scott@vtx-cpd.com

Replying to Mark Laloo 09/05/2025 - 14:29

Hi Mark,

Thanks for sharing, I agree completely. “Thyroid storm” isn’t formally defined in veterinary medicine, but we do see cats with severe clinical signs and very high T4 levels that fit the picture. Like in your cases, they’re often undiagnosed beforehand and present with GI signs, altered mentation, and sometimes cardiovascular issues.

It’s definitely an area that could benefit from clearer definitions. Great to hear your experience.

Best,

Scott

Replying to Jo T. 05/05/2025 - 18:06

Hi Jo,

Thanks for your observations, really helpful points. I agree that the aerophagia is notable, and you’re absolutely right to consider that in the context of increased respiratory effort. The final radiology report does comment on a small amount of gas in the intrathoracic oesophagus1983 and attributes this to aerophagia secondary to the reported increased respiratory rate, which supports your impression.

The radio-opaque area in the stomach you noted is addressed as well. The report describes the stomach and small intestines containing a moderate amount of gas and a small amount of heterogeneous soft tissue opaque material, interpreted as normal ingesta, with no evidence of obstruction, dilation, or plication.

As for the pulmonary pattern, the radiologist characterizes it as a bilaterally symmetric, moderate-to-severe unstructured interstitial to alveolar pattern, most severe cranioventrally and caudodorsally, rather than predominantly bronchial. That said, I do think it’s reasonable that a mixed pattern could be perceived, especially with the degree of coalescence noted. The final interpretation leans strongly toward cardiogenic pulmonary oedema secondary to cardiomyopathy, though pneumonitis and other causes remain in the differential.

Thanks again for your insights, really appreciated. Let me know what you think in light of the report.

Scott 🙂

Replying to Rachel H. 05/05/2025 - 13:31

Hi Rachel,

Thanks so much for getting in touch. This is a great case to think through, and I really like your plan. I agree that there are a few red flags that suggest she may not have classic Addison’s, and it makes sense to reassess the diagnosis now that you’ve inherited the case.

The main concern for me is the timing of the ACTH stimulation test. From what you described, the test was performed just five days after stopping prednisolone. Although pred doesn’t interfere analytