Good evening everybody and welcome to tonight's webinar. My name is Bruce Stevenson and I have the privilege of chairing tonight's webinar. Thank you for joining us with all the sport action that's going on now.
We appreciate you being with us. Little bit of housekeeping for those of you that are joining us for the first time. If you have a question for our presenter Matt, simply hover your cursor over the screen.
Your control bar will pop up, click on the Q&A box and type in the questions. They'll come through to me and we'll hold all of them over until the end. So tonight's presenter is more than qualified to talk to us as you know, from the series.
Matt graduated from the University of Liverpool in 2003 and he spent several years enjoying mixed practise before returning to Liverpool to undertake a residency in anaesthesia and analgesia. Since 2009, he has worked at North West Veterinary Specialists, which is a multi-disciplinary, multi-disciplinary specialist hospital in Cheshire. Matt is a European veterinary specialist and an RCVS recognised specialist.
Matt, welcome back to the webinar Vett and without further ado, it's over to you. Brilliant, thank you and good evening everybody. So this is the final in this series looking at various anaesthesia aspects, and we're gonna talk about controversies in anaesthesia tonight.
So there's an overview, what I've done is picked out topics that we frequently get questions about, there appears to be a little bit of confusion on, so we're gonna talk about when to give non-steroidals under anaesthesia. We're going to explore some of the opioid choices that we might have and just touch on a few aspects there. I'll answer a few questions about ketamine.
Consider fluid rates use, there was a publication a couple of years back, looking at guidelines for fluid rates, and I think it'd be quite useful to discuss some of that. And always a hot topic, we'll just talk a little bit about brachycephalic anaesthesia, maybe not really a controversial topic, but quite a, a, a topical topic if you like, and something that we get lots of questions on all the time, so worth delving into. So to start with, when I was putting this together, I, I thought I'd look at some definitions of controversy.
And one of the ones I came up with was a prolonged public disagreement or heated discussion, and I'm sure some of the things we'll talk about tonight will fall into that category. The second one I think is probably quite relevant as well as the last one to what we do on a day to day basis, so disagreement or an argument about something, not that we like to think we argue, usually because it affects or is important to many people. And I think on a day to day basis, there are lots of aspects of anaesthesia that do affect us all on a day to day basis.
We all practise anaesthesia on a day to day basis. Or the last definition I found was an area with no consensus view on best practise and for a lot of aspects that probably is quite an appropriate definition, certainly when we talk about fluid therapy. So the document that I will give you the reference for is there's some guidelines there, but it's not really a consensus statement because we don't really have a lot of evidence on some of these things, so it's quite hard to be really definitive without some evidence.
But some of the other aspects, when we're talking about some of the opioids, we will look at some of that evidence base for for what we're discussing, and how some people have looked at evidence in order to deal with some of these controversies, which tends to always be my approach. So let's start with when to give non-steroidals under anaesthesia. And why do we have the debate over this?
Well of course it's related to the adverse events that we see or effects we see with non-steroidals. And we can attribute the adverse effects we see. So the very same mechanisms that produce the beneficial effects.
So we know that non-steroids inhibit the cyclooxygenase enzyme COX 1 and COX 2. And the traditional view is that COX1 is responsible for your housekeeping prostaglandins, so we want to inhibit COX 1 versus COX 2, which is the inducible form of that enzyme, which is triggered when we have inflammation. Now maybe these two classic categories are less well defined, and certainly there is a role of COX 2, this inducible form.
In certain housekeeping aspects as well, so that's not quite as clear cut as we may have been led to believe previously. We knew that on non-steroids reduced the production of of, in particular, prostaglandins because they're the thing that we really think about associated with inflammation, but also in their key role in the maintenance of renal blood flow and gastric, mucosal blood flow. And these are the two areas that we worry about as far as adverse effects with non-steroidals go.
And of course the risks that we are all taught and we're all aware of are that with non-steroidals, there is the potential for acute kidney injury and the potential for gastritis. So really these are the two areas that we're, we're concerned about when we're thinking when do we give our non-steroidals under anaesthesia. And of course there are lots of different opinions out there.
And we've always got to just consider, is it, can we be sure it's always the non-steroidal, and I'll look at a case study and just discuss factoring that in there. Now really, if we look at cases of acute kidney injury, one of the studies that . Talks about this is the Hunt study at the bottom of the screen here.
Now this was a study that looked at adverse effects associated with non-steroidals, and they concluded that the incidence of acute kidney injury with non-steroidals under anaesthesia is very low. Now of course that could be affected by the fact that the data for this study was collected from VMD reports of adverse events. And of course we should all report our adverse events, but we don't always do that.
So of course that pool of data narrows if we don't all do that. We probably, but when you have a a very low incidence of something, you really need big numbers to be able to start looking at this on an effective basis. And of course we don't have those big numbers either.
However, having said that, we're not seeing reports week in, week out of dogs and cats suffering acute kidney injury associated with the administration of non-steroidals under anaesthesia, just to put that into perspective. Now, the second citation on this page, the low mass paper here looking at the renal effects of non-steroidals in dogs, gives some recommendations for the use of non-steroidals. This will make sense.
We know that we should ensure adequate renal perfusion if we're to administer non-steroidals, and we should ensure that our patients are adequately hydrated. When we're thinking about sicker patients under anaesthesia, we may just need to think twice about whether these two categories can be met prior to giving that non-steroidal. And I think the key questions to ask, and the way I think about renal injury or anaesthesia for renal cases is very much based on some of the human work that we have.
