Hello everyone. Thank you for joining for this next hour or so. We're gonna talk about pancreatitis.

We're gonna talk about the disease in dogs and cats, and I think there's some new information both on the types of disease each species gets and how to diagnose it and some treatment updates. We're gonna try to cover all that and let's just jump in and I used to think it was really helpful to do a compare and contrast. Between the disease in dogs and cats to help reinforce the differences in each, and now we've got to kind of rethink that a little bit.

So we'll start with the quiz question here, which is this more applicable to, dog or cat? Acute pancreatitis is more common than chronic. I think in the past, we would all have said that acute is more common in dogs.

The classic presentation of a fat pider old female dog that just ate garbage and comes in vomiting and painful, and that chronic is more common in cats. Well, it seems like based on new information and lots of histopathologic studies that chronic pancreatitis is more common in both species, but acute pancreatitis in dogs gets all the press because it's a more dramatic presentation. The bottom line here, as clinicians, I think we have to realise that when we see vaguely ill cats, we all know that any cat that has Anorexia or decreased appetite, lethargy and dehydration, pancreatitis needs to be on the differential list.

And I think we have to expand that to dogs now where if we have non-specific GI or other signs in dogs, or we have, let's say on lab work, we cannot find the cause of those increased liver enzymes in a dog. We should be thinking about pancreatitis and when we are thinking about pancreatitis in any form, just assume there's pain. That's not different.

Just take care of that. And then one thing in cats that I thought was pretty unusual is that you can feel the pancreas as an abdominal mass and about 25% of the cats with pancreatitis. I point that out to emphasise the importance of the thorough physical exam and also that every mass you feel in the abdomen of a cat isn't necessarily cancer, OK?

So, be, be aware of that. And as you know, sometimes to palpate. Cranial structures or abnormalities in the abdomen, which can be tucked up under the rib cage and hard to palpate, sometimes elevating the front front end.

Of the patient can help shift those organs or masses caudly and make them easier to feel. OK. Next question, which is this more applicable to dogs or cats?

There is no breed, age or sex predisposition to pancreatitis. This is a cat thing, OK. I think we know that there are some common risk factors in in dogs and traditionally we've thought of them.

As things like specific breeds of dogs being more at risk. Now we know that it's basically just the size that makes you more at risk, so all small breeds are at equal risk. The thinking that these particular breeds had increased risk was based on some findings of specific gene mutations like *** gene mutations in these dogs, these breeds that have pancreatitis.

It turns out that the genes are just common in the species, whether they have pancreatitis or not, and these genes don't produce anything. So it's not like they're specifically linked to the disease, they're just there, so. As of yet, to my knowledge, no proven genetic cause of pancreatitis.

Over being overweight or obese traditionally has been considered a risk factor for pancreatitis in dogs, and that is true. So we want to make sure we're doing our best to maintain optimal body condition and muscle condition score in our canine patients as well as our fema patients. Dietary discretion, a common risk factor for sure and definitely a common.

Finding in the history of a dog that comes in with acute pancreatitis. Garbage is the big one though. OK, so there's a much higher risk of pancreatitis eating garbage, which has, you know, Elements and toxins and other things in it that can irritate the pancreas, then say unusual food or table scraps.

All of that though, under the term dietary indiscretion, umbrella term, all of those are increase are risk factors for pancreatitis and dogs, high fat diet for sure diet as we know it's not a thing. At least the fat content is not an issue with cats and pancreatitis, although if you do have a cat with pancreatitis, we want to avoid a high fat diet. But in general, it's a dog thing.

Fat content in diet is a risk factor for pancreatitis in dogs, and some of the therapeutic diets, we have dogs on. Are high in fat, just be aware of that. So let's say you have a refractory seizure patient and as part of the therapy, we're on a keto diet, which has been shown in both people and dogs to help with seizure control, OK?

I fat diet. Also, if we have dogs on struvite dissolution diets, high fat diet. So just be aware, in some studies in dogs on these diets, some of them in a small amount, but some of them have developed pancreatitis.

Hypertriglyceridemia, this is a big one. So we want to keep that value under 500, yeah. Over about 850 is when we see a really significant jump in the risk of pancreatitis, and this is twofold.

If we have a dog with hypertriglyceride, gave me so bienic serum that we measure triglycerides on, we don't care about cholesterol, we care about triglycerides, yeah. Then we want to assess for pancreatitis, and then any dog with pancreatitis, we want to assess triglycerides and control that value if it's elevated to minimise exacerbating the disease. Endocrine diseases, we associate with being a risk factor for pancreatitis in dogs, but it's mainly diabetes mellitus, hypothyroidism, and hyperadrenal corticism or Cushing's syndrome, maybe less likely, but no doubt that having diabetes mellitus is a risk factor for pancreatitis.

