scott@vtx-cpd.com
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Replying to Shannon Thorell 22/06/2025 - 04:20
Hi Shannon,
Thanks so much for the feedback—and I’m really glad you’re enjoying the course so far.
That’s a very sensible point about the heatstroke lecture timing. I completely agree it would be really useful to have it earlier in the schedule during the hotter months. I’ll make sure to note that for the next round so we can better match it to the season—really appreciate you pointing it out.
Thanks again for taking the time to write, and for being part of the course.
Cheers,
Scott 🙂
Replying to Mark Laloo 18/06/2025 - 16:01
Hi Mark,
Thanks so much for these excellent questions.
1) Do you check coagulation times before pancreatic/liver FNAs? If coagulation times are prolonged, would you give Vitamin K if FFP is unavailable? How long would you treat before repeating coags?
For FNAs specifically, I’ll be honest, I don’t routinely check PT/aPTT in every case. My main consideration is whether there’s sufficient platelet numbers. As long as the platelet count is adequate, FNAs are generally very low-risk for significant bleeding, especially for accessible lesions on ultrasound.
For higher-risk procedures like hepatic biopsies (true-cut or wedge), feeding tube placement, or sampling in patients with known liver dysfunction or cholestasis, I’m much more cautious. In those cases, I will usually check coagulation times beforehand.
If there’s cholestasis or liver dysfunction suggesting vitamin K-dependent clotting factor deficiency, I often use vitamin K prophylactically. Typical protocol is:
Vitamin: 0.5–1.5 mg/kg SC every 12–24 hours for 3 doses, ideally starting 24 hours before the procedure to help minimise bleeding risk.
If PT or aPTT is prolonged and FFP is unavailable, vitamin K can help restore factor activity, but it’s not an immediate fix. It takes hours to days to work. I’ll generally complete the 3-dose course and then recheck coagulation times 12–24 hours after the last dose to confirm improvement.
In an acute bleed with significantly prolonged PT/aPTT, plasma (FFP) remains the ideal choice since it directly provides the missing clotting factors immediately.
2) Do you always supplement calcium if the ionised calcium is low and the patient is not showing clinical signs of hypocalcaemia? Do you administer calcium gluconate as a bolus or infusion or both? Does Vitamin D have a role to play in cats with triaditis and could this contribute to the low calcium?
If ionised calcium is only mildly low and the cat is asymptomatic, I usually just monitor and don’t routinely supplement. Mild, transient hypocalcaemia is common with acute pancreatitis and often resolves as the underlying inflammation improves.
If there are clinical signs of hypocalcaemia (facial twitching, tremors, seizures, arrhythmias) or the ionised calcium is significantly low (e.g. <0.8 mmol/L in cats), then I intervene.
Regarding vitamin D: in cats with chronic cholangitis or IBD (triaditis), there can be malabsorption of fat-soluble vitamins, including vitamin D, which could contribute to hypocalcaemia. However, in acute pancreatitis, this is usually not a major driver. Routine vitamin D supplementation isn’t needed acutely, but in chronic cases with documented hypovitaminosis D, supplementation can be considered with careful monitoring.
3) Doing OOH/ECC work, I see a lot of cats with acute pancreatitis and evidence of sepsis/SIRS. Quite often I have to reach for IV antibiotics and my go-to is amoxicillin-clavulanate. Is this a reasonable first line? Should we be doing more bile cultures in cats with pancreatitis? Is the gallbladder completely sterile or does it have a ‘microbiome’?
Excellent ECC-relevant question.
Antibiotics in pancreatitis are controversial because most cases are sterile inflammatory processes. However, if there’s clear evidence of sepsis/SIRS (e.g. hypotension, hypothermia, marked leukopenia/neutropenia with toxic change), empirical antibiotic use is justified.
Amoxicillin-clavulanate is a very reasonable first-line choice. It provides good coverage for common enteric organisms, including many anaerobes. For more severe cases or if there’s suspicion of biliary infection (e.g. cholangitis), adding a fluroquinolone or using broader-spectrum options may be indicated.
Bile cultures can be very helpful in cats with concurrent biliary dilation or sonographic evidence of cholangitis. Cats with cholangitis often have ascending infections with organisms like E. coli, Enterococcus, Clostridium, and Streptococcus.
Regarding sterility of the gallbladder: it isn’t completely sterile in all cases. There’s evidence of a low-level biliary microbiome in both humans and animals. However, significant bacterial infection is generally considered pathologic rather than normal.
4) We tend not to use IV erythromycin and ondansetron simultaneously due to the potential cardiac effects. Do we really need to worry about QT prolongation or is this just a theoretical concern?
Very good pharmacology question.
