Hi guys, my name's Sophie McMurra. I'm a registered veterinary nurse and a veterinary technician specialist or VTS in small animal internal medicine. I work at a specialist referral hospital called North West Veterinary Specialists in England, where I'm the head nurse of the internal medicine department.
My areas of interest are endocrinology and emergency medicine, and I'm here to speak to you today about lily toxicity in cats. So when a patient presents to you at the clinic, maybe it has a suspected toxicity because of the clinical signs that it's showing. Or maybe the owner has witnessed the patient eating a certain toxin and they've brought in the packaging, which is really useful.
We don't always have the most up to-date and relevant information on the, the clinical signs. We should expect to see how the patient is likely to respond to such toxin and how we treat it. There is a multitude of toxins that the patients can be exposed to and we can't possibly know everything about every one of them.
So we need a database that we can go to. On top of my list is the Veterinary Poisons Information Service or the VPIS. This is a 24 hour helpline.
And it provides us with all of the information that they have on a certain toxin, so the clinical signs, the toxic dose, how we can treat it, and the prognosis so that we can be clear to the owner. It's a large nationwide database and you will know if you've ever used the VPIS there's a small fee involved, but well worth it. And then afterwards they will ask for feedback on each case that's involved.
So they will ask what signs did they see? Do we know what the toxic dose that they were exposed to? What was the outcome and what treatment did you use?
So they will use all of this data to just build up their database and to help future patients who may be exposed to the same toxin. And then there's also the Vets Now Tox box, which is a service based in specific Vets Now clinics in the out of hours hospitals, and they will have access to certain antidotes or anti-venoms or things that are not widely available, and you can buy the substance off them and then just buy them one back. So that's quite useful to be aware of.
And then there's also the BSAVA poisons database which I like, but it is very limited, so it doesn't have that much information on there. Now to give you an idea on how common lily toxicity is, this is some data taken from the VPIS in 2020. And lily species remain the most common agent that they are consulted about for cats.
And of the 2,471 calls that they received about cats that year, lily toxicity made up just over 5% of all feline cases. So if you think of the amount of toxicities that are out there that cats can be exposed to, 5% is quite a large proportion, so it is still very common. The reason lily toxicity is still so common is for a multitude of reasons.
They are readily available, obviously just in your normal shops, and they're used for a multitude of different occasions. Easter, they're very popular in the springtime. They're used for weddings a lot and also funerals.
And they come in a multitude of different forms. So you can see two different types here that look completely different to each other. So there are many hybrids available that people may just think, oh, it's the common daylily that you can see pictured here, the orange one at the top.
But actually they come in many different forms now, and those hybrids make it a little bit more complex because people can be aware of the standard lily or the daylily. They may not be aware of all of the different types so that they even have lilies in their garden. And there's a huge lack of awareness amongst owners and the general public.
Yes, now some shops will have a warning written on the flowers as you buy them, but who buys flowers and reads the label? So yes, it's a step in the right direction, but the more that we can do as veterinary professionals, the more awareness we can bring to the general public and people will hopefully stop buying lilies if they do own cats or stop planting them in the garden where the cats can be attracted to the smell or they could walk past and get the pollen on their fare. And there are, every part of the plant is toxic, so they can get the toxicity through oral ingestion.
So maybe if they actually chew the leaves, the pollen, the stem, the petals, or you'll know yourself specifically these ones at the top of the daylilies, the pollen is so fair and It just sticks to everything. So if you walk past with your, just brush your clothes past it, you will have a large orange stain on your clothes. They also drop off after a few days and go on the work surface or the floor.
So if the cat goes past and gets it on their fur, they'll groom it off. But even if they haven't walked past it, if they've fallen onto the floor and then they've walked on top of it, they then groom it off their paws. And that is when we usually see them presented to the clinic when the owners actually see the pollen on the fare of the patient.
