Good evening everybody, and welcome to tonight's webinar. My name is Sophie McMorra, and I'll be speaking tonight. So before I go on to tell you a little bit about myself and start the webinar, I'd like to mention that you can ask questions throughout the webinar.

In order to do so, just click the Q&A box at the top or bottom of your screen, type your question and send it through. It won't disrupt the webinar at all. It will just read it at the end.

OK, so I'm Sophie McMurra. I'm a registered veterinary nurse and I also have a VTS or a veterinary technician specialty in small animal internal medicine. I work at North West Veterinary Specialists where I'm the head nurse of the internal medicine department.

So tonight, we're gonna talk about nursing the pancreatitis patient. So we'll start first of all with some anatomy and physiology. I think it's quite important that we understand what's going on in the body in order to understand what's happening when things start to go wrong.

So first of all, the pancreas has both endocrine and dexocrine functions. It's a long flat abdominal organ, and it lays the two lobes. One is just underneath the stomach, and the second lobe runs just alongside the duodenum.

So as the patient eats, the food will go into the stomach. It then travels down into the small intestine, the duodenum being the first part, where the pancreas is attached, the ducts, the pancreatic enzymes are made in that pancreas. They travel down those ducts and are dumped into the duodenum as digestive enzymes so that the digestive protest can begin.

Now, the majority of the mass is made up of ectocrine glandular tissue. And these just produce digestive enzymes. Now we'll go on to talk about the difference between endocrine and ectocrine.

So an endocrine gland simply means a gland that secretes hormones directly into the bloodstream, whereas an exocrine gland produces and secretes substances via a duct. So examples of these are salivary glands, mammary glands, mucous glands. So there's many different glands around the body, and it's important to remember the differences between the exocrine and the endocrine.

So the pancreas is made up of thousands of tiny little cells called the pancreatic islets, so the islets of Langerhans, and these all play a vital role in the metabolism of our blood glucose. So we have 3 different types of cells. The first cell is called a beta cell, and this produces insulin.

As we all know, with our diabetic patients, the insulin lowers our blood glucose. And it just does does that by sending the glucose into the cells so that it can be utilised as energy. Then we have alpha cells, these produce glucagon.

Now this works in the opposite way to insulin by stimulating the body's liver cells to allow them to convert glycogen into the active form, which is known as glucose. So this increases the blood glucose and the insulin lowers that blood glucose. And then finally we have the delta cells, so this produces somatostatin.

And this just prevents any wild fluctuations. As you can imagine, insulin's lowering it, glucagon's increasing it. It could be all over the place, increased, then really low, but the somatostatin is produced just to make sure it stays within a nice normal range, and there's no crazy fluctuations here and there.

OK, so the ectocrine secretions are just digestive enzymes. So as I mentioned before, you have food in the stomach which goes down into that, small intestine. We also have the gallbladder which sits kind of in the middle of our liver.

So we have gall salts and gall enzymes in there which also travel down at the common bile duct. We then, as you can see in this image, have The different enzymes produced in the pancreas which travel down the pancreatic duct. They both joined together in the common bile duct before being dumped into the duodenum, where the digestive process begins.

So, the name of that digestive enzyme which causes all the issues is called trypsin. So this is secreted by the pancreas, and it's stored as zygomine granules inside the pancreas. And the reason for that is just as a protective barrier.

So it's stored in its inactive form. When it's inactive, it's called trypsinogen. And then it's in those granules, once it goes to its target area in the duodenum, all the enzymes then are stimulated to convert this into the active form and get rid of those granules.

Now, The issue becomes when the trypsin is activated too early. So early activation of this will cause autodigestion. If you can imagine you have a digestive enzyme which digests all of the foods that we eat now inside of the pancreas.

We know how sensitive the pancreas is as an organ. Even just if the patient has abdominal surgery and the surgeon touches that pancreas, it can cause inflammation and pancreatitis. So it's, it's a very sensitive organ and now we're gonna add in some digestive enzymes in the middle of that.

So it can cause severe inflammation and necrosis, and that's all part of what can come along with pancreatitis. Now, on a daily basis, around 10% of pipstinogen autoactivates within the pancreas itself, but we can deal with that. We have inhibitors in place to tackle around 10% on a daily basis.

It's when more than 10% is activated early that we quickly become overwhelmed and we just don't have enough inhibitors to tackle it, and it's too much for us to deal with. So in those cases, that's when autodigestion will start to occur, severe inflammation and necrosis of that peripancreatic fat, the fat that surrounds the pancreas itself. This can also lead to a focal or a generalised sterile peritonitis.

And when those cells become inflamed and edematous. It's quite easy for them to rupture and start to leak into the abdomen. And then you don't, you not only have chips in, in the pancreas, we then have it in the abdomen as well.

So I'm sure you can appreciate how painful this condition can sometimes be. Now It also enters the bloodstream. So we have it on our organs, we have it transloc into our bloodstream.

