Thank you very much, Bruce, and thank you everybody for joining us this evening. So tonight we're gonna have, we're gonna talk about 3 different toxins. So we've just got a couple of pages on some toxicity information before we talk about Xylitols, we're relatively new, toxin, and then metaldehyde and also non-steroidals to finish on.

So toxicity information. So if we think a patient has had access to a toxic substance, what do we do and where do we find the most up to-date and relevant information? So we have the Veterinary Poisons Information Service or the VPIS.

So this is a 24 hour emergency helpline, and it provides information on millions of different toxins in animals. It's a global company and they provide advice on Pretty much every toxin that you may see in patients, they should have something on their database to help you, whether it be the toxic dose or the treatment that you may require, and also the prognosis and the outcome as well. So it's a really useful resource to have.

We do charge a small fee for the phone call, but it is really valuable information. And then we also have the vets now tox box as well. So this work, they work alongside the VPIS and it provides 24 hour access to antidotes, which may be required for many different toxicities.

And these antidotes are stocked for collection in most vets now clinics across the UK. So because they're 24 hours, you can collect them at any time should you need it. And then there's also the BSAVA poisons database, which is jam-packed full of lots of useful information.

And it's, it's kind of, that's a good source to go to if you just want to read up and do research on a daily basis just to broaden your knowledge on toxicities as well because there's plenty of good information on there. And now, once you gain this information, I find it quite useful to create an in-house toxicity log. So any of the info that you gain from the VPIS or from any of these other resources, it's useful to log that in-house.

Just remember to go back to it, say what treatment you did administer, what dose the patient had ingested, and then go back and write the outcome as well. So then you're creating this in-house log that you have immediate access to. And Just always take, take notice of the date.

So if it was something that you maybe only wrote a month ago, you know, it's quite up to date. If it's something that you've written a year ago and you haven't seen any toxins since, it may well be out of date or some of the science and data may have changed. So in those cases, I'd say it's still worth going back to the other resources like the BPIS, but it is a really useful tool.

And then emergency triage, this is a really important role of all staff members, regardless of whether you're a vet or a nurse, and it's important to have some well rehearsed questions that are important to ask the owner. And the aim of the telephone triage is to quickly identify if a patient needs to see the vet immediately, or they already showing serious signs? Has the patient been witnessed eating a toxin?

And then also really important to advise the owner to bring packaging with them. So this allows us to see the active ingredients, along with the concentration and it allows us to also gauge how much volume this, the patient may well have consumed. OK, so we'll move on to Xylitol.

Cylitol is a relatively new toxin, so we've probably known about it for around the last 10 years, and we're still developing more knowledge on this as well. So this is a natural sugar alcohol, so it's used by humans as an artificial sweetener. So it's contained in a lot of sugar-free products, a lot of dietary products that they may use a substitute for sugar and put in this artificial sweetener.

So the toxic dose is 0.05 to 0.1 grammes per kilo.

And then we have a hepatotoxic dose as well, because this can cause an acute hepatic necrosis. And that's anything above 0.5 grammes per kilo.

And what Xylitol does is it can cause a rapid insulin release in dogs, and this can occur within about 15 to 30 minutes of the patient eating the Xylitol, and because of that rapid insulin release, it causes a hypoglycemia. And If they have eaten a little bit more and they're in the hepatic toxic dose, then you may start to see acute hepatic failure as well, of which the mechanism is still unknown. Now, what products may contain Xylitol that we need to be aware of?

So chewing gum is a big one. Also toothpaste and mouthwash, and then any baked goods, so anything, particularly dietary products where they're substituting the sugar out, sweetener, chewable multivitamins, peanut butter. So this is one that we need to be aware of because a lot of owners stuff their con toys with peanut butter.

That should be absolutely fine, providing. It's not one that containsy at all. So always warn your owner if they do ask or they say that they stuff their corn with peanut butter, just ask them to check the packaging of the peanut butter and make sure they're looking out for one that does not contain xylitol.

And then some liquid medications it's put in just to sweeten the taste and even body care products. Now there's an image of Starburst chewing gum on the side here. This has been around for maybe a year or two, but this actually contains a really high dosage of Xylitol, and it's around 50%.

So if the patient does have access to these, they can have a much quicker onset of the signs, and you might often see more severe signs associated with this toxin in particular. So the clinical signs that we may see are those that are typically linked with hypoglycemia, and it can be anything from 15 minutes of ingestion up to 18 hours. So we'll start to see lethargy, vomiting, weakness, which may lead to ataxia and collapse.