Now dogs are not very sensitive to lily toxicity, they get gastrointestinal signs, whereas cats are incredibly sensitive to the toxic effects of this plant. So the remainder of this talk is based around cats. And it has a rapid absorption and rapid clinical signs will develop.
Now the mechanism of the toxin is still unknown, but we believe it to be water soluble. It causes a necrosis of the renal tubular epithelial cells, and it causes a profound polyurea with renal failure, which then in turn causes a severe dehydration because the patient's just urinating out a lot of its fluid. And the secondary dehydration occurs because of that.
And we believe that the toxin is eliminated within about 48 hours, although we still don't know what the toxin is, we know its characteristics and the symptoms that it can cause with these patients, and typically we believe it to be gone after around 48 hour mark. And the nephrotoxic component of the plant, we know that it's water soluble, which helps when we're treating the patient because we can diarse it out or we can, that's the goal, and it's present throughout the whole of the plant. So whether it's the stem, the leaves, the petal, or the pollen, so every part of this plant is toxic.
I mentioned earlier that there are many hybrids available. The liliium species specifically can have many different forms now. The daylily is the orange one pictured at the top, which is the most common and the one that we all think about when we think of lily toxicity.
However, there are many different forms now, so true lilies, Easter lilies, Asiatic, Oriental, just to name a few. And they are all nephrotoxic. And then we have some which are renal sparing, but they do have cardiotoxic effects instead.
So Lily of the Valley, which is pictured over on the right, is similar to foxglove in the way that it responds in the body. And while it's bearing on the kidneys, you will then see the cardiac effects of the toxicity instead. So before we delve too deeply on the nephrotoxic effects that this toxin can have on the body, we need a just a brief reminder to remind ourselves what the kidneys actually do and the importance of kidney function and the effect that it can have on the body, so that we can start understanding when we see different symptoms and different side effects, why they might be happening.
So to mention just a few, maintenance of blood pressure, usually via the RAS system, the Renin angiotensin aldosterone system, and the kidneys play a vital part in that, and that is the main system for the maintenance of blood pressure. They also maintain our electrolyte balance, the excrete, the ones that we don't need, and they retain the ones that we do. They also eliminate a lot of our waste products and toxins, which is why a lot of our toxins go to our kidneys because they are there to excrete it and get rid of it out of our body.
And obviously they play a really vital part in the production of our urine. So kidney dysfunction can have a real massive knock-on effect to the rest of our body and it can include things like our water balance and our acid-based status as well. Now the definition of an acute kidney injury is the abrupt decrease in renal function, which may include both structural and functional damage.
Now the damage causes a decrease in the excretion of those waste products. So our urea, our creatinine, those things that we think about when we look at our bloods for our kidneys specifically, and our phosphorus as well. So we may not be able to excrete those out, so therefore they will start to build.
And we maintain our electrolytes, so specifically potassium and calcium can start to become elevated because usually our kidneys will excrete those out and diarrheze them out of the body. Whereas if we have an impaired kidney function, we may start to keep hold of some of those. So you will see an abrupt rise in things like our potassium.
And you can also see metabolic disturbances, so you can see a metabolic acidosis. And because of all of these important functions that the kidneys play in just the homeostasis or the normal physiology of the body. The acute kidney injury is often not a sym syndrome of one organ, but it can play an active role in multiple different organs and just the physiology and how our body works on a day to day basis.
So we can quite easily tip into multiple organ dysfunction syndrome where it will have knock-on effects to a multitude of different things around our body rather than just the kidneys because they are so important. And the three main things that we look out for with acute kidney injury is fluid retention. If our kidneys are not able to diarrheas like they normally can, then we might end up retaining some fluid.
Electrolyte abnormalities and acid base abnormalities. So they're the three things we need to keep in mind. And they're the 3 things that we need to monitor and also see if we can correct them as and when we need to, if our kidneys are not able to.
This is where our treatment comes in. Now the clinical signs are acute in onset, and usually they will start to occur within a few hours of the patient eating the toxin or the the plant. And initially we will see gastrointestinal irritation, so maybe the patient will come in with vomiting.
