119 | Here’s exactly what you need to know about nursing dogs with pancreatitis in 2026
This episode is the first in a two-parter wrapping up our series revsiting GI disease, and we’re talking about a disease lots of us see very regularly - pancreatitis.
I wanted to cover this one because pancreatitis is a condition almost all of us have nursed, and yet it's a condition where a lot of what we were originally taught has changed.
And alongside that, we know that nursing care can make or break recovery for these patients, especially in cases of severe disease. There’s a lot to think about when caring for them, and a lot of ways we can use our knowledge and skills to give even better care to these patients.
This week, we’re chatting all about canine pancreatitis - how it presents, how it impacts our patients, and how we can use more of our skills when caring for these patients in practice. And next week, we’ll be turning things over to our cats, focusing on feline pancreatitis and triaditis, and how the disease - and nursing care - is often very different in these patients.
So if you’re ready to get nerdy with me and start discovering new ways to support your pancreatitis patients in practice, grab a coffee and let’s get into it.
The pancreas: what does it do, and what happens to it in canine pancreatitis?
I’m going to start with a brief look back to A&P, but don’t worry - I promise it will be very brief!
I firmly believe that understanding the diseases we see and how they impact our patients begins with a look at what the body systems involved SHOULD do when they’re functioning normally.
The structure of the canine pancreas
Looking at the pancreas, in dogs it is a V-shaped organ sitting between the stomach, spleen and small intestine. The right limb runs alongside the duodenum, and the left limb runs along the stomach, towards the spleen.
The body of the pancreas - the area where the two limbs meet - sits against the pylorus.
So if we think about the pancreas’s location and all the neighbouring organs its touching, we start to see a disease bigger than ‘just’ the pancreas itself (and this is especially true for cats).
The inflamed pancreas can start to irritate the stomach and duodenum, contributing to things like vomiting; it can swell, impacting the flow of bile from the neighbouring gallbladder and biliary ducts, and it can also cause irritation of the fat surrounding the pancreas, too - causing increasing pain and inflammation.
The pancreas also shares its blood supply with the duodenum, which is really important for us to bear in mind as RVNs, because pancreatic perfusion - the appropriate delivery of blood and oxygen to the pancreas - is really important in preventing pancreatitis (or preventing existing pancreatitis from worsening).
The role of the pancreas in dogs and cats
The pancreas has several key functions, split primarily into endocrine and exocrine functions.
The endocrine functions are ones we’ve discussed a LOT on this podcast - creation of insulin, glucagon and other hormones via endocrine cells within the pancreatic islets. I’m not going to focus on those today, but if you want to know more about these, I’d recommend looking at the episodes on insulinoma and diabetes we’ve already covered.
The exocrine functions are the ones we need to think about in pancreatitis (mostly).
98% of the pancreatic tissue is dedicated to exocrine function - that is, the creation and secretion of digestive enzymes, as well as other substances. The pancreatic acinar cells produce these enzymes, and the duct cells produce bicarbonate, a buffer solution, which neutralises stomach acid entering the duodenum.
These digestive enzymes include amylase - which breaks down carbohydrates and starches into sugars - and lipase - which breaks down fats - as well as proteases, which break down protein. These protein-digesting enzymes (trypsin) are secreted in an inactive form (a zymogen known as trypsinogen), which then converts into trypsin within the small intestine.
These zymogens are packaged really cleverly to prevent inadvertent activation by substances called lymosomes, with a trypsin inhibitor called SPINK1 sitting nearby ready to neutralise any trypsin which activates by accident.
The final activation step is carried out by a substance called enteropeptidase, which lives on the entrance to the duodenum. So trypsinogen only becomes trypsin once it has physically left the pancreas and arrived where it's meant to be working.
The digestive enzymes enter the duodenum via ducts. In dogs, there are two - the pancreatic duct, and then an accessory duct. Cats are different, and this is a big part of why we see things like triaditis in our cats - but we’ll talk more about that next week.