Yeah. And then certain drugs are anti-epileptic drugs, and it's usually a combination of potassium bromide with phenobarbital, a higher risk factor than just potassium bromide alone and we know we have some chemotherapeutics to be concerned about in dogs and hypercalcemia. And this is something that I think, you know, when we're talking about changes in calcium high or low, I think the best thing to remember is that we really don't have an abnormality in calcium unless we have an abnormality in ionised calcium.

So the recommendation would be anytime you have an increased or decreased total calcium, try to confirm that by getting an ionised calcium. Now, cats, no known risk factors, but You know, they can develop pancreatitis if there is a decrease in pancreatic perfusion. From either having anaesthesia, from having a traumatic episode, anything that would impair profusion of the pancreas, cardiac problems, etc.

OK. So the main goal here is when we have sick cats, OK, traumatised sick cats, under anaesthesia cats, we want to make sure we're getting adequate, but not too much fluid therapy. So that we maintain profusion, but most of the time in cats, the disease remains idiopathic.

OK, for which is this true? Current concurrent GI and liver disease is more common. This is definitely a cat thing and it has to do with their anatomy.

Of course, they have unusual anatomy that predisposes them to having both not only pancreatitis, but also liver and gut involvement and the reason for that is because Their bile duct and pancreatic duct join before the pancreatic duct enters the duodenum. OK. And dogs said they're separate things.

The pancreatic duct and the bile duct have their own entries into the abdomen, but in the cat, the common bile duct and the pancreatic duct fuse prior to entry into the duodenum, meaning there's just an open channel for communication between all of those organs, yeah. And so the common comorbidities we see in cats with pancreatitis, and this is over 2/3 of them are liver disease and gut disease. OK, so you can have pancreatitis and one of those, bioitis or pancreatitis and both of those triitis.

Also, we can see lipidosis and diabetes melos and then just to be aware that, you know, our new oral therapy for naive diabetics that aren't ketotic and aren't sick are SGL2 or SGLT2 inhibitors, yeah. Not indicated, not recommended when you have diabetes mellitus because these and pancreatitis, because those cats are more likely to require insulin and develop ketosis if they don't get it. OK, which is this true for dog or cat?

Combination of clinical findings, pancreatic lipase, immunoreactivity, and all. Ultrasound provides the most reliable diagnosis, and this is both for sure. Now, diagnosing pancreatitis, we can do this, OK?

When you read a study about pancreatitis, there has to be inclusion criteria mentioned in the study, like how did they determine that either the dogs or the cats in the study had pancreatitis. And here's an example of one study and the criteria for inclusion for pancreatitis for two or more of the following classic clinical signs you can see there. Abdominal ultrasound that showed no other cause of the signs.

Now here it's interesting, they weren't trying to confirm pancreatitis with ultrasound but rule out other causes of those gastrointestinal signs and then an increased snap CPL test. Now we can do that, yeah. So I just think, you know, it's possible to make an in-clinic diagnosis of pancreatitis and it just got easier.

Teaser there, we'll get to that in a minute. What we know is that our typical amylase and lipase on our chemistry panel are basically not useful. In cats, amylase lipase not useful at all.

In dogs, amylase, forget it, lipase, if it's exceedingly high, say 4 times higher, 4 times normal or higher, OK. Probably only pancreatitis can do that, but still, I'm not making a diagnosis unless I have a more specific test for the lipase from the pancreas. And the reason that the serum lipase on our panels fall short is that there's like over 100 lipases in dogs, yeah.

Cats probably as well. They come from different organs and so the Methodology used for the lipase on a routine chemistry panel can't distinguish between all of these different types of lipase, but we really only want to know what is going on with the lipase from the pancreas. So pancreatic specific lipase test.

And so we have You know, two general types of assays that can identify lipase, and the only ones that are truly specific for the lipase from the pancreas are the immunoassays, and they, these are monoclonal antibodies that only react with the pancreas, with the lipase of pancreatic origin. They don't cross. Any of those other 100 phases or 99 lipaes, yeah.

And you know, we know the common available immuno acids are both the snap and the SEC CPL and FPL from IDEX, and then the CPLI, so the canine and feline, pancreatic lipase, immuno reactivity from Texas A&M. OK. Then we have those enzymatic assays.

These are just assays that react with any old lipase, and they, none of them are inherently specific for pancreatic lipase. They just can't distinguish between the other sources of lipase and that from the pancreas, yeah. So, with that in mind, how do we confirm pancreatitis in the clinic cause we really want to get these animals on treatment, especially the acute ones, which by the way, yes, chronic pancreatitis is more common in dogs and cats, but acute does happen in both and is severe often and requires, you know, quick diagnosis and aggressive early intervention.