And then the later effects that we see is usually from uremic damage, so an increase in our urea causing a uremia in the bloodstream, which can have a knock-on effect and make them feel incredibly sick. And then if death is going to occur from a lily toxicity, usually it can be anything from 3 to 7 days typically. So some of the clinical signs that we may see include hypersalivation, vomiting and diarrhoea, so those gastrointestinal signs from the irritation.
Lethargy and depression, they're likely to feel lousy by this state, so lethargic and a little bit down and depressed. We will start to see our urea and creatinine increase along with our potassium and our phosphorus as well. And usually this is before the 24 hour mark, they will start to increase because the kidneys can't get rid of them.
And then the renal function can start to deteriorate and signs that the acute kidney injury can typically be seen from the 24 hour mark, but it can take up to 3 days to start showing the signs of an acute kidney injury. And along with that, you will see polyuria polydipsia, or PUPD, and this is when your secondary dehydration will start to come along. And also, we often forget about pain in patients with an acute kidney injury or any renal issues, but they usually get enlarged kidneys and they're usually quite painful in the area of the kidneys as well.
And let's not forget that kidney disease can make you, I always remember it described to me as feeling like a horrific hangover. You're really dehydrated and there's a toxin that you're trying to clear out. So headache, nausea, you can get some vomiting and diarrhoea.
So all of those things come with pain. So keep that in mind when we're thinking about nursing our patients with an acute kidney injury. And if the patient gets bad enough to have a really severe uremia, which they will have if they do tip into the acute kidney injury.
It can be bad enough to cause convulsions. And that is from the uremic toxins building up in the bloodstream causing an encephalopathy, so it's basically intoxicating the brain. You can then, you can resolve the vomiting and it can often occur again with the uremic injury, and that can be on maybe day 2 or 3 or even later.
And then after that, you may start to see your auric renal injury, and we'll talk about aura and things in a moment, but anuria just means when the the your urine production starts to to stop basically. And that just means that the kidneys can no longer function and death will usually occur imminently after that if we don't intervene. And we have seen some of the more rare clinical signs as well, which certainly don't appear in every case.
They are rare and they can include pancreatitis or pancreatic degeneration. We don't understand why, but we have, it has been seen in some cases. And you can sometimes see edoema, mainly in the pores of the patients.
And then even if we do get the patient out of this toxicity and out of the acute kidney injury, they're likely to still have long term renal insufficiencies. So chronic kidney disease is likely to to remain after, even after we've treated the acute kidney injury and got them out of the worst part of the toxin. OK, so now we know what our patient has been exposed to, we know what to expect.
We need to start doing some diagnostic aids. And we've just said that our kidneys eliminate waste products and maintain our electrolyte balance. So they're the two first things that we want to check.
So your urea and creatinine will start to increase. And sometimes you can see a disproportionately elevated creatinine in comparison to your urea. And you will see an elevation in your phosphorus and your potassium is often elevated with an acute kidney injury as well.
In some cases, we have seen reports of an increase in liver enzymes and bilirubin. And your analysis is something that we should utilise in any kidney patient. It's something that is often underutilised, but it gives us so much information.
So your analysis will show us evidence of renal tubular damage and often before we can see aotemia, so increasing our urea and creatinine on our bloods. Up to 12 hours post ingestion of the lilies. And the things that we're looking out for is our urine specific gravity, for the first thing.
So we know that urine specific gravity reflects the concentration or the kidney's concentrating ability of the urine. So we know that this patient is likely to be dehydrated. In a patient who's dehydrated, the urine should be more concentrated.
But often with these patients we will see an isostenuria, which just means it's within that range that we deem as the the normal reference range. So in a cat about 1020 to 1060. Anything with dehydration should be over 1040.
So if we have a patient who is dehydrated, but their urine is within that range, that's abnormal. And remember that we need to always assess urine specific gravity alongside our hydration status. So if the patient is dehydrated, the ord in specific gravity should reflect that, and if it doesn't, it can tell us that the kidneys have a decreased concentrating ability.