Do we have any presence of pre-existing renal disease? We've got to be able to answer that question in order to find a direct causal mechanism if we were to suffer an acute kidney injury. Have we used nephrotoxics in that patient?
And whilst nonsteroids per se aren't necessarily nephrotoxic under the correct circumstances of dehydration and low renal perfusion, then we can see symptoms associated with nephrotoxicity. But are we using any other agents? Have there been any other agents implicated in nephrotoxicity?
We typically think about. Aminoglycoside antibiotics and iodinated contrast agents that we might use for something like an intravenous urogram or contrast CT studies. Ask what the hydration state of that of that patient is.
Think, is the renal perfusion adequate? But then we've got to ask the question, how can I tell if renal perfusion is adequate? It's quite a nice study in cats, looking at blood pressure and how that correlates to different pulse qualities, the femoral pulse and metatarsal pulse.
And it's something you'll hear some people say, well, if you can feel a metatarsal pulse in an anaesthetized patient, then the renal perfusion probably is adequate because it's probably above 60 millimetres of mercury. We don't exactly know that in dogs, but that work in cats would certainly support that. So if we're trying to work out if we've got decent peripheral, decent renal perfusion, we should first maybe answer the question, do I think my peripheral perfusion is good based on pulse palpation.
So we're talking about real basics here. So these are all the things we think about when we're planning an anaesthetic and our concerns. But let's just flip this round and think, right, I've had a case today that presented 5 days after being spayed, young dog, polydipsy, because this is the classical presentation that we see with these patients, 3 to 5 days post anaesthetic.
Lethargic, drinking a bit, not eating particularly well, you take some bloods, document azotemia. Now of course, provided we didn't have any renal impairment prior to that anaesthetic, we're going to be suspicious of an acute kidney injury in this patient. We use an aromazine methadone pre-med, fairly common, you may use aceromazine buprenorphine as a pre-med, propofol induction, probably 80% of us are using propofol for induction versus 20% alfaxolone.
Isofluorine maintenance again, probably in the numbers are about 80, 20 people using Io. And we use them on steroidal and the pre-meds because we've been taught that we should practise preemptive analgesia, getting the analgesic into the patients prior to that painful stimulus. If we think about all of these agents we've used and considering renal perfusion, as peryzine is a vasodilator, that's going to trend or or or lend to a state of hypotension depending on the circumstances.
Methadone, very unlikely to cause any cardiovascular effects beyond a mild bradycardia. Nothing we're particularly going to worry about from a hypotension point of view. Propofol, we know propofol is a vasodilator as well, so on top of that Aceromazine, we're adding to that hypotensive effect, considering already what's going on with our renal perfusion with these drugs.
Isofluorine for maintenance, actually isoflune is the one drug isoflurane and ivoflurane, by the way, are the drugs that we typically forget about when we're thinking, well, what are the, the effects or side effects of these drugs. Now the volatile agents, Iso and civo are actually the biggest contributors to hypotension and impairment of renal blood flow. This is why we talk about when we talk about local anaesthetic techniques, the advantages of local anaesthetic techniques, because they allow us to spare our volatile agent use.
The advantages of sparing volatile agents are that our, we have less hypotension, less vasslation, our blood pressure is going to be better maintained, and we hope that our renal perfusion is going to be better maintained as well. So all in all we've used a lot of agents here that are trending towards hypotension and at the same time we've used a non-steroidal. So we do just need to exercise a note of caution here.
How would I consider this? There are a few other questions that I would ask if this was a case that I've been involved in. Did we use fluid therapy?
And did we use blood pressure monitoring. So this is how I would approach thinking about this case if this had happened. How could we think about agents that would maybe avoid that trend towards hypertension and just giving us that vague, I don't really know what's going on with my renal perfusion.
We could consider using an alpha 2 agonist, dex meatomidine or or or meatomidine because they cause vasoconstriction instead of that aromazine. I would use that in conjunction with methadone, and you tend to get a, a mildly hypertensive state because of that vasoconstriction. Propofol, the other advantage to using dexamedatomidine or mesotomidine in the pre-med, we're gonna get a better sedative effect so we can use less induction agent, and we're always trying to spare our induction agent because of that hypotensive effect we see.
And of course that's very good alpha 2 pre-med will allow us to spare our reafluorine as well. But maybe we could look at some other techniques as well that reduce our dependence on volatile agents. So it's worth thinking about your multimodal analgesia here, on non-steroidals if we think, well, I'm a bit concerned about using that non-steroidal.
Let's think about other things. So is there a local anaesthetic technique we can incorporate, and for a spay, a line block would be a really good example of a local anaesthetic technique to use, plus some intraperitoneal bupivaca or lidocaine around those ovarian ligaments and stumps. If we are certain that our blood pressure's good and we have measured blood pressure, then we could be safe to go ahead and give our non-steroidals.
And that tends to be my approach. Do I know what the blood pressure is? Am I sure that I've got some decent renal perfusion there?
I'm happy to go ahead and give that non-steroidal. So I'm thinking about every single case before I give the non-steroidal, and it's not just part of the give it in the pre-med routine. So I just ask you to think about about the timing of your non-steroidal.