In dogs, the pancreas is also responsible for creating most of the body’s intrinsic factor - a substance involved in the creation of B12. This is worth knowing about, because B12 levels can drop in pancreatic disease - especially chronic pancreatic disease.
So that’s how the pancreas works - but what happens when it doesn’t?
Pancreatitis occurs when something triggers the premature activation of trypsinogen inside the acinar cell.
In the majority of our patients we never find out what that something was. The current understanding is that it happens through a process called co-localisation, where the zymogen granules and the lysosomes end up in the same compartment when they should be kept apart. The lysosomal enzymes convert trypsinogen into trypsin, and the neutralising substance - SPINK1 - gets overwhelmed. And this starts a cascade of activation, where trypsin formation then activates other digestive enzymes.
At that point we get pancreatic autodigestion, leading to things like oedema, haemorrhage, inflammation, necrosis of pancreatic tissue, and necrosis of the peripancreatic fat.
The secondary complications of this have significant effects on our patients, and explain why we see such severe systemic illness in patients with awful pancreatitis.
The pancreatic inflammation and necrosis - as well as inflammation of the surrounding tissue - recruits huge numbers of neutrophils, and those neutrophils release cytokines, reactive oxygen species and proteases into the circulation.
This causes systemic inflammation (or systemic inflammatory response syndrome/SIRS), which predisposes our patients to further complications like acute kidney injury, acute injury to other organs (eg the respiratory system), and coagulopathies.
The systemic inflammatory phase is what the majority of our intensive treatment and nursing care is aimed at - essentially, everything we’re doing within the first 48 hours, when these patients are early in their hospitalisation and treatment, is an attempt to stop that patient tipping into it.
It's also worth noting that the trypsin pathway isn't the only way our patients can develop pancreatitis. There are trypsinogen-independent pathways that we now recognise as important too, and this explains some of the medications available to treat pancreatitis (though at the time of recording this, these drugs are not available in the UK).
What’s the difference between acute and chronic pancreatitis, and how do we know which our patient has?
This is an area I think many of us - myself included - have misunderstood for a long time.
We used to get taught that acute pancreatitis are the really nasty, severely-affected patients hospitalised and needing intensive care, but chronic ones have much milder signs.
And while that can be the case, distinguishing between the two is not something we can do based on their clinical signs - it’s actually about the histological changes happening inside the pancreas.
Acute pancreatitis is characterised by neutrophilic infiltration, with oedema and, in severe cases, necrosis. Critically, it is potentially reversible, because the pancreas can recover with appropriate and prompt treatment - think of it as like AKI for the pancreas.
Chronic pancreatitis, on the other hand, is characterised by lymphocytic and plasmacytic infiltration, with fibrosis and acinar atrophy - and those changes are irreversible.
Because chronic pancreatitis progressively destroys pancreatic tissue, these patients can go on to develop secondary pancreatic diseases such as EPI and diabetes. If our patients lose enough acinar tissue, they lose the ability to create enough digestive enzymes, and we get exocrine pancreatic insufficiency. If they lose enough islet tissue, they can’t secrete sufficient insulin and they become diabetic.
Interestingly, one study found that almost two-thirds of canine pancreatitis cases were chronic. So chronic disease is far more common than we think, mostly because many of these patients are often subclinical or only mildly affected, meaning we don’t hospitalise them as much.
We can also see acute-on-chronic disease, which is a flare up on top of established fibrosis. So this means that the dog in front of us who looks like a first-time acute case may well have been chronically affected for years without anyone knowing.
Because of this, more recent studies have recommended we rename acute pancreatitis ‘acute-onset pancreatitis’. That phrase describes what we can actually observe, which is that the clinical signs started suddenly - because acute pancreatitis technically relies on a biopsy and histology to confirm the diagnosis.
What causes pancreatitis in dogs, and what signs do we see in patients with it?
Most cases of pancreatitis in dogs are actually idiopathic, which is interesting because many of us have been led to believe that they’re caused by things like high fat foods.