So that's abnormal in the dehydrated patient. You can also start to see things like proteinuria a protein in your urine and glucose as well. And this can suggest glomerullar damage.
And then you can see granular or epithelial casts if you analyse it under the microscope. So we have 3 main aims when we're looking at the treatment of lily toxicity and the management of an acute kidney injury. And those 3 things that we need to remember are decontamination, to get rid of the contaminant, to get rid of the toxin so that the patient can improve and come out the other side of this.
But we need to also do it with the prevention of renal shutdown in mind. So this toxicity is targeting the kidneys because the kidneys are there to excrete it and get rid of it out of the body. However, it is a difficult toxin to get rid of, and it is something that will impair our kidneys while doing so.
So we need to prevent renal shutdown by providing things like fluid therapy so that we can aid or allow our kidneys to do their job so that they can start excreting this toxin and the waste products that it needs to get rid of in order for us to remain healthy. And then we need to enhance our renal perfusion. So if we have severe dehydration, we have an increase in our renal values and toxins and waste products, and we also have a toxin on top of that.
The last thing we need is a decrease in our renal perfusion because we're polyuric and we're urinating all of our fluids out. That will shut down the kidneys faster than anything else. So we need to make sure that we are maintaining that perfusion to the kidneys so that we allow them to continue doing their job the best that they can while trying to get over this toxin.
So we can help treat these patients by inducing emesis and providing performing a gastric lavage. So we need to get rid of anything that may be remaining in the stomach. If there's any contaminants there, we need to get rid of it so that the patient doesn't have chance to continue digesting even more of this toxin and worse in their condition.
And then we, we do a gastric lavage just to make sure that we get all of it out of the stomach. And then for the parts that have already been digested and entered the gastrointestinal tract, we need to use activated charcoal so that it can bind to the, the toxin and help it pass through the rest of the gastrointestinal tract. If we have any fur present on the, sorry, if we have any pollen present on the fur, we need to wash it off so that we are not going to leave any on there that the patient can wake up and groom again.
And then the beauty of this toxin being water soluble means that we can just provide diuresis, we can diaries this toxin out, hopefully, and we do that with fluid therapy, and that will support the kidneys while we're trying to diaries and while they're doing their really important work to try and get rid of all the toxins. We often do require very high fluid therapy rates and we'll touch on that in a moment. And that can usually be for anything from 24 to 72 hours.
And then we need to monitor our hydration status. Those fluid therapy rates can be quite dangerous if we're not monitoring them effectively enough. We can either cause a fluid overload if we give too much or too quickly, or we can cause dehydration.
So we need to monitor these very carefully. And we can look at monitoring our blood to our renal values. Are they changing?
Are they responding to our our fluid therapy? How are our electrolytes? Are there any corrections that we can intervene with and that we need to help with in order to support the kidneys?
So there's a multitude of different things that we can do just to get them through this kidney injury or this original insult. So I also mentioned earlier that often the patients can be painful in the area of the kidneys, so don't forget your analgesia. Obviously you would never use something like a non-steroidal in a renal patient, but you can use other things like opioids or whatever you deem necessary.
Gastroprotectants and antiemetics, they're likely to feel very nauseous and even if a patient doesn't vomit, it doesn't mean that the nausea is not there. So treat, make them feel a little bit more comfortable, treat the nausea and protect their gastrointestinal tract as well. Enteral nutrition feeding is vital for these patients or for any long stay patient in the hospital.
We know that an acute kidney injury is not a quick fix, so they are likely to be in hospital for some time, so it's really important that we can provide that early enteral nutrition to them to support them throughout this condition or their hospital stay. If the patient is conscious and doesn't require an anaesthetic, then the feeding tube of choice, I would recommend a nasogastric feeding tube, which we can place as nurses. If the patient is having an anaesthetic, then for something like the urinary catheter placement or the gastric lavage that we need to do early on, then I would recommend the esophagostomy tube.