So, what we can do in the clinic now is we can run a snap. Pepide snap test for canine and feline pancreatic lipase. These tests cannot confirm diagnosed pancreatitis, but they're screening tests that if they're negative, rule out the disease.

So how we use these tests and all screening tests in the manner of, if they're negative, we think, OK, not pancreatitis. So a highly sensitive screening test that is negative. So screening, the word screening and negative both have an end, right?

So a screening test that is sensitive with an S and negative with an N rules out the disease, snap, yeah. So, the negative rules out the disease. A positive result could The pancreatitis, OK, but we have to confirm, OK?

And the ways to do that now, up until now have been to send to the lab another sample to get an actual quantitative value, how high is the CPL or the FPL? And then there are cutoffs that determine, well this is borderline, this is grey zone, and this is consistent with pancreatitis. Things just changed.

Now at IDEX there's a new lipase on the catalyst machine analyzer. That is specific for pancreatic lipase. This is kind of Great in the sense that, OK, it is an enzymatic assay and as we saw from the previous slide, that none are inherently specific for pancreatic lipase.

This is a DGGR assay like other. Lipases that you get from other labs and even Is that in the lab, right? But those DG DGGRS can't distinguish between the lipase and the pancreas, the one we care about, and the other lipases.

But this one, because of the way it's engineered, they figured out how to manipulate the pH and manipulate the temperature so that this DGGR only detects pancreatic lipase. And one good way to determine that your assay is only specific or only detects pancreatic lipase is to run it on dogs that shouldn't have any pancreatic lipase. In other words, dogs that have pancreatic acid or atrophy or EPI exo pancreatic insufficiency.

There should be no pancreatic lipase in the circulation of those dogs, right? So if you run a pan lipase assay on those dogs and you get a value, you know that's not from the pancreas. So your lipase assay is not specific for pancreatic lipase.

This new DGGR assay on the catalyst analyzer reads nothing as you would expect. So it is not picking up any other lipase, meaning it's kind of specific for the pancreatic lipase and it has a really good correlation. Based on both IDEX internal and external Texas A&M validation, really good correlation with the SEC CPL and the SEC FPL.

All the stuff you want to see, the precision, the reproducibility, those values should be below 10%. They're well below 10% with as I say, minimal interference with the typical interfering substances, he lipemia, hemolysis, and you get a number, you get a quantitative value, so that you can with the snap test, it's either positive or negative and then you move on. If it's possible to get a number, while here with this availability of the pancreatic lipase on the catalyst, you only need to run that test.

And then you'll get it, is it above the normal value or is it not? OK. So just to show you some information showing the correlation between the catalyst, pancreatic lipase, and the spec CPL and FPL, you can see they're pretty much on the line for the most part, right?

And our our value is of our value of 1 is perfect and we've got our value of 0.94 and 0.96, pretty good, yeah.

And then this just shows you that. When we look at running the catalase pancreatic lipase on dogs that have pancreatic as or atrophy, in other words, no tissue, no pancreatic lipase. There should be none measured by an assay if it's specific for the pancreatic lipase and SEC pill over on the right.

Only a few samples measure any at all but well below cutoffs for what would be considered positive, yeah. And the catalyst assay, the new catalyst pancreatic lipase assay, hardly any. Specific for pancreatic lipase.

So now, diagnosing pancreatitis in the clinic just got a lot easier because we can simply run this test, get a number. And determine if we have evidence of pancreatic inflammation or not. And then of course, we're gonna put that in the context of what's going on clinically with the patient, and imaging studies we have and other laboratory evidence that supports it, but this is kind of a big deal.

Super glad to have this available now. OK, so which is this true of dog or cat? The basic lab work are essential for determining severity and prognosis.

Well, this is both, obviously, and we look at The lab work, you know, how pancreatitis can be more of a localised edematous process or it can be a hemorrhagic necrotic, more severe condition that can cause systemic inflammation, the cytokine storm that can involve all organs in the body, as I'm sure we're aware. And so we look at the lab work to see, do we have any evidence of that? Are other organs involved?

Does this become a widespread systemic problem? So the CBC nothing specific at all. But I haven't read things that if you see these, should get your attention because the disease is more severe and these are associated with a poor prognosis.

But mainly use them not to say, well, there's no use trying to treat this dog, because I see a lot of thrombocytopenia and other red things that I'll show you, so not worth treating. No, no, no, it is worth treating. It's just that these animals, you gotta stay on them and be more aggressive and way more monitoring and probably 24 hour care, all that.