Our blood goes everywhere. It goes through the heart, so we might see abnormalities on the heart, which we'll talk about later on. It goes through the kidneys, it goes through everything.

So the pancreas or pancreatitis can quite easily start as a pancreatic issue, but it very quickly becomes a systemic problem. So many, pretty much all of the cases with pancreatitis have an associated systemic inflammatory response syndrome, which is also known as SARS. And that's just because we now have part of the digestive enzyme in our circulation, in our bloodstream, travelling around the body.

Causing inflammation on those endothelial cells that are on the inside of our vessels, causing them to become inflamed, causing them to leak out fluid in areas where we shouldn't leak and there's just a massive inflammatory response. It can also lead to things such as multi-organ dysfunction syndrome, which you may have heard of, as mods, and in the severe cases, it can also cause disseminated intravascular coagulopathy, which is also known as DIC or death is coming. And that's because once the patients get this, they can recover from it, but it's a very limiting disease.

It quite often does cause death. So these patients can come in with a massive variety of signs from really mild to being managed outside of the hospital, maybe your chronic cases, to being on death's door as they arrive and some patients sadly don't recover. Now, another thing that I just wanted to mention, particularly important in cats, is something called intrinsic factor.

Now, this is a glycoprotein, which is responsible for the absorption of vitamin K and also vitamin B12, which is known as carbalamine. Now this is absorbed in the small intestine, and cats only produce intrinsic factor in their pancreas, whereas dogs also produce it in their stomach. So if a cat has this condition, they may really struggle to absorb that vitamin B12 and vitamin K.

So that's that's most important in cases which if a cat comes in and maybe the pancreatitis is caused by a blocked biliary duct. And they need to go to theatre. We need to make sure that we're aware of this intrinsic factor, and we're checking this patient's coagulation factors before it goes to theatre.

The vitamin K plays a massive part in our coagulation factors. Without vitamin K, we may not be able to clot our blood properly, and if that patient's about to go to theatre for a surgery, we need to know about that. So it's important to check for signs of TH or ecchymosis, any pinpoint bleeding on the skin, usually on the midline, the scle of the eye, sometimes in the pinner of the ear or the gums, and just be aware and maybe suggest running a coagulation panel just on one of the in-house machines if you have one.

So Pancreatitis does come in many different forms. It can be mild, severe, or acute or chronic or acute and chronic. So the acute patients usually present with a sudden onset, but if they do recover, it has little to no permanent pathological damage to the pancreas, so they can go on to lead a perfectly normal life with no permanent signs or changes after recovery.

Now, to be a necrotizing pancreatitis is life-threatening and they will need intensive care and that does carry a poorer prognosis. Whereas your chronic patients, they have a continued inflammatory protest on a daily basis. Every single day, they're tackling an inflammatory protest with this disease.

It's just maybe they've had access to a fatty meal or maybe they've had some trauma, and then they'll just have an acute flare-up. These chronic cases are the ones that will have that permanent pathological damage to the pancreas. It can start to damage the cells, so it can start to atrophy some of those beta cells which I mentioned earlier, which produce insulin, leading to a concurrent condition of diabetes.

They can get other diseases, . Many other diseases leading on from this because of the atrophy or damage that this chronic continuing inflammation can do to that organ, and it can just be something as small as a fatty diet that will just flare up this onset of an acute attack. Now, usually, we believe that this is often idiopathic.

However, genetics do play an important role in humans. They're trying to look at whether genetics plays an important role in humans. However, in dogs, we do believe that it plays a role for us.

So our overrepresented breeds are the miniature schnauzer, the cocker spaniel, terriers, or some domestic charters. Now we know that our miniature schnauzer has a naturally elevated amylase and lipase. And that's what predisposes them to pancreatitis.

So that's why we believe that genetics do play a part, even though there's no proof of that yet. It, it makes sense to us. Now, we also know that larger breeds tend to be underrepresented.

So we all know of millions of Labradors that can eat absolutely anything and never come in with pancreatitis. And it tends to be middle aged to older patients. So we used to say 5, fat, and female, but now a sex, there's no link to a sex.

It can be male or female, and they don't always have to be overweight, but they, we do tend to say it usually is middle age to older patients. Now, the take home message from this, if you take anything home, is that pancreatitis in cats is different to the pancreatitis in dogs. Cats can have different causes and usually it's a, they have a recognised association with other conditions such as IVD being the most common cholangitis or renal disease.

So maybe cats can come in with feline triaditis, so pancreatitis is just a third condition that they're struggling with. And It can also be an infectious cause such as toxoplasmosis or even FIP causing that inflammatory response across the entire body can inflame that pancreas. Whereas dogs tend to have gallbladder issues, sorry, dogs tend to have liver issues first if they do have a concurrent disease, whereas cats tend to have, it's usually the gallbladder or a bile duct problem or maybe IBD.