It's a wider bore tube, it's a long stay tube, and it's less likely to cause any blockages, and they can be sent home with the patient and managed by the owner if necessary. And it's also very well tolerated. And then if the patient does go into an acute kidney injury, I would recommend specialist referral with the the development of an AKI because they can be very complex cases and they require very intense nursing care.
So we can look at the treatment of the lily toxicity as two different sections, so prior to any aneuric renal injury. We treat with fluid diuresis. Once we, the patient is starting to get towards the aneuric renal injury, then we need to continue with fluid diuresis, but also consider the use of diuretics, which we'll talk about in a moment.
Once renal impairment has occurred, we need supportive management. So all of the other side effects that come along with renal impairment, we need to manage those. And then there's hemodialysis and peritoneal lavage, which can be successful in some cases, but it's not always financially or it's not always available to every, every patient.
OK, so let's move on to some nursing care. So we need to administer fluid therapy. First of all, we need to correct and normalise our intravascular volume.
The intravascular volume is what will improve the perfusion to the kidneys and will cause a norvolemia if they are hypovolemic from the polyurea that we mentioned. So they're PUPD and the polyuria is so profound that they will get a secondary dehydration. So first of all, increase that intravascular volume to improve the perfusion to the kidneys, and then afterwards we can start looking at looking at the more maintenance rates so that we can correct the dehydration as well.
First of all, it's that intravascular volume that is really important. We need to increase it and get the support to those kidneys. The most appropriate fluid therapy is an isotonic crystalloid like Hartmann's solution.
And take care when you're delivering such high volumes of fluid when oligura or anuria starts to creep in. So I would say when you're monitoring your ins and outs during this really vital and critical phase, I would say monitor the urinary output every hour because you need to make sure that you're correct in that fluid volume accordingly. It's not really.
It's not really going to benefit the patient to put them on a high fluid rate and leave them for 4 hours because these patients can change pretty quickly, and if they become auric after an hour of a high fluid therapy rate and you've still got 3 hours before you're checking it, you're going to start getting into other issues like over perfusion. So if you can drain that urinary bag every hour, once you've placed the urinary catheter and then match the ins and outs, it needs to be as frequent as that because these are very high fluid rates and it's a very fine balancing act nursing the acute kidney injury patient. And remember when we're looking, when we're thinking of cats with volume depletion, cats can become bradycardic with volume depletion.
I'm not sure on the mechanism of action around that, but if you keep it in mind, it's something that you need to be aware of when we're nursing these patients. So fluid therapy, when you look in a textbook, they say, oh, shock, shock rates really high. Don't, we don't ever administer the high volumes of shock rates in one go.
What has been shown to increase mortality and have a more successful outcome is smaller fluid bolus while reassessing the patient until the intravascular volume is restored. So what I would recommend is 2 to 10 mL per kg bolus depending on the individual patient and what you deem is necessary. You can start with 1, monitor the vital signs, as your heart rate decreased because, you know, if you are dehydrated and hypovolemic, your heart needs to pump faster to deliver the same volume to your body.
So as you correct that intravascular volume, your heart rate should come down, your respiratory rate should come down, your mucous membranes should become a little bit more pink if they're not vasoconstricted from if they're a little bit hoy. The pulse quality should improve. If you have if you can monitor blood pressure, the blood pressure should also improve and the patient's demeanour, as you fluid resuscitate the patients, often they will start to have a little bit of a brighter demeanour.
Obviously they are still very poorly since they're not going to come back to, you know, the normal bouncy self, but they may just be a little less, less dull and lethargic. If you give a bolus and it's not quite enough, you still think that they are volume depleted, give another one until you are satisfied with the clinical signs and the response to your therapy. And then once you've delivered the appropriate intravascular volume and you think it's restored, you can start to think about the appropriate maintenance fluid therapy rates so that you can replace those losses and that dehydration.
