Feb. 19, 2024

#114: "The Kidneys Are Not Toilets That You Can Flush": New Thinking On Managing Nephrotoxin Ingestion In Veterinary Patients. With Dr Corrin Boyd and Dr Leonel Londoño.

#114:
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Season 1

The puppy that ate the box of NSAIDs, the lab who found the bag of sultanas, cats and lilies - you know what to do: whack them on twice maintenance fluids for a few days to flush out the toxin and protect the kidneys, right? But wait. Have you ever stopped to think about HOW IV fluids increase toxin excretion? What if we told you that it DOESN'T?!

In this episode critical care specialists Dr Leonel Londoño and Dr Corrin Boyd explain why the standard approach of fluid therapy for nephrotoxin ingestion in veterinary patients not only doesn't make any sense, but can actually be harmful. We recap renal physiology and discuss a better plan than having a healthy bouncy patient on fluids in your hospital for 2 days.

Dr Corrin Boyd is  a registered veterinary specialist in emergency medicine and critical care who works and teaches  at Murdoch University in Perth, Western Australia, and Dr Leonel Londoño is clinical assistant professor of emergency and critical care and director of the hemodialysis unit at University of Florida. His research interests include renal and non-renal applications of extracorporeal purification techniques, endothelial and glycocalyx pathophysiology in the critically ill, and hospital-acquired acute kidney injury. 

 

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I once heard a story about somebody who was watching her husband cook a lamb roast.She watched him go through the process of salting it and putting all the herbs on and everything.And then just before he put it into the dish that goes into the oven, he chopped off the last 1015 centimeters of the roast and put that chopped off piece of meat next to the main roast and then put the lid on and put it in the oven.
And she said, I've been watching you cook lamb roast now for the last 15 years and every time just before you put it in the pot, you chop the end of why do you cut it off?And he said, I think it's something to do with the moisture content in the roast, but I'm not 100% sure.
But that's how my mom did it.So now this lady's fascinated.So she gets on the phone to mom in law and she says, listen, I just watched Dave cook a lamb roast and chop the end of the lamb roast like he does every time before he puts it in the pot.And he says he does it because that's how you did it.
So please, can you tell me why?Why do you chop that end off?And she says, I I'm pretty sure it's to do with flavour, penetration into the the bulk of the glamorous.But really, actually, I'm not sure because I just do it because that's how my mom did it.
So now they're both fascinated.So mom in law puts the phone down, gets on the phone to her mom, and 10 minutes later she phones back the daughter-in-law.She said, I just spoke to my mom and she said when I was growing up, when I was a kid, the casserole dish, the pot that she had for cooking lamb roasts, was too short to fit the average Lego lamb.
So she had to chop the end off to fit it into the pot.I feel like this is sometimes how we practice veterinary science.We do stuff because Once Upon a time, based on what we knew at the time we did something a certain way.We gave a drug, ordered a procedure because at that time, based on the information that we had, it made sense.
But here's my rant, But here's my rant, because what happens, what I see us doing, what I do sometimes what I do is sometimes we keep doing the same thing just because that's the way that we do it.Even when some new information has come to light, a new paper or research that has clearly shown that chopping the end of the lamb rose makes no difference to the final outcome of your roast.
Or maybe we even learn that it can make the outcome worse.But yet we still do it, which is why I chose to share this episode as the next one from our clinical podcasts.Like our previous clinical episode about AHDS or HGE and the nonsensical things that we still do to treat that condition, when it comes to how we deal with potential nephrotoxins, we have a new part so we can stop dropping off the end of the roast.
I made this episode from a compilation from some highlights of two episodes that we recorded in the last year on the topic of fluid therapy for nephrotoxin cases.We're talking NSAID grapes and lilies and all that sort of stuff.One of the episodes was with Doctor Karen Boyd, who is a registered veterinary specialist in emergency medicine and critical care who works and teaches at Murdoch University in Perth, WA.
The other one was with Doctor Leonel Londono, who is a Clinical Assistant Professor of Emergency and Critical Care and Director of the Hemodialysis Unit at the University of Florida.His research interests include renal and non renal applications of extracorporeal purification techniques, endothelial and glycocalics, pathophysiology in the critically ill and hospital acquired acute kidney injury and these two interviews complement each other beautifully.
