57 | 3 things you can do to give better care to your pancreatitis patients right now

In the first of a 2-parter on pancreatic disease, today we’re talking all about managing pancreatitis patients.

 

Pancreatitis is the most common pancreatic disease we see in practice. These patients are often severely unwell and risk developing complications like SIRS and MODS, and need intensive nursing care. In this episode, we’ll look at what pancreatitis is, how it affects our patients, and how we treat it - as well as three things you can do as a vet nurse to give even better care to your own pancreatitis patients.

So what is pancreatitis, and what happens when our patient gets it?!

Pancreatitis is an inflammatory disease of the exocrine pancreas. It is common in both dogs and cats (though cats are less-frequently diagnosed), and can be either acute or chronic, subclinical or associated with clinical signs.

To understand how pancreatitis impacts our patients, we first need to take a (short!) trip back to SVN training and A&P in particular…

Let’s take a look at the pancreas.

The pancreas has both exocrine and endocrine components. The endocrine functions take place in the pancreatic islets and are mostly to do with glucose homeostasis, and today we’re not particularly interested in those (episodes 27, 28 and 29 are for you if you are, though!).

We’re going to focus on the exocrine functions today. These take place in acinar cells within the pancreas. Here, digestive enzymes are created. These include:

  • Trypsinogen, which is converted into trypsin in the small intestine where it breaks down proteins

  • Amylase, which breaks down carbohydrates

  • Lipase, which breaks down fats

These enzymes are stored inside the pancreas in inactivated forms called zymogens and become activated when they leave the pancreas. Normally, when a patient eats, pancreatic juice (containing those enzymes) leaves the pancreas via the pancreatic duct, and enters the small intestine along with bile, and digestion begins.

These zymogens are important - because like the food these enzymes break down, the pancreas is made up of proteins, fats and other organic substances. If these enzymes sat in the pancreas in their active forms, they could break down pancreatic tissue (called pancreatic autodigestion).

When these pancreatic enzymes become prematurely activated, they cause pancreatic autodigestion - resulting in pancreatitis.

In the initial stages of pancreatitis, pancreatic juice secretion decreases and those zymogens become activated. Trypsinogen is converted to trypsin inside the pancreas, which triggers a cascade of digestive enzyme activation.

These digestive enzymes damage the surrounding exocrine pancreatic tissue, causing pancreatic oedema, inflammation, haemorrhage, and necrosis. The surrounding tissue (particularly the fat surrounding the pancreas) also becomes inflamed and necrotic, and inflammatory cells and proteins are released into the bloodstream.

These inflammatory substances then circulate through the body, where they can cause complications in other organs and generalised inflammation.

This is known as SIRS - systemic inflammatory response syndrome. Patients can develop vasodilation and distributive shock, hypotension and tachy- or bradycardia.

If the inflammatory substances cause injury to two or more organs (eg. acute kidney injury, acute hepatic failure and myocarditis), multi-organ dysfunction syndrome (MODS) results.

Am I saying that every pancreatitis patient will develop SIRS and MODS? Not at all. However, these are important complications of pancreatitis - particularly acute, severe, or necrotising pancreatitis - and we must be aware of them so we can monitor our patients carefully and intervene at an early stage.

Acute vs chronic pancreatitis - what’s the difference?

If I said, ‘Picture a pancreatitis patient you’ve seen,’ I’ll bet you’re thinking of an acute pancreatitis case.

Acute pancreatitis is the ‘classic’ pancreatitis we tend to think of - the painful dog in the prayer position with severe ongoing vomiting. It tends to be these guys who get things like SIRS and need intensive in-hospital care.

Acute pancreatitis is sudden, severe, reversible pancreatic inflammation. It usually has more severe clinical signs than chronic pancreatitis and requires inpatient management.

Chronic pancreatitis is a long-term condition characterised by ongoing, low-grade pancreatic inflammation. The clinical signs are usually less severe, and some patients may even be subclinical. Because of this, the condition can be challenging to diagnose and manage, particularly in cats.

Chronic pancreatitis can lead to permanent pancreatic damage, causing complications like diabetes mellitus or exocrine pancreatic insufficiency (which we’ll talk about in next week’s episode).

In general, cats tend to present more commonly with chronic pancreatitis, and dogs present more commonly with acute pancreatitis - though that isn’t always the case.

So that’s what pancreatitis is and how it affects our patients. But what causes it?