So in order to successfully monitor our patient's urinary output and effectively match what we're putting in via fluid therapy, we need to place an indwelling urinary catheter. And this should have a collection bag on the ends that we can drain every hour to calculate how much they are urinating. And then we need to weigh our patients twice a day to start with because these can this can give us a lot of information.
If our patient presents to us dehydrated hypovolemic, it's polyuric, and now it's caused that profound dehydration. We are made up of a large proportion of water, so our patient's body weight is likely to have reduced. When we've fluid restored them and we're we're happy that it's back to an adequate level, we should weigh the patients and that weight should then plateau as they get back to their normal stable state.
And then by weighing them twice a day or even more frequently to start with, that can tell us if our patient's body weight decreases just by fluid therapy. We may not be, we may be losing more fluids than what we desire, so maybe we aren't giving them as high a fluid volume as we should. And equally, if our patient starts to gain weight from our fluid therapy, we need to question whether the patient's urinary output is decreasing.
Are they becoming oliguric or anuric? And if so, we need to match that and reduce our fluid therapy so that we're not getting into the over perfusion realm. So body weight can actually give us a lot of information, a lot more than what you would originally consider.
So the normal urinary output of a cat or a dog is 1 to 2 mL per kg per hour. So if we're monitoring it hourly, we need to be calculating this hourly as well, so that we can make sure we're putting in what's coming out to prevent dehydration and more pressure on the kidneys. So Oliura is classed as 0.5 to 1 mL per kg per hour, and auria is anything less than 0.5 mL per kg per hour.
So this is when the kidneys fail to produce any urine and are now starting to, well, they're not producing any urine at all. So that is classed as aura, and that's what we want to avoid. So to put that into context, if you have a 5 kg cat, the normal ordinary output of a 5 kg cat, 1 to 2 mL per kg, is 5 to 10 mLs every hour.
That's normal. So if you measure the patient's urinary output and it's 15 mLs an hour, you know that that's too much. So 15 mLs divided by the 5 kg will tell you that the patient is producing 3 mL per kg per hour, whereas the norm is 1 to 2.
So the patient is polyuric, which is expected during the early stage. So then you need to match that fluid rate. So you need to, if it's producing 3 mL per kg per hour, they need to receive 3 mL per kg per hour, which works out as 15 mL per hour.
And then a really useful bedside technique, as I mentioned earlier, is the you in specific gravity. So this is a really great tool for us to assess kidney concentrating ability. It's quick, it's easy, it's cheap, and it gives us an instant result at the bedside.
Remember to always assess it alongside hydration status, and if the patient's hydration seems within the normal limits and you're happy with it, then it should sit in that isostenuric, or sorry, in the, in the normal range, so between 1020 and 1060. You may find that they are more dilute with this, and they tend to hover around the lower range or even lower than that range if they do have some active dilution with polyurea. Now if the patient does creep into the aneuric stage, we can consider diuretics.
However, the VPIS say that they're not very effective with lily-induced renal toxicity. The reason we would give diuretics or vasodilators may be given to aid with the excretion of those the waste products or the electrolytes that we mentioned, so your sodium, your potassium, your chloride, your water, and any waste products like your urea and creatinine, and the toxin as well. We want to, it can aid with increasing the renal blood flow or the glomerular filtration rate, so the flow that the blood and the the urine is flowing through those kidneys.
And it can help reduce the risk of fluid overload, although there is a very delicate balance here, we don't want to give too much or give it for too long because then all of that hard work that we're putting in to maintain that fluid balance, you can then end up diarrhezing out if you give too much of a diuretic, and then the patient can worsen because you've caused dehydration. And it's indicated if the urine production is decreasing. Despite matching ins and outs, however, the VPIS say that it's not very effective.
It's something to be aware of, but whether you use it or not is case dependent and clinician dependent. And then hyperkalemia or an increased potassium value often comes along with an acute kidney injury, and that can give its own set of clinical signs that we may need to treat. So a hyperkalemia, so an increased potassium value, can cause a bradycardia.