That said, there are some recognised risk factors which we need to know about as veterinary nurses and technicians.
Risk factors for canine pancreatitis
Breed
First up, there are some at-risk breeds and perhaps unsurprisingly based on what we’ve seen in practice, Miniature Schnauzers are significantly overrepresented. They have some variation in their SPINK1 gene, the safety-mechanism mopping up any prematurely activated digestive enzymes. Yorkshire Terriers, Cocker Spaniels, Dachshunds and Poodles also appear predisposed, and English Cocker Spaniels may actually have their own distinct autoimmune form of chronic pancreatitis.
Other risk factors
Hypertriglyceridaemia, or elevated serum triglycerides, is an important risk factor, as is Cushing’s disease (many dogs with Cushings also have hyperlipidaemia), hypercalcaemia, and obesity.
Certain medications have also been linked to the development of pancreatitis, including phenobarbital combined with potassium bromide, L-asparaginase and azathioprine.
Dietary indiscretion is a recognised risk factor in dogs, and so is blunt force abdominal/pancreatic trauma.
Interestingly, so is pancreatic hypoperfusion under general anaesthesia, which is now thought to explain most cases of so-called post-surgical pancreatitis.
The clinical signs of pancreatitis in dogs
The most common clinical signs we see include anorexia (reported in 82% of dogs in one study), vomiting (80%), abdominal pain (69%), lethargy (46%) and also diarrhoea (42%).
The stats on pain is interesting, because when we compare this to human pancreatitis, pain is reported MUCH more commonly - in over 90% of cases. And I personally think it’s quite unlikely that dogs experience less pain than humans - but the data suggests we’re still not identifying it anywhere near as often as it’s probably present.
While we’ve all got so much better with pain recognition and management over the years (I say this after 20 years of nursing where in my first clinic bitch spays were still premedicated with butorphanol), there’s still a bit of a gap in its recognition here - and I think this is an area we’re ideally placed to champion as nurses.
We know the more obvious signs of pain these patients present with - things like the prayer position, or a really tense abdomen, or being really resentful of palpation or a look with the ultrasound probe. But the more subtle signs - the changes in vital parameters, the restlessness, the trembling, the reduction in interaction - are the ones we’re great at spotting. And this will change from dog to dog, because many of our patients are more stoic than we give them credit for, meaning they may look calm and settled, but they’re actually quiet and painful.
As a general rule, if we think a dog has pancreatitis, we should assume there is abdominal pain and treat it until we have evidence to the contrary.
OK, so that’s the clinical signs these patients present with. But what about diagnosis?
Of course, diagnosing these patients is a task legally outside of our remit as nurses and technicians. However, it’s important we understand the diagnostic tests available, what they tell us, and importantly their limitations - because they’re not perfect, and they don’t all give us the same information.
And we know that while we’re not making the diagnosis, we’re heavily involved in the diagnostic process - from taking samples to assisting or even performing ultrasound scans in these patients.
So how are they diagnosed?
There is not one single test to confirm pancreatitis - instead, we need to look at clinical signs, blood results and imaging.
We’ll be performing all the usual routine bloods in these patients - biochemistry, haematology, electrolytes and ideally a venous blood gas if you have one available - alongside specific pancreatic testing and an abdominal ultrasound.
Pancreatic lipase testing
Pancreatic lipase is the most useful clinicopathological marker we have. Specific pancreatic lipase immunoreactivity, which you'll see written as cPLI or as Spec cPL for the commercial quantitative assay, has a reported sensitivity of around 86 to 94%, and a specificity of around 66 to 77%.
Sensitivity and specificity are important terms when it comes to testing - they tell us how accurate our tests are. A highly sensitive test is better at ruling a disease out, whereas a highly specific test is better at ruling a disease in.
The lower specificity number here means that we can see patients without pancreatitis still test positive. This is because an elevated cPL tells us that pancreatic lipase is elevated in the blood, but it doesn't tell us that the pancreas is 100% the reason this dog is unwell.
