Good evening everybody and welcome to a Thursday night members webinar. My name is Bruce Stevenson and I have the honour and privilege of chairing tonight's webinar. I'm sure that most of you are as keen to hear about AKI's as I am and all the latest updates.

Such an important topic for all of us. I don't think we've got any new members on tonight, so no need for detailed housekeeping. Remember, we'll carry on all the questions at the end.

Pop them in the Q&A box. And Chloe has kindly agreed to answer them at the end and enter into the discussions. So, Chloe qualified as a veterinary nurse in 2012, gained her ECC certificate in 2016, and a VTS ECC in 2018.

She has a strong background in ECC and referral nursing. She is currently the head of Priy emergency treatment services out of hours in Brighton, who also provide cardiorespiratory and internal medicine referral services. Chloe is also on the review board for the RCVS In Focus Veterinary Journal and is involved in peer review material for the Australian College of Veterinary Nursing ECC certificate.

She is highly experienced and passionate about all aspects of emergency and critical care nursing, but her specific interests include critical care patients with renal and septic patients being top of the list, followed by cardiorespiratory patients. Chloe, welcome back to the webinar vet and it's over to you. Thanks very much for the introduction, Bruce, and welcome everyone.

I'm really pleased that you could all join me tonight to talk about acute kidney injury. It's something, as Bruce just mentioned, that I'm very passionate about, and I think it's a lot more common than we might think, or, you know, we may already know that it is very common. There's a whole range of diseases, toxins, as well as iatrogenic causes, that can endanger our patients with acute kidney injury.

We'll come to that in a little bit. But first, what is acute kidney injury? So the way that we draw from this is we draw from human medicine, and their definition is abrupt and absolute, so AA.

So abrupt meaning within 48 hours, this injury occurs and the acute kidney injury pathophysiology begins. And then absolute. So there's an increased creatinine of over 25 milli litre.

And so these two together create the definition of acute kidney injury. This can be applied to both dogs and cats, and the injury can vary in acute kidney injury all the way through to acute renal failure, in our worst case scenario. But what does this mean in relation for our patients and how is this going to change our treatment plans?

So first and foremost, whenever I think about a disease process, I always really like to address the normal physiology, and this helps us to visualise what's going to happen to our patient, what systems are going to be affected, during this disease process. So what does the kidney do? Well, it's really a key organ to maintaining health.

If you think about a bridge going over water, really choppy water, the kidney is essentially that bridge. You know, if you didn't have that bridge there, you could muddle across, but you most likely die. And so because it's a key organ to maintain health, there's a lot of functions that it actually has.

So the one that we all know is toxin excretion, drug metabolization. So whilst the liver metabolises most of, medications, and toxins and stuff that come through the body, the kidney is responsible for some drug metabolization. And it is the main route for toxin excretion.

So if you think about that in terms of acute kidney injury, if it's not able to process those toxins, those toxins then build up in the body, and they're going to cause problems for your patient. It's also responsible for the maintenance of electrolytes and the blood pressure in the patient. And this is as a result of this, running angiotensin al deerone system.

So I'm not going to go into detail about that, system, but it's really important to know that, and that this is where electrolytes, you know, and solutes such as water, are passed through in the loop of the, and that the blood pressure is affected by that RAS system. So, without the kidneys, these patients would have a blood pressure all over the place, which obviously is going to affect blood flow to your other organs. And so if we don't have correct blood flow to say the heart or the brain, that's gonna end up bad for our patients again.

As we all know, it produces urine, so this takes the toxins away. It takes money away any excess electrolytes. Obviously, within that maintenance of electrolytes is the osmotic gradient.

Which also gets rid of excess water or, you know, retains water for our patients if they're dehydrated, . And so again, no production of urine is going to mean, that that backs up into our patient or those solutes aren't being allowed to be excreted, and bad news for our patient. And last but not least, there's a production of erythropoietin, as well as, vitamin D, And the production of erythropoietin is really important because obviously that's going to provide our red blood cells through the bone marrow for our patients.

So we'll come to in a little bit later. Obviously, erythropoietin, short term and acute kidney injury isn't going to be affected too much. In chronic kidney disease, we start to see, this cap on this production of erythropoietin, which is why we get, non-regenerative anaemia in these patients.

So next up, I'm, I want to go quickly over renal blood flow and glomerular filtration rate. I'm So renal blood flow compromises of approximately 20% of cardiac output. So that's around 1 litre per minute.

You can use a thick principle to calculate the renal blood flow. So you'll need the concentration of a substance both in the urine and the plasma. So this is why urine and creatinine are usually good measures for this.

And then glomerul filtration rate is the amount of fluid going from the glomerulus to the boneman's capsule per unit time. There's also a calculation for that, but I think for both of them, you don't necessarily need to be calculating these to assess whether these patients have good renal blood flow or good glomerullo filtration rate. What we want to aim for in these patients and in all patients is to continue to keep that renal blood flow consistent, which then in turn keeps that glomerullo filtration rate consistent.