We're very used to giving non-steroidal subcutaneously, but non-steroidals such as meloxicam are licence for intravenous use. And if we think about giving a non-steroidal subcutaneously, obviously it takes a while for that to reach peak plasma levels. So if we are waiting to give on on steroid, we want to give something intravenously that will achieve peak plasma levels as rapidly as possible.
Our options there are meloxicam intravenously or even rubenacoccy onsse, if you give that subcutaneously, it reaches peak plasma in about 30 minutes. It's a pretty good example of a rapid onset non-steroidal. I'd be a bit cautious about something like carprofen because carpro subcutaneously takes a lot longer and we're talking hours to reach a peak plasma effect.
So just think about the timing of the non-steroidal there. Having said all of that, and just to be devil's advocate, I have seen cases of acute kidney injury after anaesthesia where a non-steroidal has been given, but from practises that provide fluid therapy under anaesthesia and do monitor blood pressure. And in these cases, if you can answer all of those questions and say that patient was not hypotensive and that patient received fluid therapy, that's when we say this is what we call an idiosyncratic reaction.
One of those reactions, it happens in a very small number of cases and we don't know why it happens. But in order to say that we have to have ticked all of those boxes previously and be sure that we've done everything that we can do to avoid those hypotensive periods. So just be a bit cautious, let's not throw the baby out with the bath water.
We need to think and just be rational about when we administer those non-steroidals. I'm not saying the non-steroidal is always to blame and we should avoid non-steroidals. I certainly wouldn't say that because nonsteroidals provide very effective anti-inflammatory analgesic effects, which we often really, really rely on for excellent analgesia.
And in considering all of this, I think we've got to take a sensible approach and not an excessively cautious approach. Because if we say, well, actually you've just scared me, this may happen, I'm not willing to take that risk. The risk is incredibly, incredibly low.
The incidence of, of acute kidney injury associated with non-steroidal and under anaesthesia is rare. And we have some very good evidence that non-steroidals as analgesics provide far more benefits, so those benefits vastly outweigh the risk. So let's just think rationally about our use of non-steroidals.
And I just out of interest, I've got this poll here, so I'm intrigued as to what you do if you experience an adverse event with a non-steroidal. And I'm not necessarily talking under anaesthesia, this could be a dog that's chronic OA that starts vomiting on a non-steroidal or experiences diarrhoea. So just widening that context a little bit.
So do you stop the non-steroidal? Do you try another non-steroidal? Does it depend how severe the reaction is, or do you use something else?
So I'd like you to choose one of these answers, please. So folks just simply click on the answer that best suits what you believe is the right answer. And we'll give you about 30 seconds to vote on that and then we'll close the poll.
Remember this is an anonymous poll so don't be scared. Take your chance, give us your opinion. Alright, 5 more seconds for the last few stragglers coming in.
Right, let's end that poll and share the results for you, Matt. Can you see those, Matt? OK, so 33% said stop the NSAID.
0 said try another NSAID. 50% said depends on how severe the reaction is, and 17% said use something else. OK.
That's very interesting, good. I think we're obviously, we know very well that we should always stop that non-steroidal. Yes, it does depend on how severe the reaction is.
Sometimes if you stop the non-steroidal for a few days, then you rechalenge the patient with that say non-steroidal, they may be OK. There was an interesting part of the Hunt study I referred to earlier, and they documented, actually, a lot of dogs, when you give them a tablet, they just vomit anyway. So one of the comments they made is, is vomiting just a normal effect associated with giving dogs medication.
And if you discount all those dogs that just vomit anyway, you certainly reduce the overall true incidence of vomiting with non-steroidals. That's quite interesting. And of course my approach tends to be, depending on how severe the reaction is, I will always try another non-steroidal because I know the benefits associated with non-steroidals.
And if we're thinking about using a different non-steroid or something else that's, this is, I suppose it's not really controversial, it's quite debatable, is what's the washout period? And I would say that there is no firm data. People talk about 3 to 5 days, but of course that depends on the half life of the drug.
So if you think about a drug that we administer once a day, such as meloxicam. Then, we say after 5 half-lives, then we have 0 of that drug left in the body. Compare that to a drug that's administered once a month, such as mavocoxib.
We've got a much longer half-life. We've got to wait quite a long time before we're safe to administer another non-steroidal. And what do you do during the washout period?
So if we have a dog on long term nonsteroidals and they are painful, we need to consider some other options. And I'm not gonna discuss that tonight, but that's something that we certainly addressed in the chronic pain webinar in the pain series last year. So that would be a good place to go and consider the other options.
And a question for you, what washout period do you observe if you're switching from one non-steroid to another? Do you switch right away, say, where you had your meloxicam this day you can start your car and the next day, 2 days, 3 days, 5 days, 7 days, or do you observe a longer washout period, so over to you? Alright folks, you know how to do this.
Just click on the answer that suits the way you handle this situation. And we'll give you about 30 seconds or 45 seconds just to answer this. And then we will close that poll.
Right, everybody's voting nice and fast this time. So let's close that poll and share those results. Can you see them this time, Matt?
No. OK. So again, switch right away is 0%, 2 days is 29%, 3 days is 29%, 5 days is 29% and 7 days is 14%.
Nobody said longer. OK, so a bit of bit of variation there. Like I say, I think we all, we're all familiar with 3 to 5 days, but there isn't anything specific documented there, so I just ask you to consider how long that, that non-steroidal is acting for, and I normally think 3 days, in those patients.