Which is why we use a variety of tests to confirm pancreatitis, and never rely on one alone.
There are actually a few different tests used in place of pancreatic lipase - such as the semi-quantitative snap test (which tells us if a patient is normal or abnormal, but does not provide a number), the V-check test, and DGGR lipase. These are used similarly, but do not all tell us exactly the same thing.
I also want to briefly mention amylase and lipase. They’re still around, and sometimes you’ll see them on biochemistry results - but we don’t really bother with them when it comes to pancreatitis. There are lots of things that can affect levels of both, not just pancreatitis.
Imaging is often required in these patients. And ultrasound often does show signs of severe disease, but its accuracy is very dependent on the images collected, and patients with pancreatitis can still have a normal-looking pancreas on ultrasound.
Cytology or histology of the pancreas is definitive, but often not worth performing - because it rarely changes the treatment these patients receive, it can upset the pancreas further, and these patients are often poor candidates for anaesthesia and pancreatic sampling.
Our patient has pancreatitis - how will we treat them, and what do we need to know about it as veterinary nurses?
Most of how we treat pancreatitis is supportive, and these patients often need incredibly intensive supportive treatment and nursing. There are four main pillars of supportive care - fluid therapy, antiemetics, analgesia, and nutrition - and we’re heavily involved in all of them as veterinary nurses.
There’s also a more specific treatment for canine acute-onset pancreatitis, though at the time of me researching and recording this it is only available in North America and Japan.
Introducing fuzapladib sodium (Panoquell-CA1), a new treatment for canine pancreatitis
Fuzapladib is the first treatment we have that targets the actual pancreatitis itself, rather than the consequences of the disease. It's an LFA-1 (lymphocyte function-associated antigen 1) activation inhibitor, which means it blocks neutrophils from adhering to endothelium and migrating out of the capillary bed into the pancreas and into other tissues.
This means it is targeting that inflammatory phase we chatted about at the start of this episode - stopping the inflammatory response spreading out of the pancreas.
It is not available where I am, so I have absolutely no experience with it - from the studies I have read, the dose is 0.4 mg/kg as a slow IV bolus, once daily for three consecutive days. Trials have shown significantly faster clinical improvement in treated dogs over that three-day period.
As I say, this is a drug in its early stages of use - and I’m interested to see where it goes. Maybe next time I revisit pancreatitis we’ll all be using it, but either way, it’s great to see we’re getting more treatment options available for these patients alongside that all-important supportive care.
Fluid therapy in canine pancreatitis
The pancreas is incredibly sensitive to changes in fluid balance. When perfusion to it drops, the capillaries can become more permeable and ‘leaky’, vessels can spasm, and microthrombi can form - all of which further limits delivery of blood, fluid, nutrients and oxygen to the pancreatic tissue.
This means that mild pancreatitis cases can worsen in the face of poor perfusion, so fluid balance (and blood pressure) are really important areas of our monitoring and nursing care.
This doesn’t mean more fluid is always better, because there is still a risk of fluid overload - especially in nasty severe pancreatitis where we risk concurrent AKI. So like any other patient, thorough fluid assessments, calculating and addressing deficits appropriately, and ongoing monitoring after correction is essential.
Antiemetics and the importance of their use in the pancreatitis patient
Nausea and vomiting are significant complications in these patients, and they risk delays in enteral nutrition, aspiration, and further dehydration. Addressing both is an essential part of caring for these patients.
Maropitant is a potent antiemetic, but is less effective for nausea than vomiting - using additional agents, such as ondansetron - can be helpful here (under veterinary direction and prescription as always).
Metoclopramide is not an effective antiemetic, but it is a great prokinetic. If your patient develops ileus secondary to pancreatitis, it can help. However, it works on dopamine pathways in the body, and these pathways are also thought to play a role in pancreatic blood flow, so should be used with care.
