scott@vtx-cpd.com

Hello Christina,

This is a great topic!

Traditionally, corticosteroids were thought to contribute to the development of pancreatitis, largely based on anecdotal associations and extrapolation from human data. However, this dogma has been challenged over the last decade, with growing evidence suggesting that glucocorticoids do not cause pancreatitis in dogs, and in some cases, may even provide therapeutic benefit.

Several studies (Parent 1982; Bang et al. 2008; Steiner et al. 2009) have failed to demonstrate a causal relationship between corticosteroid use and the development of pancreatitis in dogs. In fact, glucocorticoids have been removed from the list of drugs considered to cause pancreatitis in humans, and veterinary consensus is shifting in parallel.

Recent literature suggests glucocorticoids may:

Enhance apoptosis (a controlled form of cell death that limits inflammation) rather than necrosis

Suppress systemic inflammation associated with SIRS or septic shock

Upregulate pancreatitis-associated protective proteins (Wan et al. 2011; Yu et al. 2014; Dong et al. 2015)

Have beneficial antioxidant and membrane-stabilizing effects, which may preserve pancreatic tissue integrity

The 2019 study by Suzuki et al. (PMID: 30868606) is a good example. It showed improved clinical outcomes in dogs with suspected acute pancreatitis treated with corticosteroids, compared to those who did not receive steroids. This echoes earlier experimental work (e.g. Imahori et al., 1984), which reported reduced histologic severity and better survival outcomes with steroid administration in induced acute pancreatitis in dogs.

So when do I consider steroids? Not routinely—but selectively:

Cats with triaditis, where prednisolone is already often used long-term for IBD or cholangitis

Dogs with suspected immune-mediated or chronic relapsing pancreatitis, particularly if concurrent IBD is suspected

Patients with persistent systemic inflammation, vasculitis, or SIRS-like responses, where other supportive care is insufficient

On the other hand, NSAIDs are a different story. While their anti-inflammatory and analgesic effects are attractive, the risks tend to outweigh the benefits in most pancreatitis cases:

Even post-rehydration, GI perfusion may remain compromised

There is potential for GI ulceration, renal hypoperfusion, and exacerbation of mucosal injury

NSAIDs are one of the agents proposed to contribute to GI barrier breakdown in people with pancreatitis, and similar mechanisms are likely in dogs

I would only consider NSAIDs in pancreatitis cases if:

The patient is fully hydrated, stable, and eating

There is a compelling orthopedic or neoplastic pain issue requiring additional control

There is no GI bleeding, no concurrent corticosteroids, and I can co-prescribe a proton pump inhibitor (PPI)

That brings us to gastroprotectants, which are frequently used—but perhaps overused—in pancreatitis. The rationale has always been that:

Hypovolemia, hypoxia, and GI ischemia in pancreatitis may lead to stress ulceration

NSAIDs or systemic inflammation may further compromise mucosal defenses

Therefore, acid suppression (e.g. omeprazole or pantoprazole) might prevent ulceration

However, this rationale is being challenged. The ACVIM consensus statement on GI protectants (Marks et al., 2018) specifically states:

“There is no evidence that acid suppression treatment is beneficial or indicated in the management of dogs or cats with pancreatitis, unless the animal has concurrent evidence of gastric ulceration or erosion (GUE).”

Further to this, Section 6.6 of the Consensus on Pancreatitis outlines:

The incidence of GI bleeding in pancreatitis is unknown

PPIs like pantoprazole have shown inconsistent effects in rodent models—some anti-inflammatory, some pro-inflammatory (refs 189–191)

A recent placebo-controlled human trial (Jung et al., 2019) showed no clinical benefit from pantoprazole in acute pancreatitis

Therefore, routine PPI use is not justified unless there’s specific concern for GI ulceration (e.g., melena, hematemesis, or known NSAID exposure)

So in short, PPIs should not be used reflexively in every pancreatitis case—but I would still use them in patients with:

Known GI bleeding or ulceration

Severe GI pain or vomiting that may suggest mucosal compromise

Lastly, it’s worth keeping an eye on emerging therapies—notably fuzapladib sodium, a leukocyte-function associated antigen-1 (LFA-1) inhibitor. It’s licensed in Japan and conditionally FDA-approved in the U.S. for treating clinical signs of acute pancreatitis in dogs. Early studies show it attenuates systemic inflammation and may reduce pancreatic injury. While not widely available, it reflects a promising shift toward targeted immunomodulation rather than purely supportive care.