By chemistry panel, you can see some of the most common changes, no surprise here. The ones in red, you know, are ones again that we have to be, you know, aware of, and if we find them, take them seriously, be more aggressive in our therapy. C-reactive protein, our acute phase protein that systemic inflammatory marker in in dogs, only if it's elevated and mainly if it stays elevated beyond 2 or 3 days of therapy, that's a negative prognostic indicator.

Hypoglycemia. Also, excuse me, negative prognostic indicator, probably because it indicates we've got sepsis, yeah, or SERS, and then hypocalcemia, any disease that causes hypocalcemia and this again is ionised calcium being low, is regardless of what's causing that, what the disease is, hypocalcemia is just bad, negative prognostic indicator. Now, in cats in particular, the correlation between total calcium and ionised calcium isn't great.

So you can have a normal total, but have a high or low ionised and vice versa. So we basically in cats specifically really wanna rely on ionised calcium to determine if we have an abnormality there. We can also see with acute severe pancreatitis, acute kidney injury.

OK, so this is something to be aware of. If you have an animal that comes in with severe pancreatitis, you're gonna have decreased perfusion to the kidneys, inflammatory mediators circulating that can damage the kidneys. So we want to be monitoring these guys for the development of acute kidney injury.

Yeah. Now we have Markers for acute kidney injury and all of these appear first in the urine. So the injury markers are in the urine.

And the reason for that is the tubules are the most vulnerable part of the nephrons, so anything that affects the kidneys will hit the tubules first and we'll see changes in the urine up to 2 days before we'll see changes in the blood. So we're relying on our STMA and creatinine and BAM to tell us if we have acute kidney injury by the time those are elevated, we're like 48 hours behind. So we have our traditional markers for acute kidney injury.

You can see here, the issue is if they're present, they're specific. So granular cast. If you see them, you've got acute kidney injury.

If you have glucose urea, the normal blood sugar. That tells you you've got something going on in the proximal tubules. They're not reabsorbing the filtered glucose, right?

However, if you combine glucose era and granular caste, only 30% of dogs with AKI have those. If you see them, AKI but you don't always see them when you have acute kidney injury. Enter cystatin B.

This is a test we do now on urine, which is an indicator of active, like right now tubular damage. This cystatin B should be in the tubular epithelial cells. When they're damaged from ischemia or a toxin or infection, those cells break down and release the cystatin B into the urine.

And that's present when you have AKI right now. Think of it as the ALT of the kidney. When you see an increase in ALT in the blood of a dog or a cat, you know two things.

You've got right now liver cells that are leaking. This is a cytosolic enzyme that leaks, we call it a leakage enzyme when the patocytes are damaged. OK?

ALT has a short half-life. So we also know that when That damage is resolved and we've treated that patient correctly, the ALT will go back down to normal. And that's ystatin would be in the urine.

If you see it in the urine, you know that right now, tubular epithelial cells are leaking, they're damaged. And then as we monitor that urine cystatin B, if it's going down, we know that returning to normal, we know our treatments are working. So, we look at cystatin B when we have a suspicion of acute kidney injury from a direct hit to the kidney, like a toxin.

Lilies and cats, grapes or raisins and dogs, ethylene glycol, you name it, or we can also have damage to the kidney from a non-kidney related problems. So secondary acute kidney injury from pyomenephritis, vector-borne disease, pancreatitis, anything that impairs blood flow to the kidneys or bombards the kidneys with inflammatory mediators, those cytokines that are highly damaging to cells, OK? So Bottom line, severe acute pancreatitis, monitor those patients for acute kidney injury by looking at the urine as well as your blood work, but it, you're gonna see evidence of AKI first in the urine because the tubules are damaged before the GFR will Go down, yeah.

And then cystatin B is a useful tool in identifying that in more patients and relying on our traditional markers that may or may not be present. OK, what about imaging in terms of helping us get a diagnosis of pancreatitis? Well, we do it, but think of it as you're doing radiographs and ultrasound.

Yes, you're looking for supportive evidence that the pancreas is a problem, but what you're really doing is ruling out other causes. OK. You should be able to find a normal pancreas.

So yes, I mean, the fact that you, we used to be able to say, I didn't see the pancreas, so it must be normal. That's no, with a good ultrasound and a good ultrasonographer, you can find it and assess it for all the things we know. Is it enlarged?

Are there changes in ecogenicity? Is there duct involvement? Is there fluid around it, right?

We know the changes, but what we're really hoping, what we're really doing with our imaging is Can we find another cause? Is there an obstruction? Do I have a mass, etc.