OK, so moving from non-steroidals onto opioids. Those of you that have attended the chronic pain webinars we did before and the acute pain webinars, we talked about a choice of opioids previously, so you will have already seen the table that we've got here. We've got our two licenced options for dogs and cats at the top there, methadone and buprenorphine, and we've got a range of doses.
So let's look a little bit about that methadone buprenorphine and some things that we just need to think about. Typically we, we've always thought of pure neurops such as methadone and fentanyl as more effective analgesics than partial neuro agonists like buprenorphine. And you've heard me talk previously about how there is evidence in dogs that methadone is more effective analgesic than buprenorphine.
But in cats, the evidence that we have suggests that buprenorphine works in some cats, methadone works in others. Part of this is probably due to the fact that there are A lot of variances between patients, maybe more in cats versus dogs with opioids. And we know that different drugs have different receptor activation profiles.
So although methadone and fentanyl both form new agonists, they don't both activate the receptor to exactly the same degree. And maybe in some circumstances we don't have a an absolute comparable dose known to us. But it's just worth thinking that if a patient doesn't seem to suit one opioid, it doesn't mean it's not going to suit another.
So I'd always encourage switching between opioids to gain a full beneficial effect. Methadone, we always talk about a dose of 0.1 to 0.5 mg per gig with methadone.
We know that the data sheet dose for Comtan is higher than that. However, if you look in those texts, then we're looking at a dose of 0.1 to 0.5, mix per gig, IV, IM, dogs and cats, and we can titrate methadone, we've, we've talked about that before.
What about morphine? So we certainly know with morphine that there are a few advantages that methadone has. We don't see nausea or vomiting with methadone, and we have NMDA receptor actions with methadone versus morphine.
So again, some good reasons to use methadone over morphine. Which are now more apparent that me I say now, methadone has been licenced for about the past, probably 8 years in dogs, a few years less in cats, so we don't really have this, this methadone morphine debate anymore particularly. In some countries where neither are licenced, then perhaps people still are having these questions over which one is more efficacious.
I think probably from an analgesic point of view, it's actually quite difficult to prove that one is any more efficacious than another, but we tend to have a more adverse effects profile with morphine, I say the vomiting diarrhoea, you know, if you give it rapidly IV then you see histamine release. So those would be some of the, the. Areas that that debate revolves around.
Certainly in the UK I think everyone's transitioned over to using methadone, it's the licenced products. I think you struggle to justify using unlicensed products when we have a full new agonist available for dogs and cats. We typically think bigger dose is better analgesia.
Yes, we do see that with methadone, the effect is dose dependent. Is the same true with buprenorphine? This was something that was looked at a few years ago in dogs that use ovarian hysterectomy as the model, looking at analgesic requirements during surgery and after surgery with two different doses.
And they were looking at snoring not 2 makes per kg, so the dose that we commonly use and a higher dose n. 4ms per cake. Questions being, does a higher dose produce more analgesia or does a higher dose produce more side effects?
What they were able to note in this study was that the 0.02 mepi dose so our our standard dose, this is the dose they use every day. We don't see any greater analgesia when we use a bigger dose of buprenorphine.
And we don't see any more side effects, so take her message, 0.02 mixing in dogs undergoing ovarian hysterectomy is an adequate dose of buprenorphine to use. And that's informed my clinical practise for a long time.
If we don't think we're getting the analgesia required with buprenorphine, then the next step would be switched to methadone. Probably not gonna see a greater analgesic effect by doubling the dose of buprenorphine. What they did find in this study was that in dogs that the vast majority of dogs, I can't remember the percentage, but it was, it was a high, it was higher than 50% required further analgesia at the 5 hour mark versus the traditional 6 to 8 hour duration of action we typically think of for buprenorphine in dogs.
So if you still have 8 hours as a duration of action buprenorphine in your head. Just think, maybe buprenorphine doesn't last that long based on this evidence and bring your pain scoring forward accordingly to make sure we're not missing those patients. We're not relying on buprenorphine to provide analgesia for as long as 8 hours.
Next subject, which I think is always it's been a question in in everyone's head once they graduate from vet school, because we're all taught or we we need to be careful about ketamine and cardiac patients because it's a myocardio depressant. We certainly know that in vitro, if you take cardiac muscle in a petri dish, in vitro, ketamine does cause a decrease in myocardial contractility. But in real life, we have the sympathetic nervous system there to balance that.
Is that effect dose related? Yes, potentially it is, but I don't think there are any studies looking at different doses. So I don't.
Necessarily avoids ketamine in cardiac disease, but I think very carefully about it and whether I'm using ketamine for anaesthesia or analgesia. And really, we don't use ketamine intravenously to induce anaesthesia on very many occasions. Probably the main example would be if we were wanting profound sedation in a cat, we might use ketamine, midazolam, ketamine, diazepam's quite a common combination in your sicker cats.
For most of my anaesthetic practise, I'm using ketamine as an analgesic, as a continuous rating fusion at lower rates. You can see this is 0.3 to 0.6 milligrammes per kilogramme per hour compared to a bonus of 3 to 5 milligrammes per kilogramme.
So we're talking 10 times a dose reduction there for the analgesic beneficial effects of ketamine. Obviously where you have questions like this, somebody wants to go and and look at it and show, OK, if I use ketamine CRI in dogs, can I see induction of any specific cardiac biomarkers that we may associate with an adverse effect on cardiac function. And they looked at half a mg per kg of ketamine intravenously in conscious dogs, then a rate of 1.2 or 2.4 mg per gig per hour.