Now, cats do not have this disease linked with fatty diets. So when we are nursing these patients, nursing our cats, we do not need to restrict fat in their diets. They can eat anything they like, and usually what I recommend is to feed according to the other concurrent disease.

So if a patient's in with IBD and it has pancreatitis alongside and it's a cat, feed according to the IBD. Not necessarily the pancreatitis because high fat diets are not triggered, do not trigger pancreatitis in. Now, it can also be triggered by other endocrine disorders.

So if a patient does have diabetes, hypothyroidism or hyperadrenal corticism, Cushing's disease, that increases the fatality risk. So if there's any other concurrent disease, it does increase that risk. So you, you could say that cats are at a higher risk and they have a higher mortality rate because of that because they quite often have that increased Comorbidity.

OK, so there's many, many different causes of this condition. So trauma being one of them. Has the patient come in with a head trauma and no other signs that have been detected.

It's been hit by a car over two days later, it's starting to show some abdominal pain. So just be aware of this in your RTA patients or any other patients that have had trauma. But the trauma could also be, as I mentioned earlier, your clinician or your vet could have maybe just touched it with a swab or with their hands during surgery, and if they've interfered with that pancreas too much, it can cause pancreatitis.

Hypercalcemia. So I've put this one in there because it's secondary to some cancers usually. So we've had a patient in with, sorry guys, I think the screen's gone off.

I'll get that back in a second. So we've had patients in with lymphoma, and with lymphoma, you can quite often get hypercalcemia. We had a patient who started to develop abdominal pain and signs of pancreatitis a few days after the treatment of lymphoma and that's because The hypercalcemia can cause it, so it often causes sequestration of the calcium into the spleen, meaning it just starts to pool, sorry, into the pancreas.

So it just starts to pool around and kind of stick to the fat around the pancreas, and that's why it can cause the inflammation. And certain medications can cause this. So if you have a patient, say a mini schnauzer who is at an increased risk, and potassium bromide, for example, is a medication that can put patients at risk of this, then we just need to be aware of what dosage we're using, maybe treat these patients slightly differently if they had, if they got chronic pancreatitis, and now we need to add in another.

And another drugs that could cause this disease, do we need to just take that, bear that in mind when we're choosing a dosage? And IMHA or immune-mediated hemolytic anaemia can cause gallstones which can go on to cause pancreatitis. And stress as well can play a factor.

But now at the bottom, I've written duodenal or biliary reflux as seen with IBD. Now we used to believe that pancreatitis was Caused by IBD or could be caused by IBD because of the close proximity of the duct. So in those first slides you see in the duodenum and the duct that just travels up and connects to the pancreas and the gall gallbladder.

Now, what we used to believe is the bacterial overgrowth with IVD would just travel up those ducts. But further studies have shown that actually it doesn't travel up those ducts, it just translocates into the bloodstream. And then as that bacteria is in the bloodstream, it's going through the pancreas and that's what causes the inflammation.

So it is a very sensitive organ. Now, the clinical signs again can be really varied depending on the severity of this disease. So often they come in anorexic, usually for 3 days plus.

Dehydration because of that anorexia, abdominal pain, now sometimes that can be difficult to detect in cats. Tachycardia, pyrexia, or hypothermia? And also some of them can be vomiting, but not all of them, so only about 50% of dogs come in with vomiting.

And we may see these patients come in jaundiced because of an elevated total bilirubin, especially if they do have a bile obstruction. And usually these are the acute cases, and then pancreatitis will just be picked up alongside, the biliary obstruction. Cation or prolonged clotting times which I mentioned earlier because of that intrinsic factor.

Respiratory distress or any other vasculitis issues that could be caused from the systemic inflammation, causing pleural effusions to start to accumulate. Well, quite often a cranial abdominal mass can be if it's so close to the organ itself, it can just cause inflammation in that area of the abdomen and cause it. Scis, cardiac arrhythmias, now this is caused by a release of a myocardial depressant factor.

And sometimes if we link up an ECG to these patients, we can see the odd VPC or the the odd abnormal ECG complex, and that's just because we have a digestive enzyme going through our myocardial cells. So it does cause some upset and it does cause some abnormalities. And pancreatitis can cause very similar clinical signs to a gastric foreign body.

They come in, they're anorectic, they have abdominal pain. They can be young patients, they can be scavengers. So I'm sure we've all been there where our vet has been convinced this is a foreign body, opened it up and can't find anything, and actually it's just pancreatitis.

So it's important to be aware of that and just perform a careful workup so that we can differentiate between the two. Now, cats do tend to show much fewer clinical signs. They just sit, they're quiet, they're anorectic.

They don't give us much to go from. So lethargy and anorexia, definitely the top two. Vomiting and abdominal pain is seen in less than half of all the cases that we see.