And if the patient's blood glucose drops low enough, we can start to see tremors, even seizures, and then they can become comatose as well. So it's important that as soon as we get these patients in, we're checking their blood glucose, particularly if the owner has witnessed them eating products that does contain Xylitol, check that blood glucose and administer glucose as quickly as we can. And then we may start to see liver liver injury occur from 24 to 48 hours post congestion.

So if liver injury does occur, we may start to see some of the similar signs, so they'll remain lethargic, maybe some melena, so the black tarry faeces, they may start to go jaundice and collapse with this as well. So we know that our coagulation factors are made in the liver, so we may start to see coagulopathy or blood clotting disorders, maybe a thrombocytopenia, so. A decreased platelet count leading to spontaneous bleeding, so tication, pinpoint bleeding on the gums and the mucus membranes, the scle of the eye inside the pinna of the ear, and also the midline of the abdomen are quite common signs as well.

And We may start to see an altered mentation, and this could be from hepatic encephalopathy from an increased ammonia. So ammonia is a nitrogenous waste product that is produced on a daily basis by our bodies. This is then taken to the liver via the bloodstream where it's converted into urea.

So that urea is then excreted by the kidneys and it's taken out as a waste product and it doesn't usually cause any issues. However, if our liver function is starting to fail or become compromised, that ammonia may not be converted into your ear and therefore it will start to build. So if that does start to build, the signs that you typically see with hepatic encephalopathy or, drooling, they can become quite, kind of disconnected from their external environment.

They can head press, so they'll press their head against the side of the kennel and circle as well. So they can start to show really severe neurological signs with this, and they can even go on to seizure. So if you do have the, Capability to check ammonia levels in your practise.

It's always worth doing for this. And it's also worth noting that if you check an ammonia level, you need to take the blood sample, spin it straight away and run it straight away. Ideally, you can even sit it on ice.

If there's a delay getting it to the lab, because as it warms to the room air, that ammonia level will start to drop. So if you run it on a sample that's already been taken, maybe an hour before, you could get a totally normal result even though the patient has a really high ammonia, so. Just remember to run it immediately if you are looking for ammonia.

You can usually run these on the, the in-house IEX machines and they're quite reliable. OK, so what investigations may we may we do for this? So, as we've mentioned, a baseline blood glucose, especially for any patient that presents seizureing, even if you know the reason why it's seizuring, we should always check the blood glucose anyway.

Biochemistry and haematology to go along with that. So we'll see a hypoglycemia, first of all, we may start to see elevations in our liver enzymes, so an increase in our bilirubin, maybe a hypoalbuminemia, so we know that albumin is a protein that's produced, synthesised by the liver. If we start to see liver dysfunction, we may see a hypoalbuminemia, so that level may go low.

Hypocholesterolemia and maybe we might see an increase in our phosphatemia as well. And then because of that increased ammonia and the liver's, inability to convert it to urea, we may see an increase in our ammonia and then decrease in our BUN. And then as we mentioned about the the liver producing clotting factors, if you do have a clotting machine in your practise, you may start to see prolonged clotting times as well.

So that's PT and APTT. So when the patient's in front of us, how are we going to treat it? So the first thing we need to do is correct that hypoglycemia.

So 1 to 5 mLs of the 50% glucose solution that we have in practise diluted with the same volume of hormones or saline, and this can be given IV over around 2 minutes. And the hypoglycemia should be managed with a constant rate of fusion ideally after the IV bolus has been given. To give that as an initial response, and then we do need to maintain it and make sure we're monitoring blood glucose closely, ideally every hour, depending how low that glucose went and how severe the clinical signs were before presented to the practise, or every 2 hours, ideally for a minimum of 24 hours.

Now we need to supplement that glucose for around 24 hours or until normal glycemia can be maintained without supplementing it. So it's not a matter of bolus in it and then seeing how they go. As this is still being absorbed into the patient's body, the hypoglycemia is still likely to be occurring as that insulin is released from the pancreas from this toxin.

Now, I'm not gonna tell you how to do blood glucose. I'm sure you've done that a million times, but just a couple of small pinpoints to to take home. So you don't always need to use the ear.

So if you do have head shy patients or patients that are a little bit nervous, you can use the paw pad and you can also use the lip, which might seem a little bit a little bit mean, but they don't tend to mind it too much. And also the alpha tracks that you can see here, most of the glucometers that we use are calibrators for capillary samples. So you can see on the image the sweet spot here, that's where they're calibrated for.