The other thing I want to mention on the topic of nausea and vomiting is that a dog who isn't actively vomiting can still be profoundly nauseous. Lip licking, drooling, turning the head away from food, and repeated swallowing are all things we commonly see in these patients, even in the absence of vomiting - and these patients also need antiemetics. As nurses and technicians, we’re ideally placed to look out for these signs, and flag them with the vet if we’re concerned additional treatment is needed.
The importance of multimodal analgesia in dogs with acute-onset pancreatitis
Analgesia is an essential consideration in all pancreatitis patients, and many cases will need potent agents to manage their severe abdominal pain. As veterinary nurses and technicians, our role in managing this, monitoring these patients, and advocating for changes to their analgesic plan is vital.
Typically, these patients will need full-mu opioids such as methadone or fentanyl, unless they only have mild pain where something like buprenorphine may be appropriate.
NSAIDs should be avoided due to both the GI signs seen in these patients, and the risk of AKI in a patient with systemic inflammation, dehydration and hypovolaemia.
Opioids, however, can contribute to ileus, slowing the GI tract, impacting nutrition, and increasing nausea and regurgitation. For this reason, opioid-sparing protocols, and the inclusion of other agents such as lidocaine, ketamine and local blocks (such as TAP blocks or epidurals) are often considered.
Early enteral nutrition in canine pancreatitis: what to feed, when to feed, and how to feed
Nutrition is probably the area that has evolved the most in the way we support these patients - and it’s one of the areas where we can have the biggest impact as veterinary nurses and technicians.
When I began training, we used to ‘NBM’ these patients. The thinking was that, for at least a short period of time, the pancreas needed to ‘rest’ before further food aggravated it, activated more of those digestive enzymes, and worsened the cycle of inflammation and necrosis.
This couldn’t be more wrong. We now know that pancreatic secretion actually decreases early in pancreatitis, because the damaged acinar cells can't respond to normal stimuli. So resting the pancreas doesn’t actually have any significant benefit.
More than that, withholding food does active harm. It causes enterocyte damage, gut barrier dysfunction, bacterial translocation and changes to the microbiome (all of which we’ve chatted lots about over the last few weeks).
Early enteral nutrition has been shown to be safe and well tolerated even in dogs with severe acute-onset pancreatitis, and it improves return to voluntary food intake while reducing gastrointestinal complications. The only real contraindications are uncontrolled vomiting despite appropriate antiemetics, severe ileus causing intolerance to enteral nutrition, or pain that clearly worsens when a patient is fed.
So early enteral nutrition is a vital consideration for us when nursing these patients - as soon as we’re happy their pain and vomiting are controlled. We need to perform regular nutritional assessments, tempt these patients to eat, and intervene with a feeding tube where indicated at an appropriate point (<3 days of anorexia).
When feeding these patients, we need to keep their calorie intake appropriate, and keep individual meals small, in the region of 5 to 10 ml/kg.
In terms of what to feed, in dogs we want a low fat (<20g per 1000kCal), highly digestible diet. We also want to avoid high-viscosity fibre in patients with vomiting or ileus, as it slows gastric emptying. We should also avoid urolith dissolution diets where possible in these patients, as they tend to be high in fat.
There’s also a lot of treatments that we don’t routinely reach for in dogs with pancreatitis.
These include antibiotics, antacids, plasma, and colloids. Antibiotics are not indicated routinely, and should instead only be used for aspiration pneumonia, evidence of bacterial translocation, or a documented infection elsewhere. Proton pump inhibitors are only indicated if there's actual evidence of gastrointestinal bleeding or oesophagitis, and plasma and colloids don't have sufficient evidence behind them to support their routine use in pancreatitis.
There are some questions about using steroids in pancreatitis patients, with one study suggesting benefits - but there’s not enough evidence to comment more than this for now, so this is an area we may see change in the future.
Where do we fit in as veterinary nurses - how can we take the lead on caring for dogs with pancreatitis in practice?