Dr. Curran explains the logic, and Doctor Leo expands on that and follows up with a very specific, very practical example.These two episodes were made for the clinical podcast where I interview specialists and ask them all of the questions that I've accumulated over my 20 idea career about their topic of expertise.
All the stuff that I used to or still get stuck on.So updates on what's new, or sometimes a revision of important things that I've long since forgotten.You're not going to find these podcasts if you search for them on your podcast layer because access to them is through a paid subscription.Once you sign up for them at vvn.supercast.com, they will show up on your podcast layer of choice.
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So if you like what you hear on this episode and you do want to check out our full feed of clinical content, go and try it out for free for two weeks at VVN.That's VVN for redvaultnetwork.supercast.com.OK, Doctor Karen Dr. Leo.And why the kidneys are not toilets that You can Flush.
I think we're live with Doctor Corin Boyd back on the last day of X of the Spring symposium.Connor, you did a great talk on fluid therapy specifically because we've this whole week's been about fluids.Yeah.We've got fluid overload.Sorry, bad fun.It's going to be a bad session.
And then specifically in the kidney patient, which is it's insightful, really great.We actually did a podcast episode with Rob a while ago to introduce the idea of that.Because traditionally certainly when I trained and and most of my career, I've got a kid kidney failure animal or whack it with fluids because we've got to wash it out, you know, wash out the azotemia and get rid of the nastiness.
And then Rob said.And then we drowned them.Yeah, absolutely.And I guess it kind of it's not as simple as that.I think we would all want it to be as simple as that because renal Physiology is difficult and I make no claim to like thoroughly remember or understand all of my renal Physiology.
But it certainly is really complex and we appreciate clinically you know we put an animal on 2 * 3 times maintenance fluid, definitely more urine comes out of the animal.We definitely can see that, but we we don't know that more that's helpful in any way.
We don't know that more toxin comes out of the animal or we don't know that the toxin is not interacting with the kidney in the way that causes its toxicity less.And it's really interesting.I went and did a literature search for evidence of that and now there's really not much evidence.
So you're talking about the the nifrituxin that's not in kidney?Failure yet?Not in kidney failure yet?Yeah, absolutely.So your talk at the start we talked about the animal that has kidney failure and then we want to be much more cautious with fluids in that than we than we used to be.
The goal was never it was not to flush them out, flush them out because they because the kidneys aren't working so so it's much easier to fluid overload.And I yeah.And I don't think, you know, tubular obstruction is often part of the mechanism of acute kidney injury.But it doesn't really make sense to try and flush the tubules by pushing heaps of fluid in, because I think people think you increase the pressure that's exerted on those tubules if you put more fluid in.
But really the body regulates GFR, right?Like we try and keep a a normal GFR.So as long as you can get GFR up to normal then trying to push more fluid in is not going to substantially increase GFR really that much.
That's not the main way that the excessive fluid is shifted from the body when you put an animal on supraphysiologic fluid rates, So it's not going to clear those obstructed tubules.You just got to let the disease process take its course and let them clear themselves if they're going to.
And if you make the kidney tissue more Dematus, you're probably going to make it harder for it to clear.The bombshell.A lot of bombshell, but the part of your talk that was really fascinated to audience was actually in the questions you're kind of done and somebody said, look, I don't know what about the animal that ingests an ifrituxin and it's not sick yet and we put it, put it on fluids and you said at the start of the talk.
So we recap that.Yeah, so that's a really intro.I'm really glad someone asked that question because it's something I like to talk about, and you know, I sometimes do talks just on that topic because I think that there is this perception out there that inducing A diuresis, whatever that means, is beneficial to preventing nephrotoxicity in some sort of way.
Now, I don't have never actually seen an explanation.I've read dozens, probably hundreds of textbook chapters that recommend this, and I've never seen an explanation of how that prevents nephrotoxicity.So I've had to work out what I think people might be suggesting other mechanisms that helps nephrotoxicity and then think to myself, do those make sense?
And I don't think they do.To me why that would be helpful is if it helps you get the nephrotoxin out of the body into the lawn, you know, being feed out quicker.Which is what I thought.That doesn't, that doesn't pan out to me for a start, just from simple observations.
We do see that, you know if we give an animal that's ingested a grape twice maintenance fluids, that dog pees a lot, right?Like it does urinate a lot more.But we can already see from just looking at the urine, grossly looking at the urine specific gravity, all of these simple things we can do easily anytime.