So if you have a patient with a central line or maybe you'd rather go peripherally, go into the cephalic main, that's absolutely fine, but the main important point is just to be consistent with your method. So if you start with the central line, continue with the central line. I've seen differences of up to 5 mL per litre, just by changing the site of where you're gaining that sample from.

So always write on your hospital sheet where you're getting that sample, whether it's capillary, peripheral, or central, so that you can keep an accurate eye on what's actually happening with that blood glucose. And then the lancet as well, if you do have the lancet that comes along with these alpha tracks, they are really useful. So you can pop a warm ball of cotton wool underneath the ear, particularly with cats, the amount of time that lancet has gone through and got me in the finger.

If you pop a ball of wet cotton wool underneath, if it's warm, it will help with a little bit of vasodilation in that area and help the blood supply for your sample. And then if you just smear a little bit of Vaseline on the top of the ear, it prevents the blood from just smearing out across the skin and it just forms a nice little blob on top of the Vaseline, so it allows a nicer, easier sample. OK, so once we've achieved normal glycemia, maybe after 24 hours, the mesis should be induced, ideally to remove the lump or chewing gum.

And this just depends on the patient. So if they are conscious and they haven't yet shown signs when they have presented to us, their glucose is actually normal at the moment, then we can do it then. But we just need to gauge how the patient is because if they are starting to show signs of seizure in or if they are really lethargic or collapse, then we may need to push this down the line of priorities and just get that normal glycemia achieved as quick as we can and then we can look at whether we need to start inducing emesis depending on how far in we are.

An activated charcoal, we don't recommend for xy at all because it doesn't bind to it, so it won't do absolutely anything for this toxin. We can also use hepatorotectants. They can be considered for hepatic necrosis and we can also use plasma transfusions for coagulopathies as well.

As we mentioned, the coagulation factors are made in the liver. So if you do start to see any signs of bleeding or any petiation or ecchymosis on the skin or on the, the eye, then, you know, you can absolutely give a plasma transfusion depending on how severe these patients are. Now, the prognosis tends to be fair with hospitalisation and appropriate supportive care.

And then if liver failure does occur, then it's, it is less common, but it can be more severe and it can also be potentially fatal in these cases as well. OK, so we'll move on to Mataldehyde. So aldehyde is found in slug or snail bait, and it can be scattered across the garden.

It comes in a few different forms. So we've got granules, which are quite commonly seen or pellets. It can also come as a liquid or a powder.

And then in the summer, we may start to see it a little bit more frequently because it's also used in solid fuel camp stoves. Now the toxic dose is 100 to 1000 milligrammes per kilo in the dog, and around 200 mg per kg in the cat. Even if a patient does receive a smaller dose than this, then we would still recommend treatment because the quicker this, this toxin is all about treating symptomatically and the quicker we we start to treat those symptoms, the quicker the, the better the outcome we're likely to see.

So, Matildehyde is thought to reduce the seizure threshold and that it does that by increasing the excit neurotransmitters. And it's rapidly absorbed into the gastrointestinal tract. So it may take around 30 minutes for the clinical signs to appear, and we may start to see an increase in our muscle activity and the production of acidic metaldehyde and metabolites, which cause severe electrolyte disturbances, and we may always also see a metabolic acidosis with this toxicity as well.

And this may cause clinical signs for up to 10 days, so this is no quick fix. So we need to really closely monitor these patients, collecting those electrolyte disturbances and looking at that metabolic acidosis to see how we can help, as that develops as well. So they are, they do tend to be your longest stay patients.

So you may see some neurological signs as well. And they can develop anything from 1 to 3 hours after ingestion. Now Mattaldehyde toxicity is known as the shake and bake, and that's because they seizure and they also tend to become hypothermic, and the hypothermia is secondary to the seizures.

So it's A catchy, catchy phrase to remember, and that will just allow you to remember what signs to look out for for these patients. So we tend to see ataxia or hyperesthesia, so they're really, really sensitive to any noise or any touch, and then they may start to tremor. You're likely to see a tachycardia and then become really agitated, and nystagmus or dilated pupils may also occur.

So nystagmus tends to be seen more in the cat rather than the dog. And they may also get blindness. So if this does occur, it usually resolves within about 2 to 3 weeks.

And then secondary to the seizures, you may start to see hypothermia. And along with hypothermia comes a list of other problems as well. So once our body temperature becomes over 41.6, our organs can start to close down and Necrosis can start to occur throughout the body as well.