It’s a real, though small, risk. Both drugs can prolong the QT interval via effects on cardiac ion channels. There are documented human cases of additive QT prolongation and arrhythmias with combined use.
In veterinary patients, such arrhythmias are rare but certainly possible, particularly in older cats or those with underlying cardiac disease.
Practically speaking, I don't often give them at the same time. I will ask Liz for input too.
5) I know some dog breeds are prone to an immune-mediated form of pancreatitis. Is this quite rare in cats? Any breed predisposition? Does histopathology of the pancreas help you decide if it’s immune mediated? Are you able to wean them off steroids completely or do they remain on a low dose long-term? Could the steroids make a difference by also managing inflammation associated with IBD/cholangitis?
Great question.
In cats, overt immune-mediated pancreatitis is less well-defined than in dogs. There’s no strong breed predisposition like in Cavalier King Charles Spaniels or other canine breeds.
Histopathology can show lymphoplasmacytic infiltration suggesting an immune-mediated component, but mild lymphoplasmacytic inflammation is also common in “normal” feline pancreata, making interpretation tricky.
When I suspect immune-mediated disease—especially as part of triaditis with concurrent IBD and cholangitis—I often trial prednisolone. Many cats respond well. Some can be fully weaned off over months, while others remain on a low maintenance dose if signs recur.
Steroids also help manage associated IBD and cholangitis by dampening the entire inflammatory process in triaditis, so they can have significant benefit beyond the pancreas itself.
6) I know they tend not to use probiotics in humans with acute pancreatitis. Do you have this concern in cats and dogs? Is it safer in chronic pancreatitis?
In humans with acute severe pancreatitis, probiotic use has actually been linked with worse outcomes in some studies, possibly due to bacterial translocation across a compromised gut barrier.
I tend not to worry too much. In acute cases, I suppose there are lots of other priorities above ethe probiotics.
For chronic pancreatitis, however, I’m more comfortable using them. There’s rationale for supporting gut health and potentially modulating low-grade inflammation, though veterinary evidence remains limited. In stable chronic cases, I think they can be a reasonable part of management.
Hope this helps answer everything.
Scott 🙂
Replying to Rachel C. 28/06/2025 - 14:20
Hi Rachel,
Yes—very similar experience here!
A lot of my clients will proudly tell me they’re adding coconut oil, fish oil capsules meant for humans, or all sorts of “skin and coat” chews they’ve found online. Like you, I worry about the evidence (or lack thereof), especially when some of them have weird and wonderful ingredient lists with no real quality control.
I will make sure Georgia sees this too!
Scott 🙂
Replying to Yvonne McGrotty 24/06/2025 - 15:46
Thanks again for everything pal.
Always amazing to work with you.
Scott 🙂
Replying to Debbie J. 18/06/2025 - 09:59
No problem.
I know these are often ‘one off’ things, but still worth knowing about.
I hope you are well pal.
Scott 🙂
Replying to Jon H. 17/06/2025 - 21:50
This is so helpful Jon.
Thank you for sharing your insights.
Scott 🙂
Replying to Jane Sedgewick 16/06/2025 - 21:01
Hi,
Thanks for your message.
I agree that 0.5 IU/kg BID is a common and often effective starting point with Caninsulin, and in well-selected cases (e.g. stable, eating, low-risk for concurrent illness), it’s likely a very reasonable choice. I suspect that differences in case selection, monitoring protocols, and owner communication styles play a large role in how much flexibility there is to start at a higher dose safely. Your point about reducing hypo risk through education is really well taken, and your audit data certainly supports that your protocol is working well.
That said, I think this is a good question to run past Rodolfo as well, since the Caninsulin-specific part of the protocol came from his recommendations. I’ll forward this along and let you know what he says.
Scott 🙂
Replying to Jane Sedgewick 16/06/2025 - 20:53
Hi Jane,
Thanks so much, these are excellent points and ones that I think a lot of us grapple with when trying to balance safety and efficacy in feline diabetes management.
You’re absolutely right that traditional teaching often discourages frequent dose changes, especially with insulins like Caninsulin, where short duration and variability make overswing a real concern. But glargine has a flatter and longer action profile, so it’s less prone to inducing a Somogyi rebound, especially at the conservative dose ranges used in this protocol (most cats remained under 4 units BID). The protocol also reduces the dose when the pre-insulin glucose is between 6–12 mmol/L, which helps mitigate the risk of overcorrection and hypoglycemia.
The idea of Somogyi overswing in cats on glargine is still debated, but the emerging view, supported by this and other studies, is that it’s likely much less common than once thought, and persistent hyperglycemia is more often due to underdosing or other causes such as stress or concurrent illness.