And why really is this important, to know, because once our renal blood flow, and our glomerulcul filtration rate decrease, we begin to see these changes to the functions of the kidney that we've just talked about. These decreases, we'll also see changes in terms of, potential infarction or or ischemia, which we will see it will play a role in the pathophysiology of, acute kidney injury in a little bit. So really, it's really crucial to the maintenance of renal blood flow and er filtration rate to our kidneys.

And like I said, whilst we likely won't be measuring it directly, it really feels sensible to think about them, especially when we think about other disease processes. So, for example, trauma where we may have a large loss of blood, and this is in turn gonna affect your renal blood flow and then again in turn affect your glomerical filtration rate. The the renal blood flow and the glomer filtration rate is controlled by homeostasis, but under strenuous circumstances, such as a trauma, this system is going to begin to fail for our patients, and it's gonna put them at risk of acute kidney injury.

So as we've just discussed, and then as we can see in this nice little diagram, that on the left hand side, changes to the afferent arterial, So as a result of renal blood flow. Or a constrict vasoconstriction. So in terms of shock, you're going to have vasoconstriction, and that's going to alter your blood flow, to your glomerulus, and then in turn your glomerular filtration rate is going to go down.

And that's a similar thing for, you know, if you've got vasodilation, then there's gonna be again, there's going to be a change to the glomme confiltration rate. So let's look into why it's so important that this renal blood flow and glomerical fluctuation rate stays the same. We're gonna go through the path physiology of acute kidney injury, and then look later on at diagnostics and treatment plans.

So there's 3 categories of acute kidney injury, and we can split this into pre-renal, intrarenal, and post-renal. So pre-renal meaning that there's gonna be an alter alteration to the blood flow, before the kidney. Intrarenal, obviously, there's gonna be a change to, of the renal blood flow in the kidney and post renal effects, obviously after the kidney.

So you've got your ureters, your urethra and your bladder and that kind of stuff. We can break it down into 4 stages. First, we'll go through, The pathophysiology and we'll break it down into the four stages that Iris have come out with.

But primarily really what it involves is any interruption to the renal blood flow. So whether this is through a disease process, a toxin, ingestion, you know, iatrogenic, change. Really, all of them ultimately are going to cause a change to that renal blood flow, as we've just talked about, will then decrease that glomerul filtration rate.

So first of all, we have this interruption to your renal blood flow. And then once it's altered blood flow, you're obviously not getting blood to your kidneys. And because of this, there's gonna be a degradation of adenosine triphosphate, so ATP.

Into adenosine diphosphate, so ADP, and then further into adenosine, monophosphate, so AMP. So then this is then further, if there's still this interruption to renal blood flow, there's then gonna be a further breakdown into adenotine Ade nucleotides. And then at this point, once they're broken down to these nucleotides, they can't go back.

So if you were to keep it, adenosine, monophosphate, then these could regenerate and become ATP again. But once we've got down to these nucleotides, this regeneration isn't gonna happen. And this is where the damage really starts to happen.

So because of this lack of ATP, structural changes begin to happen, and this could be due to cell apoptosis, which is a programmed cell death and that occurs in, multicellular organisms, and, and this could just mean like cell changes, such as cell fragmentation or death of the cell. And because of this structural change, And this cell death, we get an increase in intracellular calcium, and because we have this calcium there, this is then gonna cause further cellular damage. And as a result, decreased activity, of the sodium, potassium ATPA's pumps.

And we think as well, we don't have the ATP and these ATPOs pumps aren't going to be working anyway. So again, this then leads into further demise for our kidneys and we get ischemia, necrosis, and optosis and begins to happen to this renal tissue. And once you get to this point, this ischemia and necrosis within the kidney is then going to cause this further altered blood flow.

So you go back to this one and you go back into cycling. It's a really vicious cycle. And this is why we then break it down into 4 stages, because there's a crucial stage at which we want to try and catch this, and reverse it.

An acute kidney injury, can often be reversed, with little to no, sort of remaining effects. Unlike chronic kidney disease, you know, we're not gonna, completely cure them, whereas at AKI we can de-stage them, and hopefully, they'll have, you know, little to no changes that are going to affect them in the future. So, we can further break down this, process and these recognisable stages, that we see in practise.

These stages have been developed by, Iris, who have also developed biomarkers, for their official stage in which we'll look at in a second. But so stage one is this initiation phase. So this is your, right after your insult.

So let's say your patient has a trauma and, a major haemorrhage. This is gonna cause them, to have this altered blood flow. So this is stage 1.

Stage 2 is once you get to, this. Nucleotides, and into these ones into, you know, this breakdown, and start of necrosis of this renal tissue. So you get ischemia, hypoxia, inflammation, and cellular injury.

And it's in this phase, that we might start to see our patients, stage one unless they have, you know, unless they have something like a, a major haemorrhage, you know, if it's, something that the owner hasn't noticed, Then it's unlikely that they are going to come in at stage 1. Stage 2 maybe because we might see, start to see some signs, some clinical signs, but often when we see our patients, it's in stage 3. This is the maintenance phase.