So it is really important that we start to, that we keep a close eye on the patient's body temperature and we try to cool them as much as we can. Hypothermia can lead to multiple organ dysfunction syndrome, also known as MON, and also DIC, so disseminated intravascular coagulopathy, but also, as we may know it, death is coming. So it's not very nice if you do see this, and it can definitely be caused by hypothermia.

So as the acidosis progresses, you may start to see even more severe signs. So they're likely to be very depressed or hypermia. So they're taking deep, bigger, deeper breaths, and this tends to be a compensatory mechanism for the respiratory system.

So as an aidemia occurs, it's the body's own mechanism to try and compensate. As you take really deep breaths, you're exhaling more of that carbon dioxide, and that's the body's aim to try and reduce that asidedemia. I just taking those larger breaths and breathing out that CO2.

And then you may start to see continual tonic convulsions and they may well become unresponsive to external stimuli. Now, if the patient does present in status epilepticus, we need to rapidly stabilise this patient. So rapid assessment of the most important bodily systems, so your CNS system and also your cardiorespiratory system.

We need to provide oxygen. So seizures increase our oxygen consumption and also our glucose consumption as well. So even though glucose may not be the cause of these seizures, it may well start to be rapidly consumed with seizures.

So keep a close eye on your blood glucose. Just always just pop a mask on these patients because they're going to require a lot more oxygen. And then we need IV access in these patients, and you can also consider placing two.

So if patients are quite unstable with their seizures, then it's always useful to have two because then if one does become dislodged from the seizure and maybe the the line of the T connector pulled on something, you always have a second one there ready to administer those anti-seizure drugs should you need to. And then you need to administer anti-seizure drugs either IV if you have your excess already, if you go intramuscularly or you also have your rectal diazepam as well. And you can keep a close eye on measuring that core temperature with active cooling.

So remember with your active cooling that we don't recommend wet towels anymore. So if you pop a wet towel over the patient, we believe that it actually helps keep the body temperature, it keeps everything in, so it can actually heat up the patient rather than cool them down. And we don't want to do any putting wet, putting a load of cold water on these patients because it can rapidly cause a hypothermia.

So what I would do is pop a fan on the patient, maybe turn the aircon on in the room and make sure everything is kept pretty cool and control the seizures, that's gonna be the one thing that's gonna really affect the body, the patient's body temperature. And you can do cold water enemas, and this will also help lower the empty the lower gastrointestinal tract, so to try and get out some of those toxins as they enter the lower gastrointestinal tract, to try and empty it out to prevent any further absorption. So once this has been administered, once we've triaged the patients and we know what's going on.

We need to perform a full clinical exam to try and assess this patient, see exactly what is going on and what bodily systems are being affected. And then ideally a neurological exam as well to see how is our patient, why are they seizuring and what effects may we start to see secondary to those seizures. And then we need to run a full blood panel as well as monitoring our blood glucose.

So as we've just mentioned, hypoglycemia can occur from prolonged seizures. So I would always have a glucometer next to this patient in its, it's tray or in a bag next to it that moves wherever this patient goes, the glucometer goes as well so that we can keep a close eye on the blood glucose. Now to diagnose this, we may want to do some abdominal radiographs.

So you can quite often see radio pig pellets if it's the pellets that they've eaten, and usually they're coloured either green or blue. So you may start to see green diarrhoea. And there's no set treatment available for this toxicity, but aggressive symptomatic treatment, ideally within the 1st 24 hours, will allow us to see the best, the best recovery for these patients, and that can be within 2 to 3 days.

So it's not a quick recovery. We need to keep going with these patients and it may well even take longer than the 2 to 3 days. Depending on how severe the patient is.

Now, gastric lavage is something that we can do. So if the patient has eaten quite a large quantity, we can anaesthetize these patients to get their seizure in under control, and with a cuffed ET tube, we can start doing some gastric lavage and that will just help us to get rid of any of that ingested material that's in the stomach. And then you can do activated charcoal, administer that as a one-off dose and then repeat it as a half dose every 6 to 8 hours afterwards as well.

And then the cold water, the water enemas to lower that to empty that lower GI tract. And fluid therapy. So Hartman's solution is ideal, and it also contains lactate and buffers.