There were 50 cats in the study, and they were quite carefully selected (motivated owners, consistent feeding routines, regular follow-up). I do think this type of protocol is hard to replicate without strong client support and accessible communication, but it’s an exciting glimpse into what’s possible.
Regarding glucometers, I agree it’s a bit of a grey area. This group used the AlphaTrak 2, which is well-validated in cats and was calibrated accordingly. There’s some evidence that human meters can be acceptably accurate in well-hydrated cats, but ideally we want something species-specific or at least calibrated and validated for feline blood parameters. G-Pet is a reasonable option for those who can’t access AlphaTrak.
Totally understand the hesitation around owner-led dose changes. It’s not something to launch without careful case selection and backup, but I think we may be heading toward more collaborative models, especially with the rise of home glucose monitoring and tools like the Freestyle Libre.
Scott 🙂
Replying to Shannon Thorell 19/06/2025 - 12:56
Hello Shannon.
Let me know how you are enjoying the course. Your feedback id really helpful.
This is a great question. I will make sure Kerry and Neus see this one!
Scott 🙂
Replying to Jo T. 15/06/2025 - 18:32
Hi Jo,
I can completely relate to what you’ve shared. It’s funny, I actually spent a number of years dealing with significant night shift fatigue too. In my first specialist role, I ended up going back to ECC night shifts because I felt they gave me more flexibility and control over my time.
Like you, I remember initially feeling that I coped really well—there was almost a novelty to the night shifts, and for a while it felt like they suited me. But over time, that definitely changed, and the impact really started to show in ways that were harder to ignore: slower thinking, poorer recovery, and just a constant underlying sense of fatigue.
One thing I’ve often noticed—and I think it’s important to talk about—is how night work is often framed in recruitment. There’s usually an emphasis on flexibility and higher pay, but I think we need to look more critically at how realistic or sustainable that actually is in the long term. The toll it takes is significant, and not always obvious at first.
It’s funny you mention the moral injury of your leadership role—I experienced exactly the same thing. For a long time, I assumed that the natural next step after becoming a specialist would be to take on head of department roles or move into clinical director positions. But the reality is, those roles really didn’t suit me, and they ended up taking a very real toll on my mental health. It’s only in recent years that I’ve come to terms with that, and found a better balance.
These days I work three clinical days a week, and I’ve been able to complement that with the educational work I do with vtx—which has brought a lot more balance and sustainability to my life. At the hospital I work in currently, our ER and ECC staff are actually going through a tough period of transition, where their schedule is shifting from three longer shifts to four shorter ones each week. And honestly, it’s causing a huge amount of distress. Having shift patterns dictated in that way, without individual input, really highlights the broader issue: for many of us to have a sustainable and fulfilling career in this profession, we need flexibility that’s actually meaningful—and that means allowing people to shape schedules that reflect their individual needs, lives, and limits.
Thanks again for starting such an important conversation. What you shared really struck a chord.
Scott 🙂
Replying to Lesley M. 15/06/2025 - 18:59
Thanks Lesley,
Transfusion definitely depends on individual stabilisation. If the dog is actively bleeding, starting a transfusion too far ahead of surgery can just result in blood loss into the abdomen. Often we’ll aim to start the transfusion shortly before or during surgery so the red cells are supporting perfusion at the time it matters most.
That said, the decision to transfuse usually hinges more on clinical status than PCV alone—things like mentation, pulse quality, lactate and MAP often guide us more practically. And of course, availability plays a huge role. In some practices, the timing is dictated more by how quickly you can get a unit than anything else.
The belly wrap idea is interesting. It’s based on the idea of tamponade—trying to buy time and reduce ongoing haemorrhage by increasing intra-abdominal pressure. It’s something that’s been extrapolated from human trauma care, where pelvic or abdominal binders are occasionally used, but even in people it’s controversial for intra-abdominal bleeding.
As far as I’m aware, there’s no published veterinary evidence supporting belly wraps for hemoperitoneum in dogs. It’s mostly anecdotal, and there are potential downsides like impaired venous return, respiratory compromise and discomfort. It might be a useful temporising option in very select cases, but we really need some proper data to say whether it helps or harms.
Would be great to hear if others are using it and what their experience has been.
Scott 🙂
Replying to Aaron H. 13/06/2025 - 13:52
Thank you!
We are very lucky to get to work with you!
Scott 🙂
Replying to Katherine Howie 08/06/2025 - 20:29
Thanks Kath!
Really helpful!
Scott 🙂
Replying to Rodolfo L. 06/06/2025 - 22:32
Thank you so much for this Rodolfo!
We appreciate you wisdom!
Scott 🙂
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 🙂
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