scott@vtx-cpd.com

Replying to Jane Sedgewick 25/05/2025 - 14:34

Hi,

Yes, I completely agree with your point about the <2-hour window, I’ll still often give it a go with emesis if the object is known and hasn’t progressed. I’ve definitely seen things like socks or bits of toy sit quite happily in the stomach for a couple of days before they start to cause trouble.

Like you said, it’s got to be something soft and safe enough to come back up, but when the circumstances are right, those success rates are very encouraging.

Scott

Replying to Rachel H. 21/05/2025 - 12:09

Hi Rachel,

Great question.

In terms of timing neutering in acromegalic bitches with diabetes, the general principle is to prioritise spaying as soon as it’s safely possible, rather than waiting for full diabetic control first. The reason is that as long as progesterone is circulating, growth hormone remains elevated, and the insulin resistance will persist no matter how much insulin we throw at it. So, while some degree of stabilisation is helpful for anaesthetic safety, trying to fully regulate diabetes before spaying can become a bit of a futile cycle.

What I typically aim for is at least partial stabilisation, meaning the dog is eating reasonably well, we’ve ruled out ketones, hydration is okay, and blood glucose is starting to come down with insulin support. That can often be achieved in a few days to a week. Then I would move ahead with spaying, earlier if she’s in overt dioestrus, and a little later if we’re able to catch her before the progesterone surge.

Once the ovaries are removed, the source of growth hormone disappears fairly rapidly, and we usually see a steady improvement in insulin sensitivity over the following couple of weeks. Insulin doses often need adjustment after surgery, so close monitoring is important.

If there are any concerns about anaesthesia, or if she’s particularly unstable, we’ll sometimes work with the surgery team to delay briefly while addressing acute issues, but I wouldn’t aim for weeks or months of pre-op diabetic control in these cases. That just delays resolution of the underlying driver.

Have you got a case currently?

Best,

Scott 🙂

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 🙂