The urine is more dilute.So whilst there's more water there is there more overall top and being excreted in that more dilute urine.OK.Yes, OK.So you're increasing the water component, but not necessarily the.Yes, the toxic in that I think you would actually have to go and look with studies to try and work out does this increase the excretion.
If you're trying to make that argument, it may amaze you that I spent a long time searching the literature trying to find studies about whether fluid therapy increases the renal clearance of anything exogenously administered to people or animals.
I found maybe like four or five studies ever.Really.But looked at substances being excreted in the urine, exogenous substances that were administered to patients or experimental animals being excreted in urine found like one on like iodinated contrast stuff because people are concerned about that causing AKI.
That's a whole nother controversy.One about I mean a glycoside antibiotics in kids where they were more actually looking at it from a perspective of if we put the kids on high fluids, maybe we have to give them more antibiotics because they'll pee it out faster.
And all of these did show difference between giving lots of fluid and giving not much fluid, but tiny difference, like maybe 5% faster excretion with the fluids.So for a start, the evidence isn't there.Then I went, all right, well, let's go and actually work out what this is the interesting question, I think if you ask most of us, most vets, why does putting your patient on twice maintenance fluids make them pee more?
Do you have a good simple answer to that?You can't trick me on a Sunday morning current.I just feel like, well, there's more fluid going in, so more fluid needs to come out.More fluid has to come out, yeah, but how does the body know that?And how does it do it?It's a complex neuro hormonal system, right?And all these things like naturally erratic peptides, the Ras, all this sort of stuff gets involved.
And it has effects on the kidney in all sorts of places, not just GFR, which is the thing that people seem to focus on.They're like we have a higher GFR, but it's probably mainly not that.It's stuff happening within the tubules themselves.
A lot of that modification of water content of the urine happens right in the very distal tubes.So that's ADH all those.Sort of.And all that sort of stuff.And then natural erratic peptides, which are these substances that only come along when you have, are hyperbolemic and tell you naturally erratic means sodium peeing, so you pee out.
Sodium and water follows it, yeah.They only kind of come along when you're hypervolemic, and they have lots of effects, some of them really bad, like shedding your glycocalyx.A lot of what they do to the urine is in the distal tubules.So it's actually more urine comes out, but it's only because it's being modified right at the very end of the.
Curve.So we know physiologically all of these mechanisms happen.No one's looked clinically and said in our patients we actually put on twice maintenance fluid.What is actually physiologically happening in their kidney kidneys?I do.I have not found any studies where anyone's actually looked at that question.
So I don't think it might necessarily.We can think it's likely to make you pee out the toxin much faster at all.The other thing that people say is, well, OK, but if there's more fluid flowing through the kidney tubules, then it'll stop the toxin from sort of, you know, getting stuck in the kidney tubules and binding to things and stuff.
But then that same argument applies, right?Like that would require knowing that there was higher fluid flow right up in the proximal kidney tubules, which is where most of the damage for most toxins is relevant.Although every nephrotoxin is completely different in how it causes kidney toxicity, so it seems strange to suggest that there could be one treatment that would work for NSAID's NSAID, which I've just said of, you know a while ago.
NSAID's don't even affect the tubules directly, they.Were they're not sitting in the tubules?They're not sitting in the tubules, whereas something like grapes, we don't completely understand what they're doing.And then use something like ethylene glycol, it's crystals precipitating out throughout the tubules.
So there are all these different mechanisms, but I just don't think either the evident clinical evidence or the physiologic argument for why it would be helpful is sound just to.Stack up and then checking an animal on on fluids for two days on twice minute is not again, it's.
It's a lot of the core of this whole week, is it?It's not just that.No, I guess my concern is some of those patients will be fine whatever you do with them, right?They just didn't get enough toxin.They got good, healthy kidneys, so.They got healthy kidneys that could take the insult, or you induce the mesas for the nephrotoxin quickly enough that they never absorbed any, or they didn't actually eat as much as the owner thought, and they were never at risk or whatever.
A lot of those animals will be fine, but some of them will develop AKI, right?Like we've all seen these big NZ ingestions that do get an AKI.Some of us may have seen mean you know, some great cases that actually do have an AKI.We might see cats with lilies do get an AKI.
And my concern is if you're putting them on twice maintenance fluid to try and prevent that AKI and then at some point during that two day period they actually develop AKI and they become because of their AKI, the urine output drops, they get an oliguric or an anuric form of AKI.