Now, thing to important thing to remember is that if at first you don't succeed, in other words, your additional ultrasound shows nothing. In the pancreas, repeat it a day or two later. Serial assessment has been shown to identify more positives than just one ultrasound, especially acutely in the disease process before changes have occurred.

Now, another thing to remember, and this goes for all tests of pancreatitis, the lipase that we have on the catalyst now, the FPL, the SEC CPL. The more severe the pancreatitis, the more obvious the changes will be on ultrasound and the higher those pancreatic specific lipases will be more inflammation, right? The milder the disease, so these chronic forms, these smouldering forms or intermittent forms of pancreatitis that we know cats have, and that a lot of dogs also have, the changes in the pancreas are mild.

There isn't that much inflammation, meaning You're not gonna see that much on ultrasound, and Maybe the values the spec CPL and FPL will not be that high, OK. When it comes to ultrasound, remember in those mild cases, it might be hard to find direct evidence of pancreatic disease, therefore, just make sure you don't find another cause of those signs. Now on the therapy, the big Aspects of therapy will be no surprise to anybody.

So fluid therapy number one, you've got to perfuse the pancreas, stabilise the patient. They're all painful like we said earlier, they all get analgesics. We've got to give them enter nutrition early and to do that might require stopping vomiting and controlling nausea.

And then in dogs we have now a conditionally approved drug, the first one ever for the specific treatment of acute pancreatitis in dogs. Mentioned before that we do see acute pancreatitis in cats as well, and this is an open source article that's really thorough in describing it, and it actually has a really good drug formula, including dosages, all dosages that you need for your analgesics and in this article. OK.

When it comes to IV fluids, we have to ask two questions, which one and how much? OK. Then there's an awareness now that by overdoing fluids in any disease process, causing volume overload, we can actually cause more harm than good.

So, hypervolemia is as bad as hypovolemia. So we want to avoid that and we'll talk about how to do that. So what fluid we reach for in any condition you can think of, almost, there's only one exception to this, which we'll talk about.

Just get lactated, reach for lactated ringers, OK? This one is fine. It mimics.

Plasma, so you can give a lot of it, not disrupt electrolytes or acid-base status. It has a buffer, yeah, so it's not acidifying, and the buffer is lactate, which is non-vasodilating. So things like plasma lite, also good choices.

The buffer is acetate. There's an advantage maybe in severe liver disease to using acetate as a buffer does not need to be converted. In the liver to become bicarbia, but acetate can be vasodilating, so maybe not such a great idea in a patient who's not stable, yeah.

Lacatorings contains calcium. Important because again, anything that causes low calcium, bad prognosis, and it has a trivial amount of potassium, a small amount of potassium. So if you're thinking, well, I won't, I don't want to give lactated ringers to a black cat or an Addisonian who's in crisis because those dogs and cats potassiums are already high, forget it.

You can give lactated ringers because the amount of potassium in that fluid not gonna do anything. To further increase the potassium in the blood. Safe, safe, safe.

Now the exception to lactate mingers being your go to fluid. Yes, even in an Addisonian crisis, which we now call adrenal crisis, is if you have a dog or cat, that's say vomiting. And you find on your lab work hypochloremia and an alkalosis.

So hypochloremic metabolic alkalosis in a vomiting animal, that's upward GI obstruction until proven otherwise. And in those patients, physiologic saline is the food of choice because that has by far the highest chloride content, and that's what's required to fix that hypochloremic metabolic alkalosis and everything else, lactated ringers is fine. OK, now, they've looked at this, OK.

There's been two studies, one that compared lactated ringers to physiologic saline and pancreatitis. This is in people, and lactate and lactated ringers actually is anti-inflammatory. So the patients did better, who the ones who got lactated ringers did better than the ones that got saline because they had less severe inflammation.

And it decreased the progression from moderate to severe disease by half in half, which is crazy. Another study looked at how much fluid, waterfall study looked at how much fluid patients got and did that correlate with severity of pancreatitis. So they had sort of an aggressive fluid therapy group and a moderate fluid therapy group.

And guess who did better? The moderate fluid therapy group. OK, because no volume overload, no exacerbation.

Of interstitial edoema, which can cause impaired oxygen delivery and other problems, right? So, how much it is based on your patient, so thorough assessment, thorough monitoring, and how fast depends on how fast they lose it. So if you have hypovolemia, that's something that happens acutely, shock, OK.

Haemorrhage, trauma. You lose the fluids quickly, you got to replace them quickly, and that's usually within an hour or so, yeah. Now the way we do this is, is different than in the past.