So this will help control that metabolic acidosis and also electrolyte imbalances that we may need to be checking on the, ideally on a daily basis, depending how severe they are, and just supplement them, any that may go low and just try and treat symptomatically depending on which abnormalities you may find. Now, Another quick note just to say is when you do gastric lavage or if the patient does vomit at all, then the stomach content can be frozen and sent off to the lab. So they do also accept urine, blood, and liver samples to test for metaldehyde or acetaldehyde, to confirm the diagnosis, but the stomach content is the most accurate.

So quite often, Other tissues or other samples can be sent off and it comes back as inconsistent. So if you do have any of the stomach content there, consider freezing it and consider sending it off as an option. Sometimes the stomach content can have almost an apple cider type odour.

They can also use bran or molasses to try and sweeten these products, so they can have a quite a sweet smell to it when, when it does come out. And To move on to treatment of the seizures, we can administer diazepam and this controls the central nervous system signs. Now phenobarb should be avoided because this competes with the enzymes that degrade acetaldehyde.

So if it's competing with those enzymes that degrade the active ingredients of this of this toxin, then we may start to see worsening of our signs. So we need to avoid phenobarbital in these patients. And if static epilepticus does occur, then we may need to consider total intravenous anaesthesia, so also known as teva.

This will help control hypothermia and we can also give muscle relaxants as well. So propofol is usually quite a good choice to use for these patients. And if we do need to consider te.

We need to intubate these patients, ideally with a c tube, and that will just allow us to maintain the airway and monitor our respiration. So there's a couple of different monitoring tools that we, if we have access to in our practise, we should absolutely be using them for these patients. Sotranography is really, really useful and it's useful as a measurement tool to assess the depth of anaesthesia, the respiration, and it also tells us quite a lot about the cardiac output.

So if our respiratory rate is too high, then we're gonna be blowing out too much CO2. So our CO2 is gonna go low. Now for our respiratory rate is too low, maybe we're too deep under our anaesthesia, then we're not gonna be blowing out enough CO2, so therefore it's gonna build and it's gonna go high.

So it does help us to assess our our patient depth, whereas other signs may be more subtle or may not show straight away. And also the cardiac output must be adequate to send blood to the lungs in order for gaseous exchange to occur and for us to get a CO2 reading on Kapnograph to start with. So if we do have a patient who may tip into cardiac arrest or is getting close to cardiac arrest, then your your catography tends to be the monitoring tool that will change the quickest because that rate will just go down along with our respiratory rate as well and our heart rate.

So it is a really useful tool and it definitely has its place in the emergency the emergency patients. And we need to provide oxygen during the tea. Monitor blood pressure if we can keep an eye on your peripheral, your peripheral pulses, see how they feel, quality and rate.

And again just monitor body temperature. And we also need to remember to turn these patients regularly. So every 2 hours ideally, and remember that you can go into sternal as well.

So from the other, the left to the right, and also sternal, and that's just prevent any hypostatic pneumonia from building in the lungs. Finally, just monitor urination. So if you have a male dog and it's quite easy to place a urinary catheter, that's one option.

If you feel that's a little bit too invasive and they may not be under teva for very long, then we may just need to write on our hospital sheets maybe every 4 hours to just palpate this patient's bladder and express if they're not urinating themselves. Just keep an eye on that they are actually going to the toilet. Now, if hypothermia persists, monitor for signs of DIC.

So if we run a haematology, we may start to see platelet consumption. And the signs of DIC will start to see spontaneous bleeding. So you can see on these two images.

So this patient, the, the limb that you can see at the bottom, as I clipped this leg, you couldn't see any bleeding, but just from the clippers, which were really gentle, this petichiation or ecchymosis started to occur straight away and it did worsen into bruises. And then you can also see some tication on the gums of the patient at the top as well. And they're just the subtle signs that you may start to see that the patient's platelets are starting to be consumed and therefore spontaneous bleeding is starting to occur, and this can occur into the bodily, the third spaces as well, so into our cavities, our abdomen, and into our plural space also.

So Matilda Hyde does carry a good to excellent prognosis, and it's all down to the supportive care that we can provide, the symptoms that we can treat and the hospitalisation that we can give to our patients. And the sooner we see these patients, the better. OK, so we'll move on to non-steroidals.

So non-steroidals are readily available. We use these on a daily basis, and there's many different types of them. So there's two pictures here, probably the most common ones that we use in veterinary.