I hope that helps.

All the best,

Scott 🙂

Replying to Sarah Clements 03/06/2025 - 12:43

Hi Sarah,

Great question. CRP can potentially be useful for monitoring response in pyothorax cases, but unlike pneumonia, there’s very little published data specific to pleural infections in dogs or cats.

Most of what we know comes from extrapolation — particularly from studies in bacterial pneumonia. In those cases, CRP has been shown to decline rapidly with effective treatment, and normalization correlates well with clinical recovery. A good example is the Viitanen et al. (2017) study, where CRP-guided therapy shortened the duration of antibiotics in dogs with pneumonia without increasing relapse risk (Viitanen et al., JVIM, 2017). However, that study did not include any cases of pyothorax.

In practice, I find serial CRP helpful as an adjunct in monitoring pyothorax, particularly when:

Culture is negative or mixed

Imaging is slow to resolve, or drainage is partial

You’re considering the timing of antibiotic taper or discontinuation

A declining CRP trend usually parallels clinical and radiographic improvement, so it can help support a decision to de-escalate therapy. But because the pleural space is more complex (e.g., biofilm formation, anaerobes, limited perfusion), I wouldn’t use CRP alone to guide treatment length.

In people, CRP and procalcitonin have some use in empyema follow-up, but even there, it’s usually paired with imaging.

Hope that helps.

Scott 🙂

Thanks Janette – this is a really valuable summary and I appreciate the link to the review. The balance between neonatal vitality and maternal welfare is often overlooked in practice.

What’s your current go-to for premeds in emergency C-sections?

Scott 🙂

Replying to Josep B. 02/06/2025 - 04:52

Thanks Josep!

Scott 🙂

Thanks Mark.

Your go-to combination of buprenorphine, gabapentin, and meloxicam is very similar to what many of us reach for in the first instance, and there’s sound rationale behind each. That said, it’s worth keeping in mind that while these medications are commonly used and make intuitive sense in painful inflammatory bladder conditions, none of them have been robustly studied for non-obstructive FIC in terms of efficacy beyond placebo.

In fact, a recent consensus summary (authored by the amazing Sam Taylor) highlights that analgesics such as NSAIDs, opioids, gabapentinoids, and even frunevetmab (anti-NGF monoclonal antibody) have not yet been formally evaluated in clinical trials for this indication. That doesn’t mean they shouldn’t be used—pain management is absolutely recommended—but it does mean we need to weigh their potential benefits against the stress of administration, especially when oral dosing is difficult or negatively affects cat behaviour. Gabapentin is helpful in many cats, but we have to be honest that in some cases, the stress of medicating may actually worsen the condition by increasing perceived threat and reducing control.

Other drugs like prednisolone, pentosan polysulfate, and glycosaminoglycans have not shown significant benefit in blinded studies, although both placebo and treatment groups often improve—possibly related to better home care, handling, or reduced threat perception (e.g. giving meds in a treat or encouraging owner-cat bonding). These behavioural and environmental influences may explain why MEMO (multimodal environmental modification) consistently shows better long-term results than medications alone.

Trazodone is one I’ve seen used selectively in cats that are extremely hypervigilant or live in high-arousal home environments, but I rarely use it personally.

Amitriptyline and fluoxetine remain options in refractory or relapsing cases, particularly if there’s concurrent urine spraying or clear evidence of chronic stress or anxiety. However, these should ideally be started with behavioural guidance and close follow-up. Fluoxetine has been associated with urinary retention in some reports, and any use for behavioural modification should always accompany MEMO, not replace it.

I am not a huge fan of subcutaneous fluids in these cases. There’s no evidence it improves outcome, but it may make sense on a case-by-case basis. I wouldn’t do it routinely unless there’s a clear clinical rationale.

I’ll also make sure Sam sees this!

Consensus guideline link: https://journals.sagepub.com/doi/10.1177/1098612X241309176

Scott 🙂