We use lower volumes of crystalloids, lactated ringers than previously because we are trying to avoid volume overload and we give them more slowly. So our boluss would be 10 to 15 mL per kg in a dog, 5 to 10 mL per kg in a cat, over 15 to 30 minutes. Assess all these perfusion parameters, mucous membranes, a refill time, pulse strength, heart rate, lactate, urine production, right?

And then, not happy, another similar bolus, same time frame, do that 2 or 3 times. If you're still not happy at that point, then crystalloids have done their job. You don't want to give more because they end up in the interstit within an hour of giving crystalloids like lactated ringers, only about 25% are still in the vessels and the rest are in the interstitial tissue.

And let's say you're a kidney and you're filling up with interstitial fluid. Well, you are surrounded by a rigid capsule. So if you have a rigid capsule, but there's more and more fluid in the kidney, the pressure in the kidney increases and that causes a decrease in GFR and renal blood flow and can cause AKI and pancreatitis patients are already at risk for it, and by the way, if you are an AKI patient, hypervolemia.

Is a worse prognostic factor, more mortality if you're hypovolemic, hypervolemic with AKI than if you're septic with AKI. That's how important it is to not overdo it with fluids. If your crystalloids aren't getting you there after two or three bolus, it's time to reach for a colloid, a natural colloid like res and plasma, or if your dog canine specific albumin.

OK. These animals are often dehydrated and dehydration happens more slowly, so you can replace the fluid deficit more slowly over, say, 4 to 6 to 24 hours, depending on the condition you're dealing with and the condition of your patient. You can see the formula there for calculating how much fluid you need to replace a given deficit, which is estimated by dehydration is.

As sort of crude as that is, as an indication. We're not really good at assessing dehydration and an animal, by the way, can be up to 5% dehydrated and show no signs. So I always say, well, you got a sick patient, especially a cat, maybe not eating, you can't really find anything.

Assume 5% dehydration and correct. Can be subcu fluids if it's a stable patient or you can add that amount to other fluids if it's a hospitalised patient. Then you keep up with any ongoing losses from vomiting or diarrhoea or polyuria, and then maintenance and that's it, OK?

How do you determine if you're giving the right amount? It's about monitoring, OK? All those parameters up above.

Blood pressure as well, and then body weight on an accurate ground scale, maybe up to 4 to 6 times a day in an acutely ill patient who's getting resuscitated with relatively large volumes of fluid. And if you're seeing a 5% increase in body weight, Consider reassessing, maybe adjusting the volume of fluid you're administering. If you get up to a 10% increase, that's when volume overload occurs.

So, new, new strategy, OK, around crystalloid resuscitation. Lower volumes and slower rates of administration, OK? If you got a critical patient circling the drain and you really want to get that volume up quickly, one injection of hypertonic saline, and then if that's not doing it, we want to go to a natural college it sort of the use of things like head of starch and voluming falling out of favour.

We just sometimes can't even get them. They don't really have that many advantages over crystalloids, as many advantages as we used to think they had. So if we need to go to a colloid, try to make it a natural colloid.

They're all painful, as we mentioned, so give them the analgesic support that they need. It's usually a narcotic, and you gotta ramp up based on how severe the pain is, and frequently adjust based on serial assessment of pain. And then you can do other, you know, sort of adjunctive analgesic administration.

You can say do a fentanyl, lidocaine, ketamine, CRI. There's a bunch of stuff you can do, but I, in general, fentanyl, if you get to the point where you like morphine or methadone isn't working, fentanyl intermittently usually gets you where you want to be pain control wise. To get them to eat might mean, or to be able to feed them.

By a feeding tube might mean having to stop vomiting and our drug here of course is mirropotin. It has other properties besides being an anti-emetic, anti-inflammatory, it can be anti-nausea as well. We used to think it had visceral anaesthesia, like equivalent to morphine.

There's some question about that, but it ain't gonna hurt, OK, for all these properties, and it is the most effective limetic by far. If we need to reduce nausea, in cats, we have mirtazapine as an option. Dogs and cats, we can also use ondansetron and it's not a bad idea to consider both ondansetron and mirropotin.

Because the lack of vomiting doesn't mean that there isn't nausea, yeah. So you want to cover both. The other thing is, often these guys have functional ileus, so gastric distention can occur which is painful and increases the risk of aspiration.

So prokinetic like metoclopramide, and we're giving it as a prokinetic because it has very weak antiemetic properties, yeah. And then also if we're gonna put a feeding tube in these animals and they often require that. Get the tube into the stomach so that you can aspirate, suction any excess fluid or saliva from the ileus, relieve discomfort, minimise aspiration risk, and then you got that tube in there.

It's what we're gonna use to give our liquid andal diet and then water as a means of hydration, if we can. OK. When do we start?

