scott@vtx-cpd.com

Replying to Jane Sedgewick 20/05/2025 - 17:39

Hi Jane,

That’s a very fair and probably quite realistic point. You’re absolutely right that while CIRCI and other causes of low basal cortisol can muddy the waters, the proportion of dogs that present looking like classic Addisonians, with the full electrolyte profile and clinical signs, but actually have something else going on is likely very small.

In most general practice or non-ICU settings, the dogs with severe enough systemic disease to develop CIRCI and flat-line a stim test are, unfortunately, often those that deteriorate quickly or are already in a very guarded position. So while it’s important to be aware of the possibility, I agree that it’s probably a minority that would survive long enough, respond to supportive care, and then be left on unnecessary Zycortal long term.

Still, it’s good to know these scenarios exist so we can be cautious about interpreting a low basal cortisol on its own without the full clinical context or without following through with the ACTH stim. And you’re right, it might be worth having a look at the protocol if that initial basal cortisol is being leaned on too heavily as a stand-alone result.

Really great question again.

Best,

Scott 🙂

Replying to Jane Sedgewick 21/05/2025 - 15:16

Hi Jane,

I completely agree that the fear around NSAIDs often leads to prolonged opioid use, which brings its own cascade of problems (ileus, nausea, dysphoria, sedation). Like you, I tend to restart NSAIDs once the patient is eating again, though I’d love to see more robust data to support this approach. That carprofen paper was at least reassuring in suggesting no obvious signal for harm in clean GI cases, when used thoughtfully.

On the paracetamol front, I must admit I’m actually a bit of a fan. That may partly be because so many of my patients are on steroids, where NSAIDs just aren’t an option. I found the PLoS One 2020 study quite useful—it compared paracetamol to meloxicam and carprofen in routine OVHs and showed broadly similar analgesia with no clear adverse hepatic or renal effects in healthy dogs. I think for stable patients with no predisposing comorbidities, it can definitely play a useful role as part of multimodal analgesia. That said, I completely hear you. It doesn’t work for everyone, and there are still cases where it seems to do very little.

On the NSAID plus sulfasalazine question, I can’t find any specific reference formally contraindicating their combined use, but there’s definitely limited evidence in dogs. I often avoid using them together, mostly out of caution. Do you use sulfasalazine a lot? I’d agree with your rationale, it’s largely cleaved in the colon, so systemic interaction is minimal. The main theoretical concerns are overlapping GI or renal toxicity, which I’d only worry about in patients who are already azotemic or dehydrated.

Scott 🙂

Replying to Jane Sedgewick 14/05/2025 - 11:57

The clinical signs are absolutely key in these cases.

I have popped together a clinical sign monitoring chart for patients. I am happy to share it with you if you think that would be helpful?

Owners love this for monitoring purposes.

Scott 🙂

Replying to Suzi Bailey 12/05/2025 - 23:27

Hi Suzi,

Thanks so much for your great questions. I really hope you are enjoying the course.

1. Refractory or recurrent Giardia infections

You’re definitely not alone in seeing more of these. My current approach is:

If a dog doesn’t respond to a 5-day course of fenbendazole (50 mg/kg PO SID), I’ll typically repeat the same course first, as I find some dogs need two full rounds before we see clearance—especially in multi-pet households or where environmental contamination is possible.

Only after a second fenbendazole course fails would I consider combining fenbendazole and metronidazole concurrently (the latter at 10–15 mg/kg BID for 5–7 days), although I try to avoid metronidazole unless really necessary due to its potential microbiota impact.

Environmental hygiene is critical—daily bathing, decontaminating surfaces, prompt faeces removal, and sometimes bathing with chlorhexidine-based products if there’s heavy shedding.

I’m increasingly increasing fibre in the diets of these dogs.

I’ve also started incorporating faecal microbiota transplantation (FMT) more routinely for dogs with relapsing diarrhoea or poor recovery post-Giardia—especially those with previous antibiotic exposure or persistent dysbiosis.

2. Acute diarrhoea progressing to chronic enteropathy

Yes, this is something I’m seeing with increasing frequency. Dogs that start out with a single episode of acute diarrhoea (often due to Giardia or dietary indiscretion) seem to lose resilience and go on to develop chronic signs.

Like you, I suspect that:

Early or repeated antibiotic exposure, particularly metronidazole, may contribute to long-term dysbiosis and altered mucosal immune function.

There may be a “tipping point” in genetically susceptible dogs that progresses to immune-mediated enteropathy after an acute GI insult.

This is exactly why I’m cautious now with antibiotics in acute cases. Instead, I often use:

Probiotics (Visbiome, Vivomixx, FortiFlora)

Fibre supplementation (psyllium or canned pumpkin)

Clay binders, and

Close dietary review from the outset.

3. When to use immunosuppressives – before or after biopsy?

You’re absolutely right that this is nuanced. Here’s how I generally approach it:

If there is marked hypoalbuminaemia, GI bleeding, or other red-flag features (weight loss, anaemia, low cobalamin), I prioritise biopsy before steroids.

If the case is moderate and owners are hesitant, I will sometimes trial immunosuppression empirically, but I document the limitations clearly and try to re-approach biopsy if the response is incomplete.

If steroids have already been started and we’re considering biopsies, I usually recommend a washout of 2–4 weeks (depending on severity and taper status) before sampling to avoid histopathological distortion.

4. Metronidazole-responsive or dependent CE cases

Yes—I’ve had similar Golden Retrievers in particular that seem metronidazole-responsive even after extensive trials.

In these truly refractory cases:

I still trial antibiotics—but very much as a last resort, and with awareness of the long-term impacts.

If long-term antibiotics are required, I’m now more inclined to use tylosin over metronidazole, supported by evidence such as the randomized controlled trial by Kilpinen et al. (Acta Vet Scand. 2011):

Tylosin (25 mg/kg SID) was significantly more effective than placebo in dogs with presumed tylosin-responsive diarrhoea, with 85% achieving normal stool consistency during relapse episodes.
PMID: 21489311

I find tylosin to be better tolerated, with less dysbiosis and neurotoxicity risk than metronidazole.

I’ll also continue probiotics alongside to help mitigate any microbiota impact, and will sometimes reintroduce FMT or increase fibre support if relapse occurs on withdrawal.

Thanks again, really appreciated your insight here. Please do keep the questions coming, and I’d love to hear how your Golden cases evolve.

Let me know how you are getting on with the course.

Best wishes,

Scott 🙂