And then one at the top, the Riadil, I've been unfortunate enough to have my two dogs who died of a Rimoil toxicity. So the fact that they are palatable is great for those patients who don't want to eat the daily non-steroidal for their bad hips or whatever they may be on, but the fact that they are beef flavoured also makes them very appealing. Now, the Rimil pack itself has a childproof lock, so it's quite difficult even for an adult to get that off most of the time.

But if you have a patient who has a really strong nose and maybe a Labrador for example. They can still get access to this. So my dog actually chewed through the pack.

We had two boxes of the 100 milligramme tablets, each with 100 in each box. She chewed through both and shared it with our other dog, so they're both sadly passed away. So that's one just to take home message to say if you do dispense any palatable tablets that do have a strong beef flavour or any strong flavour to make them palatable, make the owner aware that actually Don't store them in any of the bottom cupboards, even if you think it's stored away, they're not going to get it.

If you have a patient who does want to scavenge, they could well get into that cupboard and chew through that bottle. So I would always recommend storing them out of reach and out of out of the way of those noses. So they're readily available and they are, they can be particularly toxic to dogs.

So the most common signs that we see are vomiting diarrhoea. And gastric ulceration as well. And depending on the dose, they can also then cause acute kidney injury.

And this isn't just for dogs, it's for cats also. Now the toxic effects of non-steroidals are mainly due to widespread vasoconstriction. So inducing this induces gastric ulceration.

It can cause renal failure and acute kidney injury, and we can also start to see coagulation disorders as well. So liver failure is also another side effect that we can see, and that's because it can cause liver necrosis. So with non-steroidals as a general rule, we tend to say 5 times the therapeutic dose and you're likely to see gastrointestinal signs.

Now obviously, these are patient dependent. Every patient is different, and usually 10 times the therapeutic dose can cause an acute kidney injury, and that's when we start to see the really more severe signs that definitely require hospitalisation. The clinical signs that we tend to see, they may come in because they're vomiting.

They may be anorexic, they are likely to be off their food because they feel so lousy. Hematemesis, so maybe we have blood in our, in our vomit now, and if we have diarrhoea, you may also see melina, that black tarry faeces, and these could all be suggestive of a gastric ulcer, so that's bleeding because it looks like we've got some some digested blood there. They're likely to be very lethargic and dull, really dull demeanour.

And then PUPD is also very common, particularly with kidney involvement. Now, the owners tend to often they'll notice they urinate in large amounts and they are really PUPD. But then they tend, that tends to be followed by a rapid decline in our urinary output and then we'll start to see oli urea and urea, which is when our alarm bells really need to start ringing.

And they are likely to develop a taxi as well, quite often they are a little bit wobbly on their limbs and they just don't have the energy because it is a really It's a condition that does it causes pain, pain in the area of the kidneys and it does, I always remember learning that kidney injury or kidney disease feels like a really bad hangover. So I have sympathy for these patients. So I've had some really bad hangovers and the thought of this, Being persistent for a few days is pretty horrific.

So, just to touch briefly on the main things that the kidneys do so that we can understand what an acute kidney injury is. So the kidneys have many functions within the body, so they maintain blood pressure, they maintain electrolyte imbalances or balances. They excrete waste products and toxins, and then they also help with the production of urine as well.

So if you do start to see kidney dysfunction, it can severely compromise the health of our patients, and quite often it's not a condition of one organ itself. This causes a multiple organ dysfunction syndrome, so it does play an active role on multiple different organs if our kidneys start to become affected. Now the definition of an acute kidney injury is an abrupt decrease in renal function, which may include both structural and functional damage.

So an acute kidney injury caused is a decrease in the excretion of our waste products, so they mainly are urea, creatinine and phosphate. And because it plays an important role in the maintenance of our electrolytes, then we may start to see a decrease in our electrolyte excretion as well. And we may start to then develop a metabolic acidosis.

So The sudden onset of an acute kidney injury is potentially a life threatening kidney dysfunction. And despite the advances in treatments, death rates do unfortunately still remain high, although many patients can still recover. Unfortunately, the death rates do remain high with these patients and.

Acute kidney injury, the main thing to remember the three things are they cause fluid retention, electrolyte abnormalities, and acid base abnormalities. So if you remember those 3, then you can keep on monitoring those signs, monitoring the electrolytes on a daily basis, and keep on just altering those nursing plans to make sure that we can tailor it daily for our patients' needs and we can pick up on any signs of things that we need to look out for. And any signs that the patient may well be starting to decompensate.

Now, the treatment of an acute kidney injury, or rather of the toxicity before we get to that, so ideally we want to induce a mesis. And then we can give doses of activated charcoal as well. So that works quite well for non-steroidal toxicity.

