scott@vtx-cpd.com

Replying to Liz Bode 06/07/2025 - 21:00

Hi Liz,

Thanks so much for this! Sorry for the JC spoiler! 🙂

I also love your point about being pragmatic for those cases where echo just isn’t feasible. It’s that classic balance between ideal medicine and what’s actually possible in real life.

I think this study is going to make for a great journal club discussion—looking forward to hearing more!

Cheers,

Scott 🙂

Replying to Riley D. 06/07/2025 - 15:14

Hey Riley,

I hope you are well!

That’s exactly the kind of thing I was thinking too—it’s such a tempting message (“just start pimobendan if there’s a loud murmur!”) but it risks shortcutting proper workups.

And yes, the whole treating stage B1 dogs who don’t need it is a big one for me too—cost to the owner aside, there’s that question of pushing remodelling or hypertrophy in a heart that might have stayed stable for years.

Really keen to see what Liz thinks too!

Scott 🙂

Replying to Liz Bode 29/06/2025 - 21:20

Thank you Liz!

This is really helpful!

Scott 🙂

Replying to Liz Bode 22/06/2025 - 21:43

Really helpful!

Thanks Liz.

Scott x

Replying to Lynne Holcroft 22/06/2025 - 15:16

Hi Lynne,

Thanks so much for taking the time to share this—it’s really great to hear your perspective.

Your experience with your own Maine Coon is really valuable. It highlights exactly why these discussions matter so much: even though FHNE is often recommended as the “simple” or “safe” option, THR can absolutely be a fantastic choice in the right patient. It’s brilliant to hear how well your cat has done post-bilateral THR, especially with that level of functional recovery and no ongoing meds or physio. That outcome really speaks to careful case selection and good surgical technique, but also to owners being well-informed and involved in making the best decision for their individual cat.

I think you’re spot on about how cost, insurance coverage, and local referral options can drive these choices. In my own experience, FHNE does tend to get proposed more often partly because it’s technically easier and cheaper, and maybe also because there’s a lingering sense among some vets that cats “cope” better with it than dogs do. But as you say, the owner-reported quality of life is not the whole story if they’re losing subtle aspects of mobility or activity.

Your comment about owners noting that their cats are “back to normal except not jumping as high” really echoes what this paper showed—that there can be functional compromises even when general quality of life seems good. It makes the case for giving owners the full picture, so they can balance expectations realistically.

I think you’re absolutely right that having this kind of data in our back pocket can help us have better, more nuanced conversations in practice.

Thank you again for your brilliant comments! I hope you are having a lovely weekend.

All the best,

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 🙂