Most cases of canine and feline pancreatitis are idiopathic. Despite this, we have identified several causes and risk factors, including:

  • Breed: such as Miniature Schnauzers, Yorkshire Terriers, Cocker Spaniels, Dachshunds and Poodles 

  • Dietary factors: such as dietary indiscretion, a common risk factor in dogs

  • Trauma: blunt force trauma (high-rise syndrome, RTAs), particularly in cats

  • Anaesthesia and hypotension: causing pancreatic hypoperfusion

  • Infectious diseases and certain concurrent diseases: including Toxoplasma gondii and feline infectious peritonitis in cats, Babesia canis and Leishmania infection in dogs, and hyperlipidaemia and Cushing’s disease in dogs

In humans, several medications have been strongly linked with developing pancreatitis, though no similar evidence exists in cats and dogs.

Regardless of the cause, the result for our patient is the same; pancreatic autodigestion and inflammation, pain, and potentially systemic consequences.

What signs do these patients present with?

Clinical signs depend on the species and the type of pancreatitis the patient has. 

Dogs with acute pancreatitis commonly present with anorexia, vomiting, abdominal pain, weakness, dehydration and diarrhoea.

This is very different to cats with acute or severe pancreatitis, who commonly present with anorexia, dehydration, lethargy, hypothermia, and vomiting. Cats can also present with icterus and pyrexia, and obvious abdominal pain is reported much less commonly in these patients, despite having severe pancreatitis - highlighting the importance of looking for subtle signs of pain, and trial treating with analgesia if there’s any doubt.

Both dogs and cats who have chronic or milder forms of pancreatitis may be subclinical or present with vague clinical signs of anorexia, lethargy and diarrhoea.

And how do we diagnose these patients?

Diagnosing pancreatitis can be a bit of a pain, because none of the tests we have are 100% accurate at diagnosing pancreatitis in all patients. So really, we’re using a combination of our patient’s clinical history and examination findings with diagnostic imaging and pancreatic lipase levels - rather than relying one particular test alone.

Ultrasonography often reveals an enlarged, bright pancreas with bright peripancreatic fat - but it is important to consider that operator experience impacts the diagnostic quality of ultrasound, so a diagnosis can’t be made based on imaging alone.

Most biochemical and haematological changes aren’t specific for pancreatitis. Amylase and lipase don’t really give us any particularly useful information, especially because normal lipase on our biochemistry profiles isn’t specific for pancreatitis.

The specific pancreatic lipase immunoreactivity or PLi test is the most specific diagnostic test for pancreatitis currently available. It is highly sensitive, meaning that negative tests make pancreatitis unlikely, and highly specific, meaning a positive result correlates well with pancreatitis. 

Other biochemical tests for pancreatitis are available, including a DGGR lipase test and the semiquantitative pancreatic lipase snap test.

Pancreatic cytology or histology can theoretically be used to diagnose pancreatitis, but FNAs risk delivering non-diagnostic results, and pancreatic biopsy can itself cause pancreatitis. Therefore, we rarely sample the pancreas, instead making a diagnosis based on imaging, blood results, and clinical history and then beginning supportive treatment.

Ok, so that’s our diagnosis sorted. What does our treatment plan look like?

The mainstay of pancreatitis treatment is with intensive supportive care and monitoring.

Patients with acute pancreatitis should have any underlying causes or risk factors managed where they are identified - for example, managing concurrent hyperlipidaemia in a Miniature Schnauzer with pancreatitis. 

However, very few cases have an underlying cause identified, and in most cases, supportive and symptomatic treatment is provided. This includes:

  • Intravenous fluid therapy at an appropriate rate, based on hydration status

  • Antiemetics - including maropitant and ondansetron in severe cases that don’t improve on maropitant alone

  • Analgesia - including opioids +/- additional agents as necessary

Interestingly at the time of recording this episode, a new specific treatment for acute pancreatitis is currently available in Japan. It’s called Brenda Z (fuzapladib), and it works by preventing neutrophils from moving into the extravascular tissue. A new version of this drug, called Panoquell-CA1, is currently being investigated for use in North America. However, it’s not currently available in Europe - so watch this space; perhaps we’ll get this drug in the future!

Aside from providing supportive treatment, much of our care is centred around intensive monitoring and rapid intervention if our patient begins showing signs of systemic inflammation. This means keeping a close eye on their cardiovascular status and monitoring for changes such as:

  • Hypotension

  • Bradycardia or tachycardia

  • Bounding pulses

  • Bright red MMs and rapid CRT

  • New changes to organ function on diagnostic results (e.g. increased liver or renal parameters, decreased urine output)

What about treating chronic pancreatitis?