And again, that can often be seen with a comorbidity or a concurrent disease like your IBD or your feline triaditis. Now an important thing to point out is if our cats have been starved for a certain amount of time or a few days, then these are a higher risk of hepatic lipidosis, secondary to the anorexia and the pancreatitis. And what that is is if this patient has been off their food and not eating at all, then rather than our body using our glucose as energy.

We don't have any because they're not eating. So we start to break down our fat similar to with diabetes, but the fat is taken to the liver. Now a cat's liver can't deal with that amount of fat, so it quickly overwhelms the liver and they can get hepatic lipidosis, which is an acute attack on the liver.

And this is just resolved with diet. So as the, the patient starts to eat again, the hepatic lipiddosis signs can start to disappear, but it's very important to be aware of it. Now, we run many different tests for this condition, but what will we see and do we actually know what we're looking at?

So quite often if we run a biochemistry, we might see an elevation in our urea and creatinine. Now, when you see an elevation in that urea and creatinine, it just depends. You have to assess where the origin is coming from.

So if it's not a massive increase, then it could be a pre-renal issue, meaning the kidneys are absolutely fine. It's just that the blood supply maybe isn't perfusing the kidneys, so we can't get rid of those, nitrogenous waste products because it's just not reaching the kidneys to allow them to excrete it. And that's usually seen with things like dehydration.

So are your urea and creatinine may just be elevated because we're dehydrated, we haven't eaten for 3 days, and quite often a good way of testing whether that is the case is check your total protein and your PTV alongside. So often if you're dehydrated, you'll have an elevation in your PCV and also an elevation in your total protein. And then that azotemia, azotemia is just defined as an increase in your ear and creatinine, and that azotemia should correct with fluid therapy.

Now, high amylase is a sensitive indicator of pancreatic inflammation, but it's not very specific. So we can have high lipase with many different conditions. It doesn't specifically tell us we have pancreatitis.

And We used to rely on amylase and lipase specifically before we had the likes of a CPLI, a snap test or a quantitative test that we can send off to the lab. But now we realise that it's not very specific and we don't just rely on them. So up to 20% of animals with pancreatitis can have a normal ammalase or lipase.

So we need to just be aware of its limitations and rely on the more specific tests that we have in-house. So we could have an elevation in our liver enzymes, cholesterol, triglycerides, and hyperlipidemia. So quite often you may see these patients, they're fasted.

You take a blood sample before you've even spun it down, you can just see a big blob of fat on top of this patient's blood. And that's quite often, that's quite common with hyperlipidemia in pancreatitis patients. Now, electrolytes, if you run them in-house, they're really, really useful, especially for these patients.

So we may see a hypokalemia, meaning a low potassium value. Now, often we get our potassium and our electrolytes from eating. And We can also lose it if we're vomiting or if we have diarrhoea.

So if we have an anorexic patient, our potassium intake is reduced. So we're likely to be low. But the thing to remember about potassium is it's also excreted renally.

So as soon as we put these patients on fluid therapy, we're going to encourage diuresis and encourage those kidneys to start. Getting rid of those normal potassium, sorry, those normal electrolytes that they usually get rid of on a daily basis. We're already low, as soon as you put them on fluid therapy, it's going to go even lower.

So we need to be aware of that and spike our bag, which we'll talk about in a moment. And even in those patients who may be low end of the normal range of 3.5, it will drop once fluid therapy has started because the kidneys will start to die ease that potassium out.

As it does on a normal daily basis. And hyperglycemia may be common with the necrotizing pancreatitis or the development of concurrent diabetes. Also On the last slide, it did also say about an elevation in your lactate.

Now your lactate can also go up with dehydration. So it's a really useful tool to keep reassessing, if especially if you have a little portable handheld machine. If not, usually it's on your electrolyte machine like your epoch.

If you start to rehydrate these patients, and this is caused by A dehydration that lactate should come down, the urea and creatinine should come down, that PCV and so protein should correct normalise. So the lactate can be a really useful indicator as to how How useful your fluid therapy is being, does our patient need to receive a little bit more fluid therapy maybe and lactate will tell us that because if they, if it's not reducing. Then it's either because we're not being effective enough with our fluid therapy or it's caused by a different reason, such as sepsis, maybe this is a septic peritonitis or a different kind of sep septic agent.

Now Canine serum, pancreatic lipase, immunoreactivity, which we may all know as CPLI or FPLI in cats. Now this is the most sensitive and specific test for pancreatitis, and in-house snap tests can be unreliable. I'm sure we've all done these before and it says it's a normal, a normal result, but the patient quite obviously has raging pancreatitis.

Now, It can always also go the other way and give you an abnormal result when actually the inflammation is just in the area of the pancreas, it's not that organ itself. So if you have enteritis or any kind of inflammation around the cranial abdomen, you are likely to get an abnormal FPLI snap test or CPLI. So we just need to, it's really useful.