It's really easy to really quickly fluid overload them with that twice maintenance fluids you're giving before you can clinically recognize, oh, now they've actually got an AKI and they've stopped making urine.Like you don't have a little camera sitting there in the ureter measuring urine coming into the bladder, right.
You may or may not have a urinary catheter in place, but in my experience, most of the examples where you're.Trying to.Prevent it.You don't have an urinary.Catheter.Yet you'll only put one in if they actually develop AKI later.So you're watching them pee.You're watching them clinically and often before they actually get clinical evidence of being unwell.
They may have had AKI for a little while, and you may have already fluid overloaded them.And one of the other things we talked about a bit in the talk here was that fluid overload is really bad for the kidneys.So you may already make yourself have to start from behind with these animals because you fluid overloaded them before you've even kind of really got started treating their AKI.
Wow, that's a shift.That last bit about you got fluid rushing in the top end and the healthy kidney.And then the kidney goes, oh, I'm not that healthy.I'm going to slow down, basically close the plug.And the fluid.Keeps coming in the.Edema.Everywhere really start getting because your mechanism why the fluid overload is worse for the kidneys is that that.
I understand that because it's a soft tissue organ, but in a?In a capsule, so.You shove a bunch of fluid and then interstitial space in the kidney and it.Squashes the kidney and squashes all of the tubular outflows of the kidneys.So now blood can't perfuse it and urine can't get out of it because basically it's like a tight, scrunched, closed thing.
Yeah.Oh, wow.So we'll put one little caveat on this though that I think is really important is that dehydration and hypovolemia are definitely still bad for the kidney as well.So I'm not saying never put an animal that's had a nephrotoxin ever on any sort of fluids ever.
That's definitely not what I'm saying.A lot of these animals also, especially if it's something like an NSAID, have GI signs and if they weren't treated with fluid therapy, they would be at risk of becoming dehydrated and hypovolemic because of that at those GI signs and stuff like that.
So those animals I definitely think need IV fluid therapy.You just don't use some magical extra mindset for their fluid therapy compared to what you would normally do.You just do what you would normally do.You know, if they're in shock, you give them a fluid bolus based on the severity of their shock.
If they're dehydrated, you carefully replace your sort of estimated deficit and recheck them frequently.And if they're not eating and drinking, they can have maintenance.And you watch them closely and make sure that they're not getting fluid overloaded with that plan or they're becoming more dehydrated with that plan.
So sometimes these animals still need fluids.They just don't need fluids to flush the kidneys, which are, as doctor Melissa Claus says, the kidneys are not tiny toilets.You can't flush them.Golf.So we're making that practical for everyday practice.
So the grape dog, the my cat licked the Lily, but it's still fine.What do we do with those?Do you say OK, well go home, come back if we get sick?Yeah, it depends on the owner and how worried I am the animal is going to get sick.
Some of them you're like, all right, you've definitely had a big dose of what is definitely a nephrotoxin.I think you're really likely to get sick.I usually sort of recommend admitting those for observation.And then usually you'll find those animals already probably aren't eating and drinking when they're in the hospital.
So if they're not, then I probably put them on.Maintenance fluids until I'm happy that they're gonna eat.Yeah, if they're like the dog, that's like a bouncy, happy dog.That Ada grape came in, maybe got some emesis and vomited up.The grape is bouncy.The owners are like, yeah, we can watch it.
We'll know if he's sick, then those ones I say take him home, then please just bring him straight back.And I give them this whole list of things, Drinking more, drinking less, vomiting, diarrhea, peeing more, peeing less urines changed in color.All of these warning signs, give them a list and say come straight back if there's those things.
You know, if they're really worried like people, they're like, I really want to make sure it's OK You can kind of take some blood for a baseline renal panel so you can then, you know, if they are not looking quite right in two or three days, you got a baseline to compare against, yeah.I like that approach.
The thing that I'm wondering about, let's say we've got the Lily cat, even a significant amount of Lily, but it's young kids and it's still fine, but that's a significant nephrotoxin.So really, I'm worried about that.So even then, admitting that guy to watch it, I go, well, I'm going to admit you, and then I know that you're suddenly not going to eat and drink.
Probably because that cat I would, you know, if I admitted it and was not eating and drinking, I'd probably use maintenance fluids to try and maintain hydration.Nothing to do with flashing the.Kid.Nothing to do with.Flashing I'm just giving you what you're not drinking.I don't want you to become dehydrated and hypovolemic, so I'm going to try and keep fluid balance.