And then we need to start aggressive flu fluid therapy for the treatment of this AKI. And we need to monitor our urinary output very closely and ideally, we need an indwelling urinary catheter in these patients. So in order to nurse these patients the best that we can, we need that urinary catheter in and do it straight away once the patient is, once the patient presents, we can sedate that patient if we need to, if it's a bitch, perhaps get that catheter in and then we can start off straight away.

Once the hydration is corrected, then we can start monitoring that urinary output because we get so much information from what our kidneys are doing when we're monitoring our ins and outs. Needed to monitor our electrolyte imbalances, so we tend to see a hyperkalemia, which we'll talk about in a moment. Metabolic acidosis and then remember that we, we should administer gastroprotectant and antiemetics to these patients because they are.

Likely to develop gastric ulceration and feel really lousy. And then last but not least, analgesia, so. Pure opioids agonist like methadone or maybe even buprenorphine depends on how painful these patients are, but often if you do palpate the abdomen, they are really painful in the area of these of the kidneys.

So do remember to administer your your analgesia. So, when we're administering fluid therapy, we need to administer fluid therapy to correct and normalise two different things. So the intravascular volume as a number one, and then also dehydration as well.

So crystalloids are the most appropriate, but they do diffuse out of the IV space in around 20 minutes. So it's not one hard and fast rule of we need to Give a bolus and then it seems to have worked and then we're done, just pop them on 2 mL per kg per hour or on a maintenance rate, we need to keep on assessing these patients. And we need to make sure that we're monitoring for signs of oligura or aurea as these patients can quickly become overloaded.

And something to remember with cats is they can become bradycardic if they do have a volume depletion. So if you have a hypovolemic cat, you'd expect them to be tachycardic like dogs do. But they do tend to go the, the opposite way and you may well see a bradycardia.

So if you do see that in a cat where you suspect, that they are actually quite hypovolemic, quite dehydrated, and you think it's unusual, then it may well be, it could be from electrolyte imbalances like a hypothermia as well, but it's also worth bearing in mind that it could be from the hypovolemia. Now, sodium chloride tends to be contraindicators with patients with asidedemia because it's a very acidic solution. I think the pH is around 5.

Whereas Hartman's contains buffers, and that will help correct your asidedemia. So that would be the fluid of choice. Now to talk briefly about fluid shock rate, so if you read the textbooks, it will say shock rate for a dog is 90 mL per kilo, Shock rate for a cat is 60 mL per kilo.

But what we need to do is administer smaller bolus regularly and just keep on reassessing. So it's been proven that administering smaller bolus rather than the one-off large dose drastically improves the mortality rates of these patients, sort of all patients receiving fluid therapy. So you may not, the dog may not need 90 mL per kilo.

You might get to 60 or 70 mL per kg and think actually they're doing fine. I'm gonna slow that down and I'm just gonna maintain and start correcting the dehydration now. So I would recommend usually go for 10 to 20 kg bolus.

You can go higher if they are really severely hypovolemic, and then just keep on reassessing. So assess that cardiovascular system. Is the heart rate coming down?

Is the respiratory rate coming down as we're administering fluid therapy because it should be. How do our pulses feel? Do we have access to, blood pressure to monitor that?

Is it improving with our fluid therapy? If not, do we need another bolus on top, and then just keep on reassessing and reassessing until we're happy that our patient seems a little bit more stable. And then as we mentioned earlier, the monitoring of ins and outs is really important.

So, The normal urinary output is 1 to 2 mL per kg per hour in dogs and cats. And any less than that can be oliguric at 0.5 to 1 mL per kg per hour.

And then aura is 0.0.3 mL per kg per hour.

So we also need to weigh our patients twice a day, and they should gain weight when they're correctly hydrated from when they present. And if it's decreasing, then we know that our patient is losing fluids. So to quickly explain that a little bit more, our body is made up of 60% water, so that's why our weight is important.

Our kidneys, if our kidneys aren't concentrating urine, then we have an excessive loss of urine and we need to monitor and administer the same back. And this just prevents losses because otherwise if we have an acute kidney injury and Where you have excessive loss of urine, we're starting to become dehydrated again. That's going to put more and more pressure on those kidneys and it's gonna worsen that acute kidney injury.