But we need to be aware of its limitations, and that's why we often send a sample of the PLI because that's way more specific and it gives you a figure rather than just a yes or a no. And then there's other things that we can test for. So B12 and folate, so B12, I mentioned about possibly having deficiencies in those because of your intrinsic factor, particularly in cats, and also it's likely to have an association with IBD if it's decreased.

So these are all of the tests that we can run alongside. Now, how do we diagnose this other than blood tests? So ultrasounds is a highly specific test that we can use for pancreatitis.

It allows us to detect any free fluid, any abnormalities in any other organs. Do we have any tumours or abscess or do we have that illary obstruction? We can also FNA to take a final aspirrate of those organs, maybe if it's a lymphoma that we're thinking of.

And The important thing to point out about ultrasounds is if you don't see the pancreas, it does not rule out pancreatitis. So the pancreas itself doesn't have a capsule around it. It's really difficult to see.

And it takes a really skilled ultra sonographer to be able to see them. And even when they are highly skilled, you can't always see it just because of the organ itself. So it's great if you can see it, but if you can't, you can't rule it out.

Now, the beauty of ultrasounds is this can be done in a conscious or sedated patient. Conscious if they are quite collapsed. Oh, just bear in mind that these patients that this is a very, very painful condition.

So just make sure we have adequate pain relief, ideally a pure opioid on board before we go in that probe into the abdomen because it will cause a lot of pain. Now, treatments of this condition. So first things first, let's correct this dehydration and the electrolytes.

Let's get fluid therapy on board. Let's get analgesia on board, not non-steroidals, because this is a gastrointestinal disease. And thirdly, early onset nutrition is really important, which we'll talk about in a moment.

And then other things such as antiemetics, maybe our patients feeling nauseous and antibiotics may improve the outcome in the most severe cases, and they should always be used in cath. And that's just because of the overgrowth of bacteria associated with IBD translocating into the bloodstream and being a common cause of pancreatitis. So we should always use antibiotics in cats.

OK, so hypokalemia, so our, decrease in our potassium value. Now, the normal range is 3.5 to 5.5, and we should be supplementing this because if we don't, they can get other signs such as muscle weakness or respiratory issues.

Now we have these really great stickers that we can put on to say do not flush. And if you have potassium in that bag, you need to inject it in, put your label on first to say there's drugs added to this bag so that nobody, the amount of times I've seen people put potassium in a bag and then walk away to grab a sticker to then come back and put it on that bag, assuming that's the same bag and nobody's grabbed it or used it for something else. Always put your sticker on first before you add any drug.

It's the safest thing to do. Put the potassium in an inverted position. So hold your bag upside down.

And the reason for that is because we don't want to have a bolus of this potassium at the bottom near the port. So if it's inverted, it's more likely to distribute a little bit more evenly and you need to invert the bag about 4 times to make sure we have an adequate mix. And the reason for this is because if you bowl a potassium.

You can cause severe bradycardia, cardiac arrhythmias, and even cardiac arrest. So if we have, this patient is on the potassium fluids and we need to give another drug alongside IV such as potassium, paracetamol, for example, and we want to give it through this port that you can see here. We cannot do that in this line.

So it's quite handy to have a T connector on. So maybe a T connector attached directly to the IV line itself with one port for the potassium with a do not flush sticker on, and then you can use the other port. You can even connect to an extension, and give the drug through the other line, but it's just very important that we don't inject anything into that potassium line.

And one other thing to remember is the maximum IV infusion rate is 0.5 milli per kg per hour. So just keep that value in your head.

And if these patients do need higher fluid volumes, just quickly do a little calculation in your head just to make sure you're not given this too quickly. And if we do have really dehydrated patients, quite often we'll put them on fluid therapy. We'll give all the bonuses or give whatever we need to correct that hydration, and then only once they're then stable, we'll then start the potassium infusion.

So just forget about it until that hydration is, or the hypovolemia rather is resolved. So this is also in the notes, it's a handy chart to have and it just tells you on the left you have your serum potassium value. So say the dog comes in and potassium is 3.

So how many kilocalories of potassium to add to a 1 litre fluid bag? So if it was 3, you would add 40 milli, and the maximum fluid infusion rate is 12 mL per kg per hour. So it worked it out for you, nice and easy, and this is in the notes.

It's a really useful tool to have. Now, secondly, analgesia. So this is really important to reassess each patient on an individual basis rather than just having a flat line of this is what we do for all patients.

And one of the really useful websites is called the Zero Pain philosophy. Now they do also have a Facebook page and these are two anaesthetists that I've had the pleasure of working with called Matt and Carl. They've set up this, this website to access.

To allow people to have access to video resources and techniques that you don't have to read about in the book, you can watch them do it. And another useful thing, especially for these patients is they'll put on specific pain plans. So if you have a painful pancreatitis patient, you can go on and type in pancreatitis, and they will give you a specific pain plan to use with your patients.

