treatment option for some of our toxicology cases.

The other option that we've also now got available in the UK is hemodialysis or hemo perfusion. So that's something we can offer where I work at the Royal Veterinary College. So really this is reserved for those patients which go into a kind of full blown stage of acute kidney injury.

And so what we can do is hook them up to the dialysis machine. So this is quite an expensive and can be quite invasive, and there's a tight criteria of patients which will kind of fit fit the criteria for hemodialysis. But again, we've had some really successful cases of raising toxicity dogs, so I can think of two where they were in an aneuric state of kidney injury, and we actually got both of them out of the hospital and home.

So again, something which is now available as another line of treatment in some of these cases. So where do we come into this? So nurses play a really important role in the management of these toxin cases.

So we are going to be the ones which are giving advice to owners on prevention and educating them. We're gonna be giving that advice over the phone when they call in and have that concern that that patient's had an exposure to a toxin. We're going to be involved in triage of the patient when they arrive.

It might be that we're the one that contacts the Veterinary poisons Information Service on behalf of the vet. We're probably the one that's going to be administering the Amorphine and veterinary instruction, probably the ones that are also cleaning up the vomit. Administering the activated charcoal to the patients, administering that supportive therapy whilst they're in the clinic and monitoring their clinical signs.

And again, client communication. So I think, you know, it's quite clear here that we have a really, really important role to play in the management of these cases and as I said at the beginning, they can be really rewarding cases because we can often get them, you know, fixed and out of the hospital. So just really quickly to tie up before we finish this session, so vets now have their tox box system, which I'm sure you're all aware of, but in case you aren't, so there's certain vets now hospitals throughout the UK which have top boxs available, and so they have certain products, so apomorphine, activated charcoal, and some of the anti-venom.

Vials, and they've also got fresh frozen plasma, methocarbamol, and acetylcysteine, vitamin K and also intralipids available. And so that is a resource which, if these are products which your practise doesn't stock because you don't see that many toxin cases, then it might be you can reach out to your nearest that's now hospital who has a tox box to help you at a time where you might need these products fairly urgently for a patient. CVM also have now got some licenced products, so again, Eiddog, they've got an injectable and an oral vitamin K and also a licenced diazepam, which is all now available on the veterinary market.

So you can visit their website if you want more information about those products. Other useful resources that I find quite helpful. So there's the BSAVA triage tool for anyone who's a BSAVA member.

Obviously the VPIS is a great resource. They do CPD events and have lots of information like newsletters on their website, so again, a good resource to tap into. Information, particularly for owners, so that's now the RSPCA and International Cat Care have information on toxic toxicology for clients.

There's a number of books now available, so, two of my favourites are, are just up on the slide there. CTDS lab again will do screening for certain toxin exposures, so you can contact them if you need to. And there's a number of apps available again that you can get through the app store.

So in particular I mentioned the APCC, so ASPCA have got a great app available if you find that this is your kind of thing. So I think that pretty much just ties us up for this session. So again, thank you to GHP recruitment.

Does anyone have any questions? E, that was absolutely phenomenal. It, it's so well presented and so, so concise.

I'm more than happy to say that JHP got more than their money's worth in the sponsorship and I'm sure they are very, very happy, as are all of our attendants. So thank you so much for the effort put in. .

We did get a question come through from Greg when you were talking about Emmadog and emetics for patients. And, Greg wanted to know what dose of metaomidine do you normally use for cats to make them vomit? So I think usually we we I think quite wimpy with sometimes the doses that we use, and I think we'd probably go with the theory of starting off slowly and obviously you can give a little bit more if you need to.

So I think because we want to try and avoid some of the sedation effects, we'd probably start. About 5 mcg per kilo and see if that works, and then if we needed to thinking about sedation doses, people are usually going, I think about 10 to 20 mcg per kilo. So we would start much lower, give a dose, obviously hoping that it has the desired effect of making that cat vomit without making them really, really sedated.

We can then always top that up a little bit if we needed to, and obviously we then aim to reverse that as soon as we can so we, we can, you know, wake that pet up, so that they can then try and protect their own airway and they're not going to be at risk of aspirating or things like that. Yeah, I, I've also found the same thing in our practise. We go for very low doses of it and and in most cases it doesn't need a top up.

Yeah. Folks, that brings us to the end of an absolutely amazing webinar. Once again, thanks to Elle for a great presentation and thanks to JHP for their recruitment, their, JHP recruitment for their sponsorship.

Please remember to go and look at your emails, your junk boxes and that if you haven't got that GDPR email. From us, it really is very, very important so that we can carry on communicating and we're not going to lose any of your, CPD data and everything else. I, thank you.

I really truly hope that we get to see you and hear you again on another webinar in the very near future. Thank you very much. Folks, that's it for tonight and from me, a very good night and to Lewis, my controller in the background, thank you for making everything run smoothly.

Good night folks.