Chronic pancreatitis patients often have a milder form of the disease, requiring less intensive inpatient treatment. They are often managed as either an inpatient or outpatient (depending on the severity of their signs) with antiemetics and appetite stimulants alongside an ultra-low-fat diet. 

Patients with chronic pancreatitis who do not respond to supportive care alone may require treatment with prednisolone or cyclosporine, depending on the species and their risk for concurrent diabetes mellitus.

And how do we nurse these patients?

At the start of this episode, I said there were three things to focus on in particular when managing pancreatitis patients - and here they are.

#1: Nutrition

Nutrition is arguably the most important nursing consideration for pancreatitis. Firstly, because these patients are often anorexic, and secondly, because we’re going to need to think very carefully about what we feed them.

Early enteral nutrition is vital. If you’ve ever been taught to ‘rest’ the pancreas in a pancreatitis patient, throw away your notes right now!

Feeding your patient (via the GI tract) is the most potent stimulator of intestinal regeneration. Not only that, but it can decrease production of those inflammatory proteins, and decrease catabolism of the body’s own tissue.

So get antiemetics on board, stop that vomiting, and then get food in. Place an NO or NG tube, and start refeeding at an appropriate percentage of the patient’s RER.

So we’ve got when to feed sorted, but what about WHAT to feed? Well, it depends entirely on the patient’s species and whether their pancreatitis is acute or chronic.

In all patients, we want to feed a highly digestible, complete and balanced diet. Cats have naturally higher fat and protein requirements compared to dogs, so a moderate-fat (<25% on a dry matter basis/DMB), high-protein (30-40% DMB), low-crude-fibre diet is preferred.

This differs to dogs, who require more dietary fat restriction. These patients should be fed a low or ultra-low-fat (<15% DMB unless the patient is obese or has hyperlipidaemia; these patients should be fed <10% fat DMB), moderate-protein (15-30% DMB) diet. Excessive protein should be avoided, since proteins are a strong simulus for pancreatic secretion. However, it’s vital we provide enough protein for tissue repair and patient recovery.

#2: Pain

I can’t stress the importance of this one enough. 

Even if a pancreatitis patient doens’t appear painful, there’s a good chance they are.

90% of humans with pancreatitis describe significant abdominal pain, compared with it being reported in only 58% of dogs and 19% of cats in one study - likely due to a lack of recognition rather than these patients being comfortable.

We are our patient’s advocates - we spend time with them, nursing them in the ward, administering analgesia and assessing its effectiveness. If you’re concerned that your patient is painful, even if they’re already on opioids - speak up!

Multimodal analgesia is key in these patients, and there are lots of other agents we can use - like paracetamol and lidocaine (in dogs only), ketamine and even epidurals.

If you’re not sure whether your patient is painful, speak to your vet and perhaps try a low dose to see if your patient improves. You can always top up if you need to add more!

#3: Monitoring

Acute pancreatitis patients can deteriorate very quickly, so it’s vital to detect subtle changes at an early stage. 

Lucky for us, though, as vet nurses and technicians, that’s our forte - we’re the ones doing the monitoring, and spotting those small changes is a real art that we’re really good at.

Keep a close eye on your patient, and if you’re worried, trust your gut. Don’t wait for your vitals to hit ‘textbook’ abnormal levels - if things are starting to trend up or down, intervene early.

Here’s a quick list of things to monitor in your acute pancreatitis patients:

  • Heart rate

  • Pulse quality and rate

  • Blood pressure

  • Respiratory rate, pattern and effort

  • MM colour and dryness or moistness

  • CRT

  • Bodyweight

  • Temperature

  • IV catheter site

  • Nausea, vomiting and regurgitation, and GI motility

  • Eliminations

  • Pain

  • Appetite and % RER intake

  • Hydration status

  • Minimum database bloods as needed - electrolytes, glucose, lactate, renal parameters, PCV and total solids

  • POCUS as needed - thoracic (looking for signs of aspiration) and abdominal (looking for fluid, gastric distension and GI motility)

This list is by no means exhaustive, but it gives you a great place to start when nursing your own patients!

So there you have it - my guide to managing pancreatitis patients. These patients need a lot from us, particularly if they have acute or severe disease, but with rapid intervention and careful monitoring, we can really improve their prognosis.

Did you enjoy this episode? If so, I’d love to hear what you thought - screenshot it 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

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56 | Help, my patient is losing protein! How to care for patients with protein-losing enteropathy