So it's really, really useful and you can always contact them because they get back to you really quickly. So utilise these resources, especially in those more painful cases. And it's important that we are reassessing our pain, so do a pain score.

Believe me, once you get used to these pain scores, you don't even need to look at it before you can get the pain score for each patient. It comes second nature. Have them laminated up in the wards and then each patient you'll just do it for maybe every 4 hours depending on how long their analgesia lasts and just reassess and then we usually say anything 4 or above definitely needs pain relief.

So the dog one on the left is the Glasgow pain scale, and we believe this is the most accurate for dogs, whereas the Colorado pain scale on the right is what we use and what we favour in our cats. Now the different analgesics available, methadone is a really useful drug to use. It's a pure opioid agonist, and it's great for moderate or severe pain and it can also be given via the oral transmucosa route in cats.

And it does last for about 3 to 4 hours. Quite often they'll start to pant as you administer it, but that doesn't last very long. And you can have a varied response to this, but we do have a range, as you can see, so you can start them off at the lower end of the range, and the beauty about it is you can just increase that if you do a pain score 10 minutes later and they still seem painful.

And it's also a great choice to use with multimodal analgesia such as your lidocaine CRI. Now Lidocaine is used because Useful for those. Painful patients that seem to be not really responding to any other drugs, so lidocaine quite often comes in and they will, it will deal with that.

And sensory nerve fibres are blocked before the motor nerve fibres, which almost allows a sensory nerve block at a low dose, so it almost blocks the pain to the abdomen. And you can put it as a CRI if you have that facility after Ebolus. And it has a rapid onset after injection and it just spreads around the surrounding tissues.

You do need to be aware of an accumulative effect if they're on it for a few days, and you can just adjust it according to the pain score. And it's important to point out that this does have a really low toxic dose for cats. So even the smallest of doses is really toxic, so we don't use lidocaine in cats ever.

Now this is a typical pray position, which you might see with pancreatitis. This patient was in about a month ago. He did have pancreatitis and then as we walked past the kennel, we seen that he'd adapted this position.

He did a pain score and gave him some more analgesia. That's a great image to demonstrate that position. Now there's many, many different types of analgesia that you can use.

I would say avoidburophenol and some of the weaker partial opioids. Buprenorphine certainly has its place, especially once the pain is under control and you can start to reduce down the methadone and convert them to buprenorphine or maybe in the more mild cases. We can also do local techniques or we can set up with the CRIs if you have that facility such as fentanyl, lidocaine, or ketamine.

If you don't have that facility, all the things that could be useful is transdermal fentanyl or transdermal patches which are available in fentanyl and buprenorphine. We just need to make sure that the patient has a buster collar and this is covered so they can't eat it, which I've seen before. And The thing that I'm not keen on with the transdermal fentanyl is it lasts around 4 days, and quite often they're pretty sedate with this drug.

But just on like a spot on as you would with flea treatment, often it, it flattens them and you can reverse it with naloxone, but if you reverse with naloxone, it blocks all opioids, so you can't then reverse the fentanyl transdermal solution and then give methadone and expect it to work as well. So, I, I'm just a little bit cautious with this drug and it's not my favourite, but it's definitely an option and it does have its place for certain patients. Now, nausea, vomiting, and regurgitation are all things that we need to bear in mind.

So it's important that we are aware that these patients can feel nauseous and feel really sick, which is really debilitating without vomiting, so you don't always have to vomit if you feel sick. So any signs of nausea can be salivation, maybe they're inhabitants or anorexic still, they're gulping or lip smacking or trying to bury the food when you put it in the kennel. And regurgitation and vomiting, it's important that we can differentiate between the two so that we can make an accurate, judgement because they both carry very different reasons and very different diagnostic pathways.

The regurgitation is the passive discharge of ingested material, whereas vomiting is more forceful. And they can both cause aspiration pneumonia. Now, we used to say starve the patient for 12 hours at least until they're not vomiting and then starve them with a bland diet.

Now that's not what we say anymore. We do not starve these patients anymore. The earlier you get that nutrition in, the better the outcome has been proven.

They're more likely to gain more body weight, obviously, and they have a much better chance to survival until discharge. Now, the main reason for that is because our gastrointestinal lumen is lined with enterocytes, cells that line the GI lumen. Now they get their nutrition directly from that lumen to the food that we eat.

None of it comes from the bloodstream. So if we're starved for days and days, they can start to atrophy and start to break down and not work anymore, and then you'll end up with a secondary, gastrointestinal issue. And It also reduces the risk of a GI bacterial translocation, as we mentioned with our IBD patients, and it just prevents malnutrition.

So the earlier the onset, even if they're vomiting, start them on food and do anything that we can with regards to the likes of feeding tubes, which we'll mention here. So Nasoesophageal feeding tubes or nasogastric tubes are ones that we can place as nurses. If these patients come in and they're too poorly for a GA.