So this is the damage that's already done, potentially, there's more damage being done, as I talked about. There's a vicious cycle. But really, we call this the maintenance phase because at this point, the kidneys are injured.

And this is the phase that is crucial for us to try and minimise the time in this stage. So the longer that they're in stage 3, the less likely they're going to fully recover. So this can last from days to weeks, .

We often see azotemia angioremia, with these, and potentially these patients are going to be ole uric and auric. And this is why we often see these patients in, because the owners have noticed they're not drinking or they're drinking more and they, Not urinating. And so as I've said, this was a really crucial stage that we're going to be treating our patients in, and we'll go through the treatment plans.

And stage 4 is then we lead into recovery. A, azotemia is going to improve. At this stage, you might get marked polyurea, because of the, lack of urination.

Once you rehydrate these patients, and get them back on track, they often, have a, post diuresis. And as I've said, it may return to normal or there may be some residual damage. And this definitely depends on how long these patients are in stage 3.

If we can catch these patients in stage 1 or stage 2, then there's likely going to be no, you know, no residual damage. So as I've talked about, there's the Iris, acute kidney injury grading scale, so it's 1 to 5, and this is for dogs and cats, and it's based on the faster blood creatinine, as well as urinary flow rate. They have started to look into S SDMA as well.

But there's still a work in progress, and the whole actual scale is still a progression of development, because they, they're still researching it, it's not as well established as the chronic kidney scale. But what it's really there for is just to help, given an appropriate prognosis of these patients, and also to give a measurable scale of improvement or deterioration. So What they do hope to do is to include recommendations for testing, for treatment and for monitoring, to sort of mirror those irri guidelines for, chronic kidney disease.

So this is a nice little table that I got from their website. It's easily and readily available, but it just goes through the different, stages, the different grades, and the blood creatinine. So remembering this is just a fasted, creatinine as well, and then just a nice little clinical description.

Where these patients slot into. So it's useful to have, as I said, it's a it's an objective, way of measuring whether your patients are getting better as well. Now we're just gonna go over common causes, .

And as I talked about, they can be split into pre-renal, intrarenal, and post renal. So I really like whoever drew these diagrams. They're very nice.

I found them on Wikipedia. But, as I said, relates to anything that causes decreased blood flow, and that could be. Maybe from absolute absolute loss of fluid, as is demonstrated in this diagram on the left-hand side.

And as I've talked about, this can range from sort of your major haemorrhage to burns, vomiting, diarrhoea, even, you know, if these patients have had, large volumes of, diarrhoea or vomiting over a short period of time. So as we talked about that, acute episode is in within 48 hours. Then these patients are going to be at risk of absolute absolute loss of fluid.

And so as that suggests, you lose fluid, this is going to decrease the amount of volume and, and therefore you, decrease your renal blood flow. And often this is because of shock, and that kind of stuff, . Or we can have relative loss of fluids on the right-hand side over here.

So your body fluid is going to be exactly the same, but it's just going to be redirected elsewhere. So, as I've just talked about a shock, you know, you have distributive shock that, you know, it's gonna send the volume of blood that the body has to where it thinks it needs to send it. And more often than not, this is not the kidneys.

And again, congestive heart failure, it has the blood there, but the heart can't pump, pump the blood. I'm Other causes of pre-renal, changes of blood flow, so pre-renal, acute kidney injury. The most common one that we'll often see in practises is non-steroidal anti-inflammatory, so NSAIDs, such as Metaca.

And whilst these are COX-2 inhibitors, you know, once, you give a large overdose of these, they become non-specific, so, so they can cause prostaglandin inhibition. And so as a result of this, it's gonna cause vasoconstriction to the renal blood supply. So even just one overdose, for example, in Metam, and Marxam Bohringer actually suggest any overdose that these patients have put on fluids, and it's treated as, you know, you know, as a, as an overdose.

And that's because it's such a high risk of causing acute kidney injury, that You know, if you know that you've given an an accidental overdose or the owner is given, you know, 2 doses in one day or something like that, that you already know that this patient is potentially going to be in stage 1 or stage 2. And at this stage, you know, at these stages, it's quite easy to reverse that damage, and whereas if we leave it, we obviously get into stage 3 and potentially a long maintenance phase. Another cause of pre-renal Acute kidney injury is ischemia, so this may be a reduction of blood flow to somewhere else.

So when we talk about that, we could talk about thrombosis, neuralists and nephrolis. I've put them here because it kind of comes under this umbrella, but actually they are intrarenal and post-renal. But when we think about, ischemia, we often sort of neglect to think about septic patients, and especially the ones that are secondary to pancreatitis, because these really fit into this, vicho's trial.

So there's an altered blood flow, there's potentially endothelial injury in these septic patients. And as a result of this, we got a hypercoagulability, so there's potentially going to be, you know, throm thrombosis in either the you know, in, in veins or arteries surrounding the kidney or within the kidney itself. And so there's also a mismatch of this oxygen supply and demand, especially in these septic patients, and this is going to result in hypoxia, altered waste removal, and therefore accumulation.