So a lot higher than those rates that I quoted previously for analgesia 0.3 to 0.6 mg per gig per hour.
There's several biomarkers they looked at as well as mean arterial pressure and heart rate. So in both those doses, the heart rate did increase over the 1st 4 hours. That's fine.
It has a if you look here, we've got those two different dose groups. The heart rate started just less than 120. In the higher group it's going up to just less than 140 and then peaking just above 140.
It's probably not a huge increase. OK, at two points it's significantly different from that lower rate, but still it's not a particularly concerning increase in heart rate. So yes, high dose ketamine will increase heart rate.
But I don't think that's particularly of concern, and I would never use a rate that high anyway. Increased heart rate is not something I typically see with the ketamine rates I'm using. With the ECG, these patients they didn't see any arrhythmias, they did see some changes in the QRS morphology, but none of which were of concern.
I mean arterial pressure was increased at certain time points, but really there's not a huge increase from a baseline of about 105 up to just over 110 for mean arterial pressure in this group. Some of that could be attributed to to normal variation. Not something we can worry about particularly.
The bio with regards to biomarkers creatinine kinase MB was one of the cardiac biomarkers that they used and didn't see any significant changes in the ketamine groups. And troponin one, probably biomarker were a little bit more familiar with measuring there were all those levels were below detectable values in all of the samples. So, effects of those doses of ketamine in life patient, like healthy patients on cardiac biomarkers and cardiac function, very little effect.
So people are just starting to question, OK, should we really be worried about using ketamine in these patients? Like I say, I use ketamine mostly for analgesia, less for anaesthesia. I may be a little bit cautious with ketamine and it's probably not the most appropriate agent in, let's say a sick cat with cardiac disease.
So that's probably the only circumstance most people use ketamine at anaesthetic doses. I think we have a lot of of other options that we can use in those in a very small subset of cats, but anaesthesia for cardiac disease is a slightly separate topic. Just for example, if I had a cat, 6 year old cat, hypertrophic cardiomyopathy needs a fracture repair, this is a typical protocol that I might use.
It's methadone 0.3 mg per gig in the pre-med, afaxolone for induction. Epidural bine and morphine, we're gonna get great analgesia for that.
What we're looking for is rate control, so we don't want our heart rates to go any higher. Remember, these cats with HCM very tend to have rapid heart rates, very small chamber size, so we don't get a great cardiac output because of that, that hypertrophy. We're looking at really good analgesia, so we can get on and fix the fracture without the cat responding with no sympathetic stimulation at all, keep our hearts as stable as possible.
We can use some loam, obviously, we talked about the benefits of nonsteroidals, and when that epidural starts to wear off and epidurals in cats, I don't think it lasts as long as dogs, we're gonna use a ketamine continuous rate fusion during that recovery period at that 0.3 meg per gig per hour rate. We paints called the cat and provide methadone.3migs per gig as required.
So that would be typically how I would incorporate ketamine into a cat, anaesthetic protocol in a cat that has hypertrophic cardiomyopathy. Moving the ketamine on to our next topic which is fluid therapy. I think what we tend to focus on is which fluid maybe.
But what I would encourage you to think about is why we're using the fluids that we're using. And are we using fluids for maintenance or are we using fluids for replacement? And obviously this depends on assessment of patient prior to anaesthesia.
Our fit and healthy patients, we're using those fluids for maintenance and counteract against hypertension like we talked about in that spay example. If we think about something like peritonitis or pancreatitis, these sick cases, we're using those fluids mainly until in the initial stages, until we've replaced those volumes lost. In the latter stages of anaesthesia or hospitalisation, we're then using fluids for maintenance.
So just think about that distinction when you, when you're looking at patient thinking should I use fluids in you, are you dehydrated? Do I have a replacement challenge here prior to meeting your maintenance needs? Typical rates that are considered in this paper below.
So this was the, these are the guidelines produced by the Journal of the American Animal Hospital Association, which are free to download if you search those. The rates that they suggest for routine anaesthesia would be 5 mL per kilo per hour in dogs and 3 mL per kilo per hour in cats. But again, those recommendations aren't particularly well supported, but.
Following on from the human world, we seem to be moving away from these higher rates of fluids and, The concept that pouring a lot of fluid into patients is seemingly quite outdated because we've got to consider where that fluid goes. When we put fluid into the vascular space, if it's an isotonic crystalloid, we know that typically only 20-25% stays in the vascular space after an hour. The rest of that's leaking initially.
You've got to ask the question, where is that fluid accumulating? So again, it comes back to thinking about why am I using this fluid and therefore which, which rate am I using depending on my, my indication for that fluid. And of course monitoring, monitoring becomes relevant and we'll talk about some monitoring in these case examples.
So as an example, we have a 14 year old cat undergoing a dental, it's got IRS stage 2 kidney disease. So we ask ourselves the question, are we looking at maintenance or are we looking at replacement? And potentially in this cat, depending on the hydration status, which of course is the cat, can be quite difficult to assess if we have subtle dehydration.
I don't think we see obvious dehydration in those iris stage 2. Once that disease progresses, we definitely see we're familiar with our our crispy kidney cats. Don't think you see those cases with an IS stage 2 that.