Or a sedation, maybe the esophagostomy tube is my favourite, but if they're not well enough to receive one of those yet, we can still get some early onset nutrition in by placing a nasal esophageal or a nasogastric tube. Now, nasal esophageal is usually the preferred tube. Nasogastric, we used to say plays a more it may be more likely to cause regurgitation because it prevents the cardiac sphincter from closing, but studies of that have shown that actually they're not more likely to regurgitate with either of those, one tube over the other, so whichever you prefer.

And I suppose the one plus side of the nasogastric sits in the stomach. If if these patients do have delayed gastric emptying, maybe a bit of ileus, then we can aspirate some of the fluids or some of the food off before we go administering a load more. Now, a nasoesophageal or nasogastric, so we usually measure to the 9th rib from the nose for the 13th rib, the nasogastrix, and just allow enough out of the nose to then curl it round and staple it or stitch it to the head.

So these are really useful. So we often use minims, so the, local anaesthetic that we put in the eyes for, for eye patients. So you can put these in each nostril.

I would always do both sides because quite often they'll tolerate one side more than the other. And you can always also put them in the eyes. So if you put the drops in the eyes, it travels down and coats the back of the, the nasal cavity and the throat, which is where we're about to feed our tube.

So always do both. As you're feeding, if you have somebody else straining the patient, you just hold the muzzle, you direct the tip of the tube. Towards the centre of the nose and ventrally slightly, so medially and ventrally.

So towards the centre and then pointing downwards and then as long as you hit no resistance, feed it in up until where you've marked on the tube and then there's a couple of different ways to check placement. So usually we'll take a radiograph to just make sure it's sat in the right place. You can also inject a little bit of sterile saline, a few drops, if they cough, you know, it's in the lung.

And you can also apply some negative pressure. So if you have Negative pressure there likely to be in the stomach. If you have a load of air coming back, you're likely to be sat in a lung.

And some people also mention that you can link up the Capnograph if you have a Capno machine and just see if you're getting a trace. So you obviously shouldn't get one in the stomach, but you would get one if it's in the lungs. So don't wait for your vet to suggest that we place one of these tubes to tomorrow, one of these tubes the next day.

Suggest that you place one of these nasal esophageal feeding tubes so that we can get early onset nutrition on because you know. Why it's so important, we should be doing, we should be pushing, and it's important that we utilise our skills as RBNs. Now, what type of nutrition do we choose?

So there's many different types. So it must be low fat in the dog, which is different to low calorie. And let's just prevents any further stimulation of those pancreatic enzymes.

Now, the term low fat can be difficult to determine and Often some of the commercial diets can range from 20 to 70% fat, so it's quite difficult to say what is classed as low fat. But one of the important things to mention is find out what they're already eating on a daily basis and just make sure it's lower than that, because they might be on a really high fat diet, but they may be on just 20% fat diet and If you then give them something else that you consider low fat, but it's more fattening than what they're already on, then it's defeating the object. So just find out what they already eat at home before you make that decision.

Now some of the prescription diets are ideal, so low fat or if we are tube feeding some of the gastrointestinal low fat liquid diets are perfect for my favourite. We also have things like enteral care, chappy or cottage cheese, and boiled chicken or boiled white fish is great, but this shouldn't be a long term diet. It should only be to tempt the patient to get them eating and also just to to stimulate their appetite, but we then should be trying to wean them onto a specific, full canine diet.

And One thing that I think is really important is if we have a nasogastric or a nasoesophageal tube in place, maybe our patient's eating a little bit of chicken or a little bit of fish, but that's not a reason that they shouldn't be receiving their full RER for that day. So we can just top them up. So if they've eaten a little bit of chicken, just top up that feed with some of the enteral care or some GI low fat liquid.

And we can just make sure that this patient isn't going to become malnutrition and we we're able to do that with those tubes. And remember that cats do not require a low fat diet, so feed to treat the concurrent disease such as the IBD or the diabetes. And the, the food that are useful in cats is the likes of convalescence or enteral care, liquid diets.

And finally, one of the calculations to work out your RER is this one, which is appropriate for between 2 and 30 kg, which is the majority of our patients, and it's 30 times the body weight in kilos plus 70. So that gives you your RER so that you can make sure these patients are receiving this volume of kilocalories every day as an absolute minimum. And we need to make sure that we're not just bringing in an anorexic patient.

And weighing it on day one, but never reweighing it again. These patients should be weighed daily as a minimum, ideally if we can do it twice a day. And remember, the fluid makes up about 60% of our body weight.

So if they're already dehydrated, they're already anorexic, we're then going to pump them full of fluids and start feeding them, they're likely to gain weight. We need to be weighing these patients and adjusting that RR accordingly. Now if you try and keep that value in your head, you can do it anywhere.