In nutrition within 48 hours of the onset of signs. OK, not 48 hours after they have been in the hospital, but after the onset of signs. And often the average time it takes, the average time between the beginning of signs and the dog with pancreatitis presented at the clinic is 48 hours.

OK, so sometimes we gotta get these guys the vomiting under control so that we can start feeding them internally, . The day they arrive. OK, so we all know that parental nutrition is over.

In almost all cases, we want to rely on enteral for its protective effects on the gut mucosal barrier, which basically minimises translocation and all of the downstream effects of that er sepsis, multiple organ system, multiple organ dysfunction syndrome, etc. It's all about enteral, and this is not it. We're not putting food in a cage, the sick cats in particular, because what will that do?

Cause food aversion. This is not providing nutrition. This is providing nutrition, so get the tubes in, yeah, and then.

You know, for most cats, and almost, you know, most dogs, you can use a very linear formula for determining resting energy requirements. OK. So that's animals between 2 and 30 kilogrammes, that's the majority.

You can just use that simplified formula, but for very large or very small animals, you want to use the, the formula that has the Raised to 0.75 power, OK. But for most of our dogs and cats, you can use the linear formula, OK?

And then ideally we want to give a third of RER day one, increase that to 2/3 day two, and then full RER by day 3 to 5. Great, if you can do that, great. If you can't do that, great.

Give them something. OK, trickle in a small few CCs an hour. Give them any fraction of this so that they will get some glutamine to those enterocytes to keep them happy, OK?

We don't want to force the issue and then risk exacerbating vomiting or discomfort or aspiration, just give them some nutrition and in order to do that, again, we might want to use. Opitin ondansetron, gastric suctioning, metoclopramide, you see that there. And then we want to give them, especially if you're a dog, a low fat liquid diet.

So Rocaine and Jerry low fat liquid is fine. The human product Vivanex is also fine. It's got zero fat in it.

More important in dogs and cats, but it is kind of hyper osmolar, so you can get some diarrhoea. That's OK. Just give the amount that you need and to minimise any sort of adverse effects.

What else besides fluids, analgesic, and nutrition? And things that help you give nutrition like anti-medics and anti-nausea drugs. Well, antibiotics rarely necessary unless you've got a really acute severe dog or cat that has evidence of SERS or sepsis.

So higher low heart rate, higher low temperature, higher low nutritional count, low blood sugar, or you have a disease that requires antibiotics. They want to be pretty broad spectrum with your choice. GI protect.

Not standard, only if you have some other risk factor for erosion or ulceration of the GI tract, right? Corticosteroids, there's news here. So, first of all, they don't cause pancreatitis, right?

If they're indicated in a given patient with pancreatitis, give them. And cats often have those concurrent intestinal and liver diseases that would benefit from Prednisolone, yeah. Fine.

Give them prednisolone. If you have sort of a chronic intermittent relapsing pancreatitis, decreased appetite, give them prednisolone. Dogs.

I, as of yet, have not gotten on the bandwagon of giving dogs with acute pancreatitis. Leukhticoids. However, there have been 5 studies, 4 of them were experimental in dogs where this was done, and it didn't hurt.

OK, so there's good evidence that giving prednisone, or an equivalent dose of dexamethasone, acute in the pancreatitis, you know, course in dogs reduces histologic severity, fair evidence for shorter hospitalisation and lower C-reactive protein. In a study out of Japan that looked at this, they actually saw that the CRP decreased earlier and mortality significantly decreased versus dogs that did not get prednisone. So given early may be beneficial, and another little teaser, what do, what is one of the effects that glucocorticoids have that could be beneficial with pancreatitis or any infla inflammatory disease, they prevent Neutrophils from leaving the bloodstream.

OK, we want some to lead the bloodstream to enter sources of inflammation or infection, take care of that, but if we overdo it, then the neutrophils exacerbate inflammation. That can take sort of a localised pancreatitis and make it more severe. So, prednisone works in dogs with acute pancreatitis.

One of the key Thoughts about how this works is it minimises the transudation of neutrophils out of the vascular space into the tissue where when they release their proteases and other chemotactants and cytokines, you can develop the cytokines store. OK. One thing to also be really attentive to, especially in cats with pancreatitis is they're at risk for cobalamine deficiency, B12 deficiency, for a couple of reasons.

One, intrinsic factor which is required to bind and protect cobalamine in the stomach until it gets to the absorption sites in the ileum, prevent it from being degraded, intrinsic factor in cats is only produced in the pancreas. So if the pancreas isn't working and inflammation also means non-function. So not producing intrinsic factor, then you can develop low carbalaine because it gets degraded in the stomach and intestinal tract.