It can also cause arrhythmias and tall spiked T waves. Now the T waves, when I say tall and spike, they're usually at least about 2/3 the way of the height of the QRS complex, if not just as tall. And potassium luckily is one of the main electrolytes managed by fluid therapy.
So depending on how high it is initially, a lot of that may start to come down with your diuresis because we're about to give loads of fluid therapy which will diurese the potassium out. So that would be the initial treatment anyway. And it just depends as to whether you need to treat it.
It depends whether you're actually seeing the side effects of the hyperkalemia as to whether you, you deem it necessary. But generally anything less than 7 to 7.5, that is hyperkalemia, but anything less than that, we would say use fluid therapy rather than anything else.
Now patients who are seeing the clinical signs, and they are generally the ones whose potassium is elevated higher than 7.5 millimo per litre. You can see those cardiac effects and you can give calcium gluconate 1 mL per kg diluted and give that slowly IV over 3 to 5 minutes, and that will just stabilise the cardiac myocytes.
So those the cells of the cardiac muscle will just become more stabilised. However, it does nothing to the potassium value. It simply puts the patient into a more cardiac stable state.
So your, your potassium value will still be increased. So we know that we can get insulin to reduce potassium. But we know that insulin also lowers our glucose because it's a co-transporter.
So if you give insulin, your glucose will be sent into the cells and it will co-transport with potassium and send the potassium into the cells as well. Now we have a spike in our potassium, which is why we're giving insulin, but we don't have a spike in our glucose. So what's gonna happen?
We're gonna, we're gonna see a drop and we're gonna see a hypoglycemia. So it's really, really vital that we administer glucose in the form of a CRI alongside, and we monitor that closely with a glucometer to make sure that we are maintaining a normal glycemia after the . The administration of insulin and neutral insulin.
And then they are usually painful, so with an acute kidney injury, they may have abdominal pain and they may have a headache, they may feel really groggy, nausea, vomiting, diarrhoea, all of those things make you feel really terrible when you're poorly, and they can also come along with pain. There are many different, well, there's a few different pain scales available for cats. This is one of them, the Colorado pain scale, so we should be performing these regularly and providing adequate analgesia alongside.
These patients are often very poorly. They don't want to be up bouncing about in their kennel. They're often lay down and just stay in a very similar position.
So that's the perfect patient to link up your multiparameter machine while they're in their kennel. This will allow you to monitor any trends, any sudden changes you will detect instantly. And it allows you to be hands free.
You don't have to keep meddling with the patient. They won't build that association with every time you come near them, you're going to do something that's not very nice or might be painful. Link up if you have the ECG dots, you can tape them to the pole loosely and link up your ECG.
You can pop on a a blood pressure cuff so that you can monitor your blood pressure. And if you do have a thermometer probe, depending on the patient, they may even tolerate this with a cover on and some lubrication, pop it in rectally and just pop a little bit of tape on the tail so that you can keep that . Keep the monitor on the on the screen as well.
If they don't tolerate it or they find it stressful, then the temperature is not a big deal. But if we have a patient who's sat, they're still they're quite poorly, then we, we should ideally be checking it at least twice a day. OK, so just a quick recap on what we've covered and what we need to remember and what nursing things we can do with these patients because they are very intense patients to nurse, and they're great for us to utilise our nursing skills and our knowledge and put our knowledge to the test.
So 3 things to remember when it comes to the treatment of lily toxicity and an acute kidney injury, decontaminate, to get rid of any contaminants where we can, fluid diuresis to help the kidneys diarrhease those toxins out and to support the perfusion to the kidneys. And correct any imbalances or abnormalities such as your water imbalances, your electrolytes and your acid base balance as well. If the kidneys can't do it, you're in this critical phase.
We need to see if it's something that we can do and we can intervene and we can help. We need to place a urinary catheter, which we can do as nurses, an indwelling catheter with a bag so that we can measure what's coming out, and then we can match what's going in. Calculate your urinary output.