We probably do need some replacement. When we ask the rate question, is the is the rate the most important thing or is it actually time on fluids? So those kidney cats, they're probably better coming into the practise the night before and having fluids overnight at a slower rate to replace some of those lost fluids, get them in a better state for anaesthesia.
Or if you can't hospitalise them overnight, then probably coming in first thing in the morning, 3 hours of fluids prior to that procedure. It's gonna be much better than starting with a dehydrated cat and trying to catch up under anaesthesia. And we would typically think about using isotonic crystalloids, so either Hartman solution or 0.9% sodium chloride.
Harmless solution is more balanced solution, so that would be my first choice in this case. There are very few indications where I actually use saline, again, that's the topic for another webinar. And under an anaesthesia we're gonna monitor this patient's heart rate, so provided they're not responding to any.
Painful stimulus that we can look at the heart rate. If our heart rate is particularly high, you think, well, actually, is that a sign that you're dehydrated? We're going to monitor our, our blood pressure and in cats, we typically think about immune arterial pressure more than 70 or 80 millimetres of mercury as being our target to maintain that renal perfusion.
And of course that's something really important in this cat that already has some renal disease. We don't want any exacerbation of that kidney disease. So by following these quite simple steps, I think you can be quite well assured that this, the cats aren't going to, you're not gonna see any exacerbation of that disease under anaesthesia.
Contrast this with a dog, a seven year old German Shepherd in need of a splenectomy. Oh, we think a maintenance replacement. We need to think very carefully about how much this dog has lost, what's it lost and where has it gone.
And our routine lab work can help us, as can our pre-anesthesia monitoring. So simple things like heart rate, pulse quality, even before we get as far as thinking, well, do I need to get a blood pressure on this dog before we anaesthetize him? Let's just palpate and pulses, let's work out what our rate is.
If in this German Shepherd, your heart rate is 160 and the pulse quality is poor, that dog definitely needs fluids before we go ahead and anaesthetize. And do we need rapid replacement? Let's make a decision based on how the dog looks.
One thing we do need to think about in this case, where this is different from that cat case, if we have a bleeding splenic mass, if we increase our blood pressure too much, we're going to increase the tendency to bleed and more of our precious red cells are gonna end up in the dog's abdomen, which is then going to end up in your suction container when really we want them in intravascular space. So we're working really hard to make sure that we don't lose any more of those precious red cells. The approach here is a concept called hypotensive resuscitation.
So we are going to give some fluids, but we're going to monitor our blood pressure and try and give just enough fluids to get our mean arterial pressure above 60 millimetres of mercury prior to induction of anaesthesia. And then we're working with our fluids administration to keep that pressure just above 60. Until the moment that we have control over the haemorrhage.
As soon as we have control over the haemorrhage, we can start pushing the fluids a little bit harder. So question for you, this seven year old dog comes in, PCV is 25%, TP 40 grammes per litre, we can clearly see that this dog has lost blood. Which fluid would you choose first?
0.9% saline, hormone solution, gelliusin, or blood? And I mean, first choice, the first thing you're gonna grab off the shelf and start putting into this dog.
Matt, we don't have that loaded as a poll. OK. That's fine.
. I'll give you the answer then. The first thing that I would think about, and in all situations, your first line fluid is always an isotonic crystalloid. So now we think, OK, fine, this dog has lost blood.
If we start pouring blood straight in now, then we talked about the risk of increasing our blood pressure and losing further red cells, and we don't want to waste our precious blood. The first thing that we're gonna want to do to give us some volume expansion is going to be a simple case of giving Hartmann's solution. And my choice here is a 10 millo bolus of Hartmann solution and reassess, and then repeat that, and then repeat that.
So we're just gonna repeat those 10 millo bolus of Hartman's until either we have decent perfusion pressure on our pulse palpation or we have that mean arterial pressure above 60 millimetres of mercury. Once we have control, then if you have blood available, then blood makes perfect sense. You've lost blood, let's replace like with like.
So blood is a very sensible second option here. If you don't have blood available, then the second option would be geliffusing it, a colloid. So the advantage of the colloid is, it's a big molecule, they sit in the intravascular space and they hold some of that Hartman's solution that we said actually an hour later, most of it's gonna have leaked out.
The gelliusin is gonna help hold the Hartmann solution in the intravascular space and give us that benefit there. So if cost and availability with no object, I'd go for blood. If blood is not an option, then geliffusing is the second best.
That's fluids, as far as controversies go, and I'd encourage you to go and read that there's guidelines from the from the Journal of the American Animal Health Association, Hospital Association. Paracetamol, we've talked quite a lot about paracetamol in previous webinars with acute, and chronic, but if you didn't attend those webinars, just a brief mention on the difference in doses that we see with paracetamol. So formulary doses tend to be 10 mg per cake and we're talking dogs here.
The licence dose for PA LV, which is a licence preparation with codeine in the UK, is 33 MBs per kg, so it's quite a big difference there. My doses, I tend to use Parddale 33 MBs per gig, so the dose that's licenced 3 times a day for 5 days because that's the licence dose. Thereafter, whatever we do is going to be off licence if we need to use Padale long-term in this dog, and maybe this is a dog that can't tolerate a non-steroidal, so we're looking for another option.