Yeah. Also, cats with pancreatitis can have chronic neuropathy, OK, and that can also impair carbalamine absorption. So, Measure it and supplement it if the value is less than 400.

Now that is within the normal range, but kind of lowish in the normal range, so we don't wait until the cabalamine is less than normal to supplement. We wait till it's less than we supplement when it's less than 400. The reason for that is at values less than 400 nanograms per litre, that is associated with intracellular cobalamine deficiency.

All right. And then in acute patients, injectable is preferred. You can see the protocol there.

Now it's weird that, you know, giving cobalamine orally will work because the reason that it's low is that it's not being absorbed by the ilium in most instances. However, there is some absorption of B12 throughout the GI tract, so stable patients, long term therapy and option is to give oral cobalamine. And you can see the protocol there, but this is just a thing to remember, especially in cats.

If their cobalamine is low and we don't fix it, then often we don't get the response we want from our other therapy. OK, now the, this is crazy. We now have an approved drug for, well, a conditionally approved CA stands for conditionally approved drug for pancreatitis in dogs.

Only dogs. OK, if there's a drug that you see with conditional approval. Just only use it as Directed, because if you go off label and have a problem, you can use your licence.

OK, so just anything that has conditional approval, just follow the rules. This is no time to be going rogue, OK? Anyway, what this drug does Panicquil, OK.

Is its trade name. This does kind of what prednisone does, only better, OK? This inhibits neutrophil binding to the endothelium and therefore, the beginning of the process of them exiting the vascular space, entering the tissue, and releasing all of their harmful chemicals and chemokines, etc.

OK? And this ends up with Having less inflammation and sort of dampening the inflammatory responses. And you get improvement quicker using this drug than not using this drug, OK?

This is a 3 day, once a day injection. Given IV over about 15 to 60 seconds. And so when do you use this drug?

Anytime you have acute pancreatitis in a dog, whether you have One that you're going to admit or not admit, treat as an outpatient for whatever reason, diseases, mild owners can't afford the animal to be in the clinic. So this can be done inpatient or outpatient. The owners just come back for 3 days and you give them the injection, along with all the other therapy.

This replaces nothing, OK? This is just an adjuvant to. Our toolbox, in addition to our toolbox for acute pancreatitis in dogs.

This has been used now for a couple of years and when I go to lectures by people who are using it, they like it. Now, often these are people that work at universities or specialty clinics and their pancreatitis dogs do pretty good anyway cause they've got the staffing and the 24 hour, they can do it all, but still, they feel like this is helping and they're seeing very few side effects. So.

This is something to consider and use in our dogs with acute pancreatitis. And then we know that there's some sequela that you can develop from pancreatitis. One thing I'd like to point out is that often there's a functional biliary obstruction.

The pancreas is swollen and edematous. And it can impair biliary flow, OK? This is functional, it goes away when the pancreatic inflammation resolves.

So these dogs can look pretty non-icteric for a while and then delayed, have a delayed increase in bilirubin, you're like, what is happening? Things are looking well, but the bilirubin is getting higher. You get your ultrasound, you can see some changes in the bile duct.

Be patient, stay the course. Continue your therapy. These dogs do not go to surgery unless they're, you know, I don't know, there's biliary leakage or something along those lines.

You can do percutaneous. Aspiration of the of the gallbladder to minimise. Things make things improve, but this is not an open abdomen surgical cholecystectomy kind of situation, OK?

And then remember also that AKI can develop secondary to Severe pancreatitis, we wanna monitor that and that means staging these patients when they're with us in the hospital every day for acute kidney injury for the iris, AKI grading guidelines, OK? And you can detect the development of AKI if you see a creatinine increase. Of greater than equal to 27 million moles per litre in 48 hours, and this may be values well within the normal range.

So look at the value, don't just look to see, don't just look at the values that are flagged as either high or low. Look within the reference interval and if you're seeing a creatinine increase by that much or more in 40. That's a sign of AKI as is decreased urine production, defined by the iris grading system for AKI is less than 1 mL per kg per hour over 6 hours.

You can use other things to monitor, obviously your lab work you just saw significant changes. We want those all to be improving over time. If you're using C-reactive protein in dogs to monitor, if it's elevated to begin with, use it to monitor if it remains.

Elevated after 2 or 3 days of therapy, change something, it should normalise, you know, relatively quickly. You can also follow your pancreatic specific lipases. They don't go down linearly, so give them time, maybe wait a couple of weeks and see if you're seeing the appropriate trend downward if they remain elevated.

Maybe worth going back in imaging wise to see if you're developing any kind of complications, OK? With that, I want to thank you for your attention and enjoy the rest of your day or evening. Thanks.