And as a result of this, ischemia, the tubules undergo injury and if it's severe, then, you know, death by optosis or necrosis is gonna occur too. There's been recent studies as well, that have shown that SDMA is a really great biomarker for sepsis, and I think this is because it's such a huge risk, risk of, acute kidney injury in our septic patients. So as well as, CRP, SDMA sort of up there as one of the biomarkers to to assess, recovery in our septic patients.

So I think it's important to remember that, when we are looking after our septic patients that they are high risk, of acute kidney injury. So again, one of these wonderful diagrams, and this one sort of shows how tubular necrosis, so within the kidney, will cause a backup, in pressure. So if we talk about the renal blood flow, and this is now going to be altered, and whilst your, gluerical filtration rate might increase, there's going to be little to no exchange of those solutes that we talked about such as potassium, urea, and then there's going to be a low output of urine due to this lack of filtration, and lack of osmotic gradient.

So as a result of that, we get this azotemia that we've been talking about, that's present in our, patients. Medications that are Intrarenal toxic, so the nephrotoxic in our patients. There are a wide spanning range, cisplatin, so it's a chemotherapy medication, and that is really well known as being nephrotoxic, and often these patients, if they're having cisplatin, will have concurrent, fluids as well, with them.

And it's because it causes renal damage through oxidative stress. It causes DNA damage, and inflammatory responses. So all three of those are going to contribute to altered blood, blood flow, as well as, Altering, you know, oxygen available to those cells and so therefore cell death.

So as I've said, we should monitor these patients preemptively, you know, monitoring their renal profile before we give them this medication to make sure that they're stable enough to give it, and providing, you know, diuretics, potentially and, and also adequate intravenous fluids. Other medications that are well known, so aminoglycoside, antibiotics, so gentamicin, being, the prominent one. And it binds to weak proteins, and it's excreted through, glomerular filtration.

Cic sites, in the tubules bind to gentamicin. It also inhibits the phospholipases, which then they accumulate and this is going to cause, inflammation, . And lack of filtration.

As well as I'm often Medications will often bind to phospholipases. I'm And they, they also cause introduction of myeloid bodies, which results in tubular necrosis. So we think of myeloid, bodies, they're gonna cause, inflammation to the kidney cells.

Other substances that are nephrotoxic, tricyclic antidepressants, As well as other antimicrobials. So in penicillin, tetracyclines, like quinolones, or froquinolones, you know, even diuretics can do, appomorphine. Vitamin D analogues, and doxorubin and acetaminophen, so paracetamol and cats especially.

So causes that we see, commonly from, owner's perspective, you know, from the home environment, lilies, obviously in cats, it's, Not known fully why and they're nephrotoxic, it's sort of thought to be the crystals, but the whole plant is toxic to these animals to cats, and not just the stamens, so the leaves as well. And I think, we still see quite a lot of those. I think it is starting to become more common knowledge but it's also, you know, just educating our pet owners on, you know, toxins, you know, common toxins to them.

Grapes and raisins again, it's something we see really commonly, most commonly in dogs, again, not really known why the pathophysiology, but it is known to be nephrotoxic. And as with lilies, you know, there's no, there's no minimum toxic dose, it's a wide range. Ethylene glycol, so antifreeze.

I think we're seeing this less and less nowadays. I think, the public, the general public are a lot more aware. I've been You know, that, that really, it's, you know, sort of a death sentence for, for pets, really, if they have ethylene glycol.

And the way that this is toxic to our patients is that, you know, produces calcium oxalate, and as well as oxidotic injury, so this can cause intrarenal and post renal, acute kidney injury. So further on to infections and diseases that we might see as well, pyelonephritis, I think being more common than leptospirosis, but it, I think as well leptospirosis gets forgotten about, but, it, you know, this causes an inflammation to the kidneys, . And, it's then gonna cause this decrease the blood flow.

And pyelonephritis, you know, we've got that perent material, and we've got, And we've got inflammation. So on the right, actually, that image is like a dog that had pyelonephritis. So as you can see, it's very hyperchoic, the structure is not normal.

So then in turn is obviously gonna cause altered blood flow to your kidneys and not allowing those toxins to come out. You know, intrarenal, infections and diseases, often kidney infections are gonna affect it, and both this can then lead to urethral obstruction, which is then gonna lead into your, post renal acute kidney injury. So this is anything past the kidneys.

So you've got urethral obstruction, you might have, urethra obstruction, which is very painful for these patients. Urethrals tears, and blocked bladders, and your abdomen's due to ruptured bladders. All of these are classed as post-renal acute kidney injury, and I think this sort of section of acute kidney injury sort of gets forgotten about because it's often dealt with and, and we don't think too much about the kidneys, but we have to really consider, that these patients are high risk of acute kidney injury.