Then what we do is off licence, we're gonna be having a conversation with the owner that we use this based on our experience. And you may have a dog that the 33 mg per gig TID works very well for, and we continue with that, and I have had cases where I've done that. You may have cases where you can reduce the dose down to 10 gigs per gig, 15 mg per gig, 20 gigs per gig, and carry on, but you will have cases where you drop down and you don't see that same efficacy.
So if you find something that works, then I wouldn't be afraid to use that higher original licence days for longer than 5 days. If I'm using the IV preparation. We're giving a product IV we tend to do that in hospital in the acute period, because we're given an IV we have a greater bioavailability, therefore it makes sense we can use a lower dose.
So 10 migs per gig tends to be the dose that we use, not with a huge evidence base. We did some work, comparing paracetamol in dogs that couldn't have a non-steroidal versus dogs that could have a non-steroidal. We think the 10 mg per cake keeps those patients comfortable.
The other option we have is an oral suspension as well, and we tend to use the oral suspension at 10 mg per gig as well, although you may question, well why don't you use that at the higher 30 mg per gig dose. I don't have an honest answer for that. I put one slide in on local anaesthesia because I don't think it's really a controversial area anymore.
There are clear benefits. We have marked reduction in opioid consumption. We see lower pain scores when compared to opioid continuous rated fusions.
We know that. Local anaesthesia doesn't impair wound healing, so we can put local into wounds and it's not going to impair wound healing. And we have a whole range of preparations available on the market.
So I don't really want to consider local anaesthesia as a controversial area. I would encourage everyone to go out and use local anaesthesia and refer to previous webinars if you want more information on that. It's just one of our Other topics to consider is alpha 2 agonists, and something that's quite controversial is the use of alpha 2s in cardiac disease.
I think we were all taught, probably 15 years ago that you shouldn't use alpha 2s in older patients or patients with cardiac disease because of the effects that cause bradycardia, mild hypertension, and a reduction in contractility. So I want you to think about those three components when we look at the subsequent use in certain cases that we're gonna look at now. Bearing in mind that these are the effects that alpha 2 has caused, do I want to cause these effects in my patients?
If we have mitral valve disease, the contractility in those patients is usually good. Our aim is to reduce afterload. We want to maintain the heart rate.
Cardiac output is rare and contractility dependent. And if we think about mitral valve disease therapeutically, what do we treat with? We treat with an ACE inhibitor which reduces afterload.
So let's just think, do our alpha 2s reduce afterload? What do they do to our contractility? Remember, we want to reduce afterload to reduce the flow across that, incompetent mitral valve.
Have we got that question loaded as a poll, yes or no to alpha 2s in mitral valve disease? Yep, we do have and I've just launched it. OK.
Right folks, you know the story. Just click on the relevant answer and we'll give you 45 seconds to answer this one or maybe a minute because it's a little bit more thought provoking. Come on guys, we're a bit slow in voting this time.
Everyone's gone to watch the football. It's time. Yeah.
Either that or they really have to think deeply at this one. Right, I'm just gonna give you 5 more seconds quickly and then we're going to end this poll. Right, let's end this poll quickly and share those results.
So nobody voted for the 1st 1. 60% voted for aim for reduction of afterload. Nobody the 3rd and 4th 1 and 40% voted for what do we treat with.
OK. What I normally think about with these cases is whether we want to. Our our approach, what this should be, are we saying yes or no to alpha 2 agonists, and if you think about the effects that alpha 2's cause, I'm gonna say that, I would advise against using alpha 2 agonists in these cases because they increase after load and they increase the flow across that mitral valve.
So. Mitral valve disease, we're not gonna use alpha 2s in those cases. I'll just go through this next one with aortic stenosis and just explain the advantages of using it after using these cases.
Contractility is usually good. Our aim here is to reduce after load. We want to see a milder reduction in that rate, because where you've got that stenotic aortic valve, every time that heart contracts, it's taking longer to squeeze that blood past that stalmotic valve.
So if you think about how we treat these therapeutically, we use a beta blocker such as atenolol to reduce the rate. If we think about how our alpha 2s work, they reduce rates and cause a a bradycardia, which is dose dependent. So actually we can use alpha 2s in aortic stenosis so long as we use a lower dose.
So lower dose, I'm talking 1 to 2 mcg per kilo of either meatomidine or dexamedatomidine. Quite a nice option in those cases. The rationale is very similar for hypertrophic cardiomyopathy as well.
Maybe even more so because we think contractility we we actually have a hypercontractile state with hypertrophic cardiomyopathy. And we may have dynamic outflow obstruction as well, so there is definitely an advantage here to a slight reduction in contractility and a reduction in rates as well. And thinking about how we treat those cats, we want to be using agents that are going to reduce that contractility and slow that rate a little bit.
So again, alpha twos make quite good sense. Dose low dose, 2 to 5 mcg per kilo of either meatomidine or dexedomidine tends to work in cats. Remember, we use slightly higher doses of alpha 2s in cats because they, they are less sensitive than dogs are to alpha 2 agonists.
So I would use alpha 2s in a hypertrophic cardiomyopathy case. Some of these recommendations can be quite case specific, so actually, if you do have a case that you've got to anaesthetize, I would actually just recommend calling your local referral centre and talking to the anaesthetist about that case specifically, but don't be surprised if they say, well, actually I would use an alpha 2 in certain types of cardiac disease. But aortic stenosis and hypertrophic cardiomyopathy are really the two that we would see in general practise that would be appropriate, but not mitral valve disease.