Theoretically, if the owners could watch it, it could still send it home or.Maybe cats are a bit harder because you know the Lily cats I do.If it's a true Lily, I do get really worried about them and cats can be really subtle in their clinical signs.So a lot of times those, you know, it's a case by case decision to discussion to have with the owners, but I feel like observing them in hospital and maybe doing some baseline bloods and then bloods 24 to 48 hours later to see if creatinines going up is really useful.
I find also just anecdotally, I don't believe that this is evidence based, but it might be and I just don't know about it.But anecdotally, I think that those renal ultrasound changes, the classic AKI renal ultrasound changes that you sometimes get, you know, a bright rim around the kidneys, a little bit of free fluid around the kidneys.
I feel like those changes that I sometimes we see them, sometimes we don't in AKA eye cases.But I feel like in my experience, they're really common in Lily cats, so doing point of care ultrasound of the kidneys the next day as well, can often be really helpful to me and those cats, because I all right often already by the next day, if they're going to get an AKI.
You see, you know that fluid around the kidney, that bright rim around the cortex, and you're like, OK, these kidneys look bad now, these cats, even if the creatinine hasn't gone up yet, it's going to.Yeah, so start treating it like a kidney cat.Yeah, but we can send the written Grape Dogs home.
That's called Corin.Thank you so so much for.That no worries.Hey, just.Before Doctor Leo tells us about why putting that puppy who's just eaten non steroidals onto twice maintenance fluids for three days doesn't make any sense and what you should do instead, I just wanted to give you a quick update on our specialist support space.
Now, if you haven't heard of it, we created an online space that you can use on your phone or on your laptop to get access to a list of specialists to help you with your tricky cases.It's a very nifty little space where you can share photos or files or even chat live if the case requires it.So these are for the cases where you are just a little bit stuck.
You can't refer it for some reason or you don't need to refer it, but you just need to ask somebody a little bit smarter than yourself.What's happening here?What does that blood mean?Can you look at this X-ray for me?Can you help me with the decision on this?And our specialists are growing.Well, actually, let's say the list of specialists is growing.
I'm pretty sure that all the specialists we have on the space are fully grown adults.We started with a couple of medicine specialists and an emergency and critical care specialist, but in the last couple of months we have added a dermatologist and recently an oncologist as well as a diabetes expert.So somebody specifically for those tricky diabetes cases, including information around the new basal insulin treatment protocols.
It is a paid space but we've tried to keep it as affordable as possible for about $15.00 a month and we are working on practice subscriptions.If you want to check it out I've put a link in the show description wherever you're listening to this.And if you want to find out about practice subscriptions shoot us an e-mail at info@levatevault.com OK, back to Doctor Leo and non steroidal anti inflammatories.
So next topic is the Oh my dogs eat in a whole box of my ibuprofen or name your anti-inflammatory.I don't know what's popular in the US virus.It's often.Ibuprofen is the most common.One there.So the traditional approach, it's all kind of forever as well.
Let's get to you in hospital.Obviously, if there's decontamination options, we won't go into that.But the fluid part of that is to go.We've got to get you on fluids for 48 hours because we want to make sure that we perfuse your kidneys and flush out the NSAID, right?Yeah.Does that make sense?Nope.Again, going back to pharmacokinetics of NSAID, if you look at NSAID, they're 95% bound to albumin if you're doing fluid diuresis.
Not flashing albumin through the glomerulus.No.Unless you know how a healthy glomerulus.Yeah, right.Yeah, because albumin weighs 69,000.It's staying well and truly.Is a big molecule glomerulus.Let's pass some very small molecular weight proteins, but they're reabsorbed by the proximal tubular epithelium.
But the glomerulus doesn't let Albuvein pass unless there is an existing glomerulopathy.So what's the reason to do fluid diuresis on a dog with NSAID?There is none.That's it.So how do we clear NSAID's?Is it adipatically cleared?Well, there is both ways.
Some of them are hepatic, some of them are renal.OK.So the so the little bit of unbound percentage will get peed out, but but it's only like a did you say 95%?95% or more?5% of circulating insiders and what's the what's the half life?I know it is drug to drug.
But most of them are between 8:00 and 12:00 hours.So that's why we make that recommendation.Because again, when you give recommendations for fluid therapy to incretion through the kidneys, you want to do three times the half life of a drug to achieve at least a 60 to 65% reduction of the drug from circulation.