As nurses, we can do all of these calculations and present it to the vet each hour to make sure that we are keeping up with the renal injury and not doing anything that can worsen this patient's condition. This is a critical stage and we need to be on top of it with our fluid therapy. We need to remember that this can be painful.
They can have a painful abdomen and specifically in the area of the enlarged kidneys. They can also have almost a hangover effect, so headache, vomiting, diarrhoea, nausea, all of those things come with pain and feeling really, really poorly. So assess the pain score with a pain score that you have in your clinic and analges appropriately.
Don't forget about early enteral nutrition and enterocyte nutrition, because that's vital for any patient who is a long stay patient in the hospital. Consider the the placement of a nasogastric feeding tube in the conscious patient. That's a nurse skill.
We can do that as nurses. If it's undergoing an anaesthetic, then place an esophagostomy, long stay tube while they're under the anaesthetic. And then calculate your rest and energy requirements and remember to change it every day according to what the patient's new weight is.
So 30 times the body weight in kilos plus 70 will be fine for most patients unless you're under 2 kg, and then you can use a different calculation. And that early enterocyte nutrition is vital. We can also use the liquid diets that are available now, and we can even link it up with a syringe driver.
Draw the fluid up into the syringe, attach it to the feeding tube. Set the syringe driver to go in over 20 minutes or half an hour, and it can trickle feed in, which allows us to have our hands free to do the rest of the nursing care and to groom our patients. Remember to use your multiparameter machines if you do have them.
Again, it allows you to be hands-free and maintain that bond with the patient so that they don't become aversive to you going in. The patient is not going to eat on its own because they are feeling terrible and will do for some time. So this is why our our enterocyte nutrition and our nutrition that we can get in is vital.
And then finally consider the referral to a specialist hospital for an acute kidney injury, these really are critical patients. They require one on one nursing care and regular interventions. If you consider something like dialysis or peritoneal dialysis, that would require referral to an even more specialised referral hospital such as the RVC or there are a few of them around the UK.
So there are some options there, and we should consider the referral, especially if an acute kidney injury is present. And then finally we'll cover the prognosis of a lily toxicity, and this is completely dependent on dependent on how quickly the patient was brought into us in the clinic and how quickly we have responded with our fluid therapy and how effective our fluid therapy is. So if the fluid diuresis was initiated prior to any aura, so usually within the 1st 48 hours of ingestion, then it carries an excellent prognosis, which is great.
Even if we do get them over this initial injury and insult to the kidneys, and there's just discharge to go home, then a chronic renal insufficiency or injury is likely to result. So this will be a patient with CKD chronic kidney disease for the rest of their life. However, if oliguria and anuria does occur, then the guard, the prognosis is then guarded and fatalities have been reported, so some patients can sadly die from a lily toxicity if they are not brought into us early enough or if our sometimes even with the most .
Effective therapy, they will still go into this auric state, and sometimes it's too far for us to kind of bring back and correct that injury, depending on the volume of the toxin that the patient has ingested and when our therapy is started. So very varied. OK, so that's all from me.
I hope you've enjoyed it. I want to say a massive thank you to the Veterinary Poisons Information Service for providing so much really vital and up to-date information on lily toxicity. For us as veterinary professionals, we need to just continue to raise awareness to the general public, raise awareness to the owners of our pets, even if they don't have a cat, a friend might have a cat that they might buy lilies for.
If we do kitten checks, tell them about certain toxicities in those kitten clinics so that they can avoid buying these things throughout the cat's life, and we can just raise awareness. Things like social media are really useful. I have my own veterinary page, as you can see here, veterinary nurse medicine geek.
I'm on Facebook and Instagram, and I regularly post things about all things, internal medicine, including the likes of toxicities and your emergency medicine as well. So if you are on social media, please follow me and I hope you've enjoyed today's talk. Thank you very much.