That's the one thing to remember. Our final topic of the evening is just touching on some aspects of brachycephallic anaesthesia and less of I I I think the, the breeder maybe the breeds are slightly controversial, perhaps the anaesthesia aspects are less controversial. Should we use gastroprotectants, well, a lot of, a high proportion of these dogs either reflux or regurgitate, and a lot of owners don't actually know it or notice it.
I think it's safe to assume that you are a brachycephalic, therefore you are probably refluxing even if the owner doesn't say you probably are. I would ask the owner to admit, but don't be surprised if they say, oh no, my dog, my dog never does that. From a gastroprotectant point of view, we tend to use omeprazole 1 week per kg.
We know that there's some evidence showing that omeprazole can reduce the incidence of reflux under anaesthesia in dogs. It makes sense to use it in these patients. Of course they may already be on a gastrict protectant such as omeprazole.
I just noticed today in the journal of Small Animal practise, there's a review of different gastroprotectants, so I haven't read it in time for this webinar but I'm quite eager to read that and see what the consensus there is. Again, a topic that wouldn't come as any surprise to any of us are brachycephalics at increased risk of complications under anaesthesia. Absolutely, definitely, yes, and we should be telling our owners this, that there is a greater risk associated with anaesthesia in these patients.
The risk is airway obstruction, risks associated with aspiration. If they regurge or reflux then aspirate, there's a huge risk of developing aspiration pneumonia. And of course there's risks that go along with obesity and maybe confound some of those other factors.
So you think there's much controversy around which analgesics we'd use. I treat these patients from an analgesic point of view, exactly the same as any other patient. I, I, I have some slight concerns when I hear people say, well, I'm worried about using this agent or that agent or should I just use lower doses.
I would use exactly the same doses as you use in other breeds. We don't want to encourage deprivation of analgesia in these patients for fear of the unknown. And typical pre-meds that we might consider.
ACE for those of you, Aceromazine opioids, pre-meds, I've given an alpha 2 opioid option here as well. So we can use Aceromazine in brachycephalic, actually a really nice option for gentle sedation that lasts a reasonable length of time. And we can use alpha 2s in brachycephalic as well, provided we have IV access and we can control that airway.
So we would never pre-med with a high dose of alpha 2, put that dog back in the kennel unobserved because they're going to obstruct. We can use a dose of alpha 2 intravenously on the table right before induction, where we have a nurse monitoring the patient, and we have all of our air airway equipment and oxygen available. So alpha 2s are absolutely fine.
The advantage of alpha 2s is we can antagonise them after the procedure and have our brachycephalics awake and walking around rather than sedated in the kennel. Of course the benefits that we're trying to achieve with our pre-medication are analgesia, anxiolysis, relaxation, gentle sedation, and hopefully an antiemetic effect, although we're not entirely sure of the advantage there. Whether sorry, whether any drugs do confer an advantage I should say.
What do we need prior to anaesthesia? We need secure IV access. We've just talked about sedation, we've talked about having oxygen available.
I like to keep an airway kit with those patients that follows them around the hospital, so even after recovery from anaesthesia, if they do suffer an acute airway obstruction, we can reinduce, reintubate, get airway control. Likewise, regurge kit that contains a suction catheter and an ability to suction and lavage the oesophagus should that patient regurgitate under anaesthesia. And of course a quiet environment in which to, to do all of those things that is monitored very closely and that patient is observed at all times.
Induction of maintenance of anaesthesia, I wouldn't necessarily try something different just because they are brachycephalic stick with what you know, familiarity is of course best. And thinking forward to recovery from anaesthesia, that can be an advantage using drugs that we can antagonise or reverse. We need to be proactive in thinking about our temperature management, so these patients aren't hypothermic in recovery and taking a long time recover to recover.
We want them back on their feet, as normal as possible, ideally going home as soon as possible. We discussed analgesics, we're going to pain school these patients and provide analgesia as required. And the key really here is the ongoing monitoring, and I think you can never trust that everything's going to go fine with the brachycephalic.
So I would always have monitoring on hand for those patients as required. If we need a little bit of anxiolysis, what are our options? Just lost in this slide here, Aceromazine, if you use acepromazine in the pre-med, we can always repeat that Aceromazine.
If you've used melatomidine in your pre-med or dexamedotomidine, we can always repeat a low dose of alpha 2 just to give a little bit of relaxation. We're not trying for complete sedation, we're just trying for that anxiolysis effect. So just to summarise that series.
You've looked at a whole. Host of topics broadly related to anaesthesia. And examine the human factors and some safety factors.
We considers new drugs and new ideas on all drugs. And we had a complete review of monitoring as well. And tonight we've considered some of the, the controversies that I think are relevant and things that generate questions.
So now if you do have any questions, then I'd be quite happy to answer those. Matt, that was an amazing end to a fabulous series and thank you so much for all the time that you have given us on these webinars. The, the amount of learning and the clarity and that has been absolutely fantastic and tonight was exactly the same.
Thank you very much. It's a pleasure. Folks, we don't seem to have any questions coming through for Matt.
So, Matt, I think you've answered everything. You've certainly got the brains working. And it's just up to me to thank everybody.
Thank you for your time. Thank Anna in the background for the controlling and to all the attendees. Thank you very much for your time tonight.
And we look forward to seeing you on another webinar, Matt. Thank you and good night.