So Let's talk about the clinical signs and then the diagnostics and treatment. So the clinical symptoms are sort of what we talked about them being oliguric, and auric, so. Often these patients are going to be coming in potentially straining to urinate, you know, frequently looking like they're going to urinate, not passing anything.

They may not be urinating at all, and not trying. In some instances, they may be polyuric, it's very rare, to see them. In with polyurea, but it is, you know, it's possible.

And so it's just important to remember, remember that. Often these patients are going to be dehydrated, and very lethargic, you know, there's Toxins going to be building up in the body. They may have hypersalivation, they may be collapsed, you know, they may have shock as well as dehydration.

Often these patients are going to be vomiting, due to the toxins build up, due to the azotemia and the uremia, as well as diarrhoea cause obviously this is going to upset the gastrointestinal system as well. And then obviously later worst case scenario, and we may have these patients having seizures, due to the buildup of, blood, urine and nitrogen. So how do we know the difference between, how can we tell the difference between between acute kidney injury and chronic kidney injury.

So the way that I like to think about this, is, if you think of acute, we mean it as an acute cat. So, chronic cats are not cute often. They may be to the owners, they may, you know, they may be very sweet cats, but, you know, often they've got scarf, they've got awful fur, they're skinny, you know, they, they don't look cute in, in a, Stereotypical cute if we, you know, if we're bagging everything into one thing.

Acute ones are cute because it happened so quickly, it hasn't had a chance to change their physical appearance, . So this is one telltale sign. Since your physical exam, you know, often like I said, these, these cats haven't lost lots of weight, And you know, it's going to be very short-lived.

History is important as well. You know, taking history for any potential toxins that they're exposed to, medications that they're on, preexisting conditions that they already have, as well as, you know, how, what is the timeline for this illness. Has this patient suddenly become ill, you know, in the last couple of days or weeks, or is, has this patient been unwell or losing weight slowly or, you know, drinking more over a longer period of time?

Renal sizes again can be an indicator. So often in our chronic cats, we have really shrivelled up little raising kidneys, whereas with, acute ones, often they will swell and they're really painful, and they're quite easy to palpate, . And so this is what we're kind of looking out for when we find acute kidney injury cats or dogs.

And as I mentioned before, non-regenerativenia. So chronic cats with that production. Eerythropoietin, .

And I'm The And that's going to cause a non-regeneration, so it's not going to allow any regeneration of red blood cells. This, that means that acute kidney injury, the regenerative anaemia, is more likely to be, The difference between these two cats or dogs. So what are our diagnostic biomarkers?

What are we going to use to assess whether these patients are getting better, assess how sick these patients are? So, complete blood cell count, so your haematology, as I said, often you'll see an anaemia, you may see a neutrophilia, especially if these patients have got inflammation or infection. And we can do blood smears to sort of assess whether this is regenerative or non-regenerative anaemia.

Biochemistry, most importantly, what we might see is increasing, that urea, increasing creatinine. Often we'll see an increase in potassium because we think about the solutes aren't going to exchange, and whereas often the potassium is excreted through the urine, this isn't going to be able to happen, and you're going to get an increase in potassium. So as I said, with chronic cats, this is gonna be the opposite.

Often, often you get a low potassium in your chronic cats. You might have a decrease in total proteins, as well as a decrease in calcium. But this may be different, if we're talking about certain drugs that we talked about earlier that there may be an intracellular calcium, so your ionised calcium might be increased.

So acid base, so if you have access to blood gas analysis, then you can assess whether you, you have a metabolic acidosis or alkalosis, and the reason why we're gonna have this acidosis, It is because the kidneys are a buffer system within this acid-based balance. So you often, because of the buildup of potassium, and the lactate as well, you get this lactate acidosis. Which then will further cause a metabolic acidosis.

Urinalysis is obviously really important, during the dipstick and a urine specific gravity. You know, you may have eyes in the uric, they may, obviously not be able to concentrate the urine, or Maybe the potentially it's gonna be protein urea, or glucose urea cause, you know, these kidneys aren't able to philtre properly, so there's just gonna be stuff coming through the urine that isn't normally filtered. Urine culture and sediment, I think, it's useful, to exclude any potential bacterial pathogens, and identify an active sediments.

So, you know, identifying whether these have got rewrite crystals, calcium oxalate crystals, you know, if there's any sediment, if there's any blood, this can really help, with your diagnosis. Radiographs are really important in these patients, so we can identify, urinary calculi, as well as looking at how big those kidneys are. Sorenomegaly, and this might indicate conditions sort of, such as renal lymphoma, .

Utter obstruction, which might cause hydronephrosis. So as we talked about, urethral obstruction is really painful for these patients and they get a backup and these kidneys become large and really painful to touch. And ultraography is really useful as well in these patients, not only so that we can measure the renal pelvis, and sort of Mark that as we go through treatment, but also measuring the bladder size, especially in the first stages of these patients if they're aneuric or oliguric, you know, trying to assess the difference between the two sometimes, you know, you may, you may have this patient on fluids for say 8 hours.