So even though the fluid rates can end up really, really high for these patients to an alarming rate, which is actually quite scary, If we don't administer that same volume back, then we are going to worsen those those kidneys and they are going to start to really struggle. So that's why it's really important to match those ins and outs and whatever it is coming out, we need to make sure we're matching what's going in. So if aura does start to occur or urea, that's when we need to just be a little bit more cautious and weigh our patients if they're gaining weight, then we need to be careful that we're not administering too much because we can overload them quite quickly as well.

And we can also administer rosemide to the aneuric, aneuric patients just to try and to promote diuresis and to try and get those kidneys to excrete some of that urine and start working a little bit better. And dialysis is also an option as well. So they'd need referring to somewhere like the RBC in London for dialysis if that's an option for the patient.

Mhm Now, another side effect of an acute kidney injury is hyperkalemia, so an increase in our potassium value. So potassium is a major intracellular cation. And In volumes over 7.5 mm per litre, we need to give fluid therapy.

So fluid therapy promotes renal diuresis. So as we start to excrete our urine, our kidneys excrete potassium as well. So it'll naturally bring down the volume.

Just with a natural urinary excretion. But then if it is over 7.5, we may need to look at administering insulin.

And this is to reduce that potassium value. So we know that we administer insulin for our diabetic patients because it sends the glucose into the cells. Now, glucose is also a co-transporter with potassium, so it does the same for our potassium.

So when we give insulin, it will just send that potassium and the glucose into the cells and lower that, potassium concentration within the bloodstream. But remember that it will also lower your blood glucose as well. So we need to administer some glucose alongside this and monitor it and maybe put them on a CRI just for a short while until normal glycemia is maintained.

And then if we do tend to see any cardiac abnormalities that you can see secondary to a hyperkalemia such as your bradycardia, your arrhythmias, your tall spike T waves on your ECG, then you can give 10% calcium glutinate, so about 1 mL per kilo. And we just dilute this and give it slowly IV over around 3 to 5 minutes. Excuse me.

Now that will not affect your potassium value at all. There's nothing at all to your potassium. It simply just protects the heart from any abnormalities and disturbances that can be caused by this electrolyte and the excess volume of the electrolyte that we we have in these patients.

So we will just provide some cardiac stability. And then just finally, non-steroidal toxicity can be something that keeps them in the hospital for a little while, maybe 7 days or potentially even more depending on the severity. So remember our nutrition and how important it is.

So. We need to calculate the patient's RER and we need to recalculate this every single day as our patient changes body weight. So 30 times the body weight in kilos plus 70 is a nice easy sum to remember and that gives you your daily RER.

Your nurses involved with this, nurses can place nasal esophageal feeding tubes, and these are ideal for these patients. You can trickle feed if you have syringe drivers, you can pop liquid food to trickle into the esophageal feeds and tubes, nasal esophageal, and you can administer bolus as well. However, this patient will receive the food.

As long as there is food getting in, then it's really important for these patients and it will help with their recovery. Now, prognosis is variable for a, a non-steroidal toxicity, and it just depends on the severity of the signs and how bad the disease has become. So the recovery phase can last up to 12 weeks, so don't give up on these guys too quickly.

The important thing is that we're starting to see the blood go in the right direction. So if our patient still remains asotemic for the 12 weeks, that's absolutely fine as long as it's going in the right direction. So if our treatment is helping, and it's just reducing that azotemia bit by bit, then we're going in the right direction.

And it's important to note that the degree of aotemia on presentation does not correlate with the patient's outcomes. Some patients can be severely aotemic and make a recovery. Some patients may only be mildly aotemic, but may end up not making a recovery at all.

So it just depends on the monitoring of the aotemia and just keep on, keep an eye on that it's going in the right direction and don't give up too soon. OK, thank you very much. That was good timing before my voice goes.

I'm happy to answer any questions if you have any. Sophie, thank you very much. That was incredibly clear and very, very practical.

So thank you for your time tonight and thank you for persevering with the voice that was starting to croak there in the end. Thank you, Bruce. Right.

Sophie, we don't have any questions that have come through yet. I think your presentation was just so practical that, that everybody fully understands exactly what it was that you were trying to get across to them. So, very well done.

And once again, thank you very much. Thank you very much, Bruce. It's good to hear.

We're not going to keep you any longer because I can hear that you really are battling with swallowing and drinking and and trying to suppress those coughs. So folks, a great thank you to Sophie for her time tonight and to you for attending, to my controller in the background. Thank you as always for making things happen seamlessly.

And from myself, Bruce Stevenson, it's good night.