I want to finish today’s episode by looking not just at the specific nursing tasks we’ve mentioned, but by talking about our overall role in managing these patients.
We can - and should - play a key role in the overall support and management of these cases in hospital. Nurse-led medical care is something I’m really passionate about (as you’ll know by now!) and there are lots of ways we can have more autonomy in nursing without treading on our vet’s role.
On admission, we're often involved in history collection (or at least, we can be!) - and this should include diet, treats, table scraps, supplements, and every medication the dog is on.
We’re often triaging these patients when they present as emergencies, or looking out for subtle change when we’re monitoring them in hospital.
We can use our knowledge, our skills, our ability to know what could happen with our patients to think outside of the box and look for changes beyond the treatments written on the hospital sheet.
We can perform regular hydration assessments when the patient isn’t written up for them directly.
We can chart the patient for more regular pain scores.
We can dot the patient up for weight measurements more frequently if we’re worried about fluid overload.
We can perform a nutritional assessment, calculate intake, and advocate for a feeding tube.
We can actively look out for complications, rather than dealing with them when they arise.
And then we can continue that care at and beyond discharge - talking to them about low-fat diets if they’re indicated at home (and what that really means), creating feeding plans for the clients to follow, telling them what to monitor, and checking things are still OK a couple of days after the patient goes home.
There are so many ways we can do more with these patients - and with that, more ways we can use our knowledge and skills in practice.
Did you enjoy this episode? If so, I’d love to hear what you think. Take a screenshot and tag me on Instagram (@vetinternalmedicinenursing) so I can give you a shout-out and share it with a colleague who’d find it helpful!
Thanks for learning with me this week, and I’ll see you next time!
References and Further Reading
Chawanlawuthi, W., Sakcamduang, W., Phochantachinda, S., & Chatchaisak, D. (2025). Survival outcomes and prognostic indicators in canine pancreatitis: A retrospective cohort study of acute kidney injury and concurrent diseases. Veterinary world, 18(10), 2969–2980. https://doi.org/10.14202/vetworld.2025.2969-2980
Cridge, H., Lim, S. Y., Algül, H., & Steiner, J. M. (2022). New insights into the etiology, risk factors, and pathogenesis of pancreatitis in dogs: Potential impacts on clinical practice. Journal of veterinary internal medicine, 36(3), 847–864. https://doi.org/10.1111/jvim.16437
Cridge, H., Parker, V. J., & Kathrani, A. (2024). Nutritional management of pancreatitis and concurrent disease in dogs and cats. Journal of the American Veterinary Medical Association, 262(6), 834–840. https://doi.org/10.2460/javma.23.11.0641
Lim, S. Y., Cridge, H., Twedt, D. C., Ohta, H., Nuruki, T., & Steiner, J. M. (2024). Management of acute-onset pancreatitis in dogs: a Narrative Review. Journal of the American Veterinary Medical Association, 262(9), 1231–1240. https://doi.org/10.2460/javma.24.02.0107
Liu, P. C., Teng, K. T., Lin, T. L., Sung, C. H., Cheng, T. L., & Chou, C. C. (2025). Assessment of point-of-care quantitative serum canine pancreatic lipase testing for diagnosing acute pancreatitis in dogs. Frontiers in veterinary science, 12, 1421103. https://doi.org/10.3389/fvets.2025.1421103
Steiner, J. M., Lainesse, C., Noshiro, Y., Domen, Y., Sedlacek, H., Bienhoff, S. E., Doucette, K. P., Bledsoe, D. L., & Shikama, H. (2023). Fuzapladib in a randomized controlled multicenter masked study in dogs with presumptive acute onset pancreatitis. Journal of veterinary internal medicine, 37(6), 2084–2092. https://doi.org/10.1111/jvim.16897
Steiner, J. M. (2025). Pancreatitis in dogs and cats. Available at: https://www.msdvetmanual.com/digestive-system/the-exocrine-pancreas/pancreatitis-in-dogs-and-cats