How do you know whether that fluid is having any effect if that cat or dog is not urinating? So by measuring the bladder size on the ultrasound, so you measure, width, by height, by, length, so you just need two views for that, and it's. Really easy and simple to do, but you can measure the actual volume within the bladder.

So you can measure whether that fluid is actually having any effect on your patient, whether they are producing urine or not. And they might not be urinating, but at least they're doing that. And we'll come to other ways that you can monitor that, but I think this is the most objective way that you can do it, and it's a really good diagnostic biomarker.

I'm So Our main objective when we treat an acute kidney injury, is not to treat the acute kidney injury directly itself. So it sounds a bit backwards, but what we want to do is we want to be providing, we want to be treating the primary disease, And all the underlying disease, as well as providing support. So we'll talk about the supportive treatment in a second, but what we really want to consider when we have this primary disease, you know, do they have an infection?

Do they have an obstruction for the infection, are they going to have antibiotics? You know, obstruction, are we gonna deobstruct them unless it's a urethra, obstruction? Are we gonna refer them that?

You know, have we, do we know that they had a toxin exposure? What's that toxin? Is it reversible, you know, are we giving misoprostol to, To our patients that have had non-steroidal anti-inflammatories.

And you know, is this an acute on chronic episode? Is there a history of a chronic kidney disease? And these patients have potentially had no access to water, and now they, they're having, or they've, you know, they've had an altered blood flow because, You know, they've, they've had a different disease or they've, you know, potentially, got this now acute and chronic situation.

And also is a concurrent heart disease because this is really gonna affect our, treatment plan. You know, it's concurrent heart disease. How bad is it?

What, you know, what are the limitations of that heart disease because we're going to be giving these patients fluids. We want to give them a lot of fluids. And at this point, It's kind of a, you know, between the devil and the deep blue, that, you know, you pretend, you want to treat that acute kidney injury because it is a key organ to maintaining health, but potentially you're gonna push that heart over the edge, and give them, pulmonary edoema or heart failure.

So, fluid and electrolyte considerations, this is like the mainstay of treatment for our patient. There's really lots of factors, . To considering these patients, but primarily we want to restore the loss, if they've had a loss, as well as we want to increase that urine output.

We want to correct the acid base, we want to correct those electrolytes because these in the short term, are going to be the factors that could kill our patients. You know, long term, this acute kidney injury left untreated is going to kill our patients, but short term, you know, if these patients have got a severe metabolic acidosis, they're going to die. So we need to consider is a shock or dehydration or both.

Obviously remember the two are very different. Shock, needs an immediate, replacement, whereas dehydration needs a little longer, you know. What type of shock have we got?

Often there's an obstructive shock and we talked about that potentially is going to be a distributive shock, . And if it's a distributive shock, how are we going to address that, you know, do these patients need antihistamines, And thinking about the concentration of urine, if your patients will be concentrated urine, Or really dilute urine already, you know, just remembering that we're going to be giving this patient more fluids and it's become even more dilute. I'm So thinking about as well the fluids that are being administered.

So considering the type and the volume, so we potentially we could give a hyper hypertonic, bolus to our patients, but if they're dehydrated, you know, we want to be replacing the losses, . You know, do we want to be giving these patients bolus of fluids when they come in? Probably yes.

You know, getting blood pressure to a normal level. We really want to be optimising that blood pressure in our patients. So really getting over that systolic of 90, .

Millimetre of mercury as a minimum. And you know, thinking about what's in your fluids. So, you know, this, you know, these patients potentially have a high potassium.

Hartman's is probably the best solution, as a crystalloid, whilst it has like, you know, traces of potassium in it, it's, you know, It's an alkalizing fluid, so we want to give an alkalis fluid to our metabolic acidotic patients, whereas saline is gonna be it's, you know, it's an acid fluid and so potentially gonna be making that worse. So, Hartman's is probably the, the one of choice. You know, we want to reduce our sodium overload, as well.

And then just monitoring our acid base, you know, monitoring our electrolytes, making sure that these are coming down. So serial monitoring of sodium, potassium, calcium, phosphate, And as well as this, you know, that we think these patients are, are having diuretics. We'll come to this in a little bit, but .

You know, what we want to think about is, that these patients are well hydrated before we, even consider giving them diuretics or Manitol. I'm So we talked about the urine output. So these patients, as I said, are gonna be alluric or auric potentially, and they're gonna need this therapy to increase his urine, urine volume and encourage his output.

So when we're thinking about what we're doing, We're giving these patients fluids, but so the urine flow might increase, . But your renal blood flow may still be affected and your American filtration rate and not, you know, these are still going to be decreased. So you might Overhydrate these patients and it's a real risk in our patients.

And this is why central venous pressure monitoring, is the gold standard, for monitoring our fluid input because, you know, we can measure, the response to that, the intravascular volume status. And the way that we would do this through a central line, if you are going to send your patients off referral for, you know, For dialysis, then it's probably best to avoid putting a central lining because they're gonna do that for the dialysis. So As I've just said, providing these patients with this excess fluid.

So if they're not, if they're oliguric and they're still not putting that fluid out and you've hydrated them, you know, you've calculated your dehydration plan, you've given them the right amount of fluids that would take to be, to take the patient to, what would normally make these patients ebulimic, . This might send them over the edge, and this is going to cause some pulmonary and cerebral edoema, potentially. So we want to be monitoring for neurological changes, as well as obviously listening to lungs, frequently.

So this really I'm talking about, When we're talking about monitoring the urine output and preferably the central venous pressure, but you know, blood pressure, you know. Non-invasive blood pressure is fine as well. We want to be monitoring these if we're going to start giving You know, diuretics, so you can give riseamide, so CRI or sequential dose and often what we'll do in our hospital is a CRI, a very low dose CRI, concurrently with fluids, and this is after your patient, you know, after you've tried, 24 hours of fluids and your patient's still aneuric, you know, you've hydrated that patient and now you get to the point that, you know, the bladder is not, The bladder is not increasing anymore.

It's increasing a little bit, but you're not getting that urine output that you want. You can start to think about roamide. Obviously ACG monitoring as well, if we're thinking about, Our electrolytes and things like that.

If we've got high potassium, we want to make sure that we're monitoring, make sure that he waves are still there and giving calcium gluconate as a cardio protectant, before we Get that potassium down. Once these patients are hydrated, we can consider Manitol bolus. And so we can give potentially, a 0.25 to 1 grammes per kilogramme, slow bolus over 10 to 20 minutes.

So remembering that Manatol needs to be at room temperature, you know, no crystals present in the, in the fluid. It needs a heinate philtre, and it just needs to be given very slowly. And there's such a High risk with Manitol, and that this is really sort of a last ditch attempt as well as sort of renal vasodilators and, and Iotrope.

So, for example, a dopamine low dose, and given in conjunction with frusamide to sort of push that fluid out. I think if your patients are getting to this sort of point when you're considering this, you know, your vasodilators, and your and your on onotropes, you might want to start thinking about referring these to have dialysis, because potentially it's too late for these patients. But as I've said, blood pressure is really essential in monitoring these patients, often become hypertensive, this might need, treatment.

and so because The treatment is really limited in these patients because a lot of anti-hypertensive medications sort of only available orally, and a lot of these patients are vomiting so sort of precludes this, . But this is why then we need to go through to gastrointestinal considerations. So nutrition is really key to the recovery from acute kidney injury.

Most of these animals are gonna have reduced appetite, as, as mentioned because of the vomiting, and they're gonna be in a state of negative nutritional balance. And so they really need this protein and energy to regenerate this damaged tissue. We can place feeding tubes, and often it's really handy because then obviously you can get these oral medications in and you know that this patient is then gonna be, you know, is gonna be receiving fluids, especially in your patients that have got cardiogenic disease, you're then decreasing the amount of intravenous fluids that you need because you're providing fluid, you know, via the gastrointestinal system as well.

I'm And So, what we really sort of aim for is that we want high quality protein, but low amounts of it. So 2 to 2.8 grammes per kilogramme per day for dogs, 2.8 to 3.8 kilogrammes grammes per kilogrammes per day for cats, Obviously, especially with cats, we really need to be considering refeeding syndrome.

So this patient been completely anorexic for more than 4 days. If so, we don't want to be, you know, we don't want to be shoving food in the, in the, you know, whacking it in, in the hopes that we're going to get this patient better because this is going to cause more problems with the phosphate, you know, with an increase in phosphate. So we really want to be careful with this, and creating, you know, low feeding plans.

You know, if these patients have been anorexia or they've been picking, obviously introducing that nutritional feeding plan, at a quarter of a time. Because these patients are nauseous or vomiting because of this emia, centrally acting antiemetics such as Murroetin and or Dansetron, and Danstrom IV is really expensive, often I'll find, but the tablets work really well. But as we just said, if they're vomiting, they're not going to have those.

So if they've got a feeding tubing, great. If not, mirropotin works really well, and once these patients then have that mirropotin on board, we can start to give them on Dansetron. .

Because it is, it works really well. Metoclopramide, so a dopamine antagonist, can be given. I really recommend it as a constant rate infusion.

There's been a lot of studies to prove that it, you know, it doesn't really do much, as a bolus, and if these patients are on fluid, we've checked that there's no obstruct you know, gastrointestinal obstruction. This is really gonna help with gastric emptying, and, you know, prevent this regurgitation or vomiting. Proton pump inhibitors, so omeprazole 0.51 to 1 megs per cake per day.

You can give it orally, but also you can get an IV. It works really well, IV, you can give 1 MB per cake, twice a day. And this really works just when, you know, for inhibiting, The I'm The proton pump inhibitors, so it inhibits gastric acid and being so acidic, and therefore, if they are vomiting, it's not gonna be as bad.

Or histamine to receptor antagonist, Which is gonna inhibit the gastric acid production as well. And for metadine or anitidine, 5 megs per kg or 8 megs per kg, respectively, per oral, 3 to 4 times a day. Again, you can get this IV.

I've been to a lecture recently where they suggested vanistine as well as the CRI works really well. But personally, I haven't seen this, done. Pain relief.

So acute kidney injury, as I've said a couple of times now, it's really painful in our patients, and we've got to consider as well these patients are gonna have concurrent diseases. So sepsis, potentially osteoarthritis in our older patients, or pancreatitis, all of which are gonna need pain relief. So as we talked about, non-steroidal anti-inflammatories, .

A sort of a no go in these patients because we've already got this reduced blood flow. We don't want to be creating more problems for them. And ketamine use as well, and that's just because they're sympathetic effects, so vaso constriction and potential with this ketamine use.

So these kind of roll those drugs out. You may be able to use low dose ketamine, but it's probably, not, not useful in these patients. Acetamine offence or paracetamol in dogs works really well if they don't have any, preexisting liver disease.

I find IV paracetamol, 10 mg per kg, twice a day, every 12 hours works amazingly. Obviously, never ever give it in cats. It's toxic.

We don't want to be causing more problems, but definitely for dogs, I think it is an underused drug, That is readily available, it's cheap, and it works really well. I'm thinking about fentanyl patches in these patients, you know, if we're not, if we're thinking about trying to get them home. Or, you know, long term, we might, you know, if these patients got osteoarthritis and we just want to make sure that this acute kidney injury is gone, putting fentanyl patches on them works really well.

Gabapentin, again, cats and dogs, It's, I wouldn't use it on its own, but definitely in these patients it's definitely a good adjunct for pain relief. Tramadol, again, it's, it's OK. I think I'm in combination as a multimodal plan, you know, for these osteoarthritis patients are going to be, you know, as a potential.

But in these ones, we might be doing CRIs, you know, so. Potentially fentanyl or, methadone. Lidocaine in dogs, an ML, CRI, they work really well because you can just taper them, backwards and forwards, as, as and when needed, .

And just making sure that these patients are not painful, you know, really listening to I'm watching the behaviour and pain scoring them so you've got more of an objective, . Score for them, because pain scoring is, you know, essentially is subjective, but I'm just making sure that you and your team pass from team to team, how you've been scoring them, what system you've been using, what behavioural changes you have noted as being, a painful, Observation, because obviously some people take one behaviour as being painful, whereas others don't. So, I think it's really important to remember that.

So treatment ceremony summary, so as I said, we prevent any further toxin exposure, I'm using antidote. So I just put down here because in humans, they have, it's actually, Diuretics, ACE inhibitors, antibiotics, and in humans, it's metformin, and then NSAIDs. These are things that we consider toxic to the kidneys, but obviously, we don't use metformin that often in animal patients.

So I've changed it to metabolic. So, for example, sort of chemo or, metabolic changes, Or you could just call it done. I'm back just in case anyone has any questions.

Yeah, well, thank you very much for your time tonight and thank you for sharing all your knowledge with us. It was very, very much appreciated. I do have one question for you.

The question, I'll just read it to you. It says a male 5 month old cocker spaniel was given a 5 times dose of loxicon. What do you recommend as treatment?

So as we've talked about with these, these patients are gonna need to be on fluids, a 5 time dose, potentially you're looking at, wanting to send them for, dialysis. I have seen them in practise. We give mesoprostol, so I can't a cytotech is, I think, is the brand name, so Mesoprostol, definitely, the problem is obviously given that, you've got activated charcoal, you, .

If, if it was an oral dose, often people give activated charcoal, but I would say that the mesoprostol in this case is more important. It is a cytotoxic drug, so just making sure that obviously it's handled with gloves, but, I think this is really key to the treatment and epsinulalcrate, in these patients is really important as well, I think. So really, hard going on the gastrointestinal support as well as the renal support.

But I think definitely having these patients, you know, that patient in on fluids for at least 48 hours I would say, and just monitoring the urine output. I think the big advantage in those cases is that most people that do it straight away, so you're getting your AKI in phase one or stage one, which is really a huge, that's what it's really, it's really handy to know, you know, like it happens in practise all the time, you know, things get given accidentally twice, or, you know, owners realise that the, you know, the wife's given the dose in the morning, the husband's given. The dose in the evening, you know, it's easily done.

But at that stage, you know, you already know it's happened. You're catching that in stage one or stage 2, so you're in a really, advantageous position to, you know, to give even just 24 hours of fluids, and, you know, in this instance, mesoprostol to, to reduce those chances of having, acute kidney injury or having any long lasting damage. And then just monitor your bloods, obviously, that's a great and your urine output.

Mhm. Yeah. Definitely.

I'm, yeah. Good. Chloe, thank you so much for coming back on.

I really, really do appreciate that. And you missed me, thanking you to the audience for all the time that you've spent with us tonight and the knowledge that you have imparted. So thank you for that.

No worries. Thank you very much for inviting me. And folks, thank you all for attending tonight and look forward to seeing you on the next webinar.

From myself, Bruce Stevenson, it's good night.