You don't need to go and check a book. You don't need to go and check the computer, just calculate it while you're with the patient and then work out the food accordingly. And long term diet should be low fat.

And remember this is different to low calorie. And no feeding of high fat snacks or any table scraps, and it's important that we speak to the owner and get onto their level, provide them with a suitable alternative. So this is usually where they'll slip up because they've had a roast dinner and they wanted to give some to the dog.

So give them healthy alternatives such as pasta or chicken, maybe potato or vegetables, carrots is a great one. And just teach the owner also to spot trigger signs. So look out for signs of nausea, signs of pain if they become anorexic, lethargic, or they start to vomit again, and also try and avoid periods of stress if and when possible.

So the prognosis varies massively because of the nature of this disease, but generally, the prognosis is guarded with the severe cases. But the less severe acute cases may resolve and do really well with just a low fat diet long term at home. And some of the severe acute cases may never recover just because of that systemic disease that is caused.

This is a really interesting condition that was as nurses can look after and we can really choose a multimodal approach, many different things, and I would encourage everybody to try a nasogastric or a nasoesophageal tubes, and these are the ideal patients. To trial them in because it will benefit them and it's something that we can do as nurses and it's a great skill to learn even if you've never done it before, to suggest that one of the vets or one of the other nurses helps you along to learn a new skill. OK, so that's all from me.

So if you do have any questions, please pop them in the Q&A box. We're just gonna switch over the screen so that I can have access to the questions. And if you do have anything, just pop them in the Q&A box.

Now your screen will have gone white. Don't worry, it's just us switching over to the other screen. So that we shouldn't OK, so we have some questions come through already.

So in pancreatitis or diabetes mellitus, what happens to the delta cells? So the delta cells aren't necessarily affected in diabetes, but because we have no insulin, it's too much for those cells to maintain a normal glycemia. So because we have issues with our beta cells, they're not producing that insulin.

Or blood glucose just goes on a wild fluctuation. So it's just too much for those delta cells to deal with. We need that insulin in order to send the glucose intracellularly, so we can't get into that cell, no matter how much delta cells produce any somatostatin to try and prevent any wild fluctuations.

We cannot get that glucose into the cells because we don't have the insulin. So unfortunately, they can't really play much of a role with the likes of diabetes. We have a few more questions.

Is pancreatitis becoming more common? So that's quite an interesting one. So one thing to consider is, is it becoming more common or are we getting better at diagnosing it and picking up those signs.

So yes, our patients are probably receiving more high fatty diets and more high fatty snacks than usual. So yes, it could be becoming more common. But equally, we now have snap tests.

We have pancreatic CPLI or FPLI tests, which are really useful for us to use and it's a very specific tool for us to use as a diagnosis. So I think it's, it may be not so much that it's becoming more common, but just that we're getting better at detecting this condition. And is it better to use liquid food or solid foods when starting food?

Absolutely any food you can get into this patient, any food that they will eat is as good as the other. So whether it's solid or whether it's liquid, it doesn't really matter. If they have a feeding tube then ideal, but if they will eat by a mouth, always go via the more natural method.

So if let them eat by your mouth, if they want to eat something solid, and then we can just pop them up if and when we need to with a liquid diet, but you know, as long as they're low fat, then I wouldn't say one is better than the other. And could a severe case of pancreatitis in cats cause a severe anaemia? So with cats and dogs, they can get anaemia of chronic disease.

So quite often if we have a patient who does have chronic pancreatitis or chronic anything, renal disease, maybe the renal, the kidneys are struggling alongside any other condition, then they can get a chronic anaemia. And that's just caused secondary to the other conditions, . The renal conditions being a primary one, which can certainly happen in cats, and the reason for that is erythropoin is produced in the kidneys.

That stimulates our bone marrow to produce more red blood cells. Now, if we have a renal disease, maybe as the origin, pancreatitis could be secondary to that. Our erythropoein may not be being produced as well as it should be because our kidneys aren't working and therefore the bone marrow won't be stimulated as much as it should do.

So you can often get a secondary anaemia or the other possibility could be if it's secondary to an IMHA. IMHA can cause gallstones, which can cause pancreatitis, and IMHA causes a really severe anaemia. So if you're asking about it being severe, I would think that the anaemia is probably more the primary issue.

Rather than it being caused by the pancreatitis, but if it's just a mild anaemia, maybe a reduction of 10% or something or or less, then it could be just due to chronic disease and they can get that with any chronic disease. It doesn't have to be renal and it doesn't have to be pancreatitis. So, yes and no for that one.

You can get anaemia but not necessarily just from the pancreatitis. OK, and that seems to be the end of the questions. So I just like to say thank you so much for everybody for joining us this evening.

There will be a feedback form that pops up in your browser. Just a couple of questions if you can just pop a few answers down and give some feedback, we can tailor the future webinars to meet your needs. And thank you very much for joining us this evening and I hope you enjoy the rest of your evening.