So three times the half life.That puts us at 36 hours or so of hospitalization with most dancers.Yeah, if we were going to do fluid therapy for NSAID now how about naproxen?Do you get naproxen?You don't know naproxen?I've heard of it, but not common for us so.
Tell me about it.Naproxen is a very common human, NSAID OK, and we see a lot of exposure to an NSAID here in the US.Is naproxen the the active ingredient?That's OK.Yeah.And the half life of Naproxen is 72 to ours.
So technically, if you have a patient that ingests naproxen, you have to put that patient on fluids for 9 days.And it's also albumin bound.Like all that.Yeah.This might.Yeah.Let me think about this before I ask it.So, like, how do the NSAID damage the kidneys?It is to do with blood supply, right.Right.
So it's not.It's not directly nephrotoxic by the chemicals sitting in the tubule damaging tubular cells, because the other theory with why do we put animals on fluids Is because you don't want the toxin to to linger in the tubules you are.Once it's through the glimmerase, you've got to get the hell out of there.But it's not.
No, and then it's not directly nephrotoxic.Again, the damage to the kidneys is mediated by prostaglandin inhibition and when there is no prostaglandin, there is no apheren artery or basal dilation, right?So technically you have a vasoconstriction, the hypoxic damage to the.
Kidney is sad because it's not getting enough oxygen, basically.Pretty much so yeah.This dogmatic approach of fluid therapy for the answer dog doesn't really make a lot of pharmacological sense.And I that's a very strong consensus in the IRIS Society amongst nephrologists is there.
You know, I'm part of the IRIS AKI guidelines, and we discussed that in patients with NSA toxicity fluid therapy.There is really no evidence to prove that it makes a difference.Feel like you should say the sentence You don't need to put your NSA toxicities on fluids for 2-3 days, and then you should drop that microphone and walk away.
You you look at it for patients because technically you know, IV fluids can have a detrimental effect too.Yeah, right.Especially if you're not monitoring body weight.You can overload even if they have some clinical AKI with no isotymia, they can retain water.
So they have that.And then one point I was very well taken in the audience was workload for our ICU nurses.Oh yeah, and it promised.They almost always puppies.And they're almost always really annoying.Exactly there for 2-3 days back in the heads of ensuring the drip lines.
Exactly.You know, we talk about how sure stuff sometimes the hospitals are, how difficult is to get ICU nurses and then we're overloading them with work.Surely there's no evidence to support the use of fluids on anset toxicity.
Now I think that we also have to categorize our patients too, because you have the dog that just ate the anset swagging his tail, right?You make him vomit, vomits good amount, you give him some charcoal or some cholesteramine, maybe some IV lipids, OK, And then you send them home.
But also you have the dog that ate 2000 Nicks per gig of ibuprofen and comes in comatose, so that animal has to stay so.So you know, I'm not saying that no, it's even completely contraindicated because at the end those animals, if they're really a risk of AKI with a high dose, you cannot decontaminate because they're neurological, then those animals will benefit from staying and looking at all their options for decontamination such as IV lipids.
Therapeutic plasma exchange has become very popular.OK.So for the GP technician faced with the healthy dog, that's just eats and so it's decontamination really and and then home and then keep a close eye on him and if it becomes unwell let's let's come back in.
It'll be warranted to monitor creatinine at least 2448 hours.You can send them home with some coasteramine because we know that was a good point from the audience today was, you know, you have patients that you may send them home with activated charcoal, but they can become hyper natural, yeah, yeah.
So you can give them a single dose of charcoal and send them home with coasteramine.Which is a brand new one.I I did a podcast about a month ago about cholesteromine and that was about the first time I ever heard of it.Yeah.And so in theory it should work for the instance we don't have data that supports it or?
Well, you know, if you look at the enterohepatic, so the toxins that have enterohepatic recidivation, those toxins are bound to cholesteromine in bond, yeah.So it should work.It should work.That's really useful.Awesome.
Thank you so much for sitting down.I appreciate it.Thanks.Super insightful.Before you disappear, I wanted to tell you about our new weekly newsletter.I speak to so many interesting people and learn so many new things while making the podcast, so I thought I'd create a little summary each week of the stuff that stood out for me.
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Dr Corrin Boyd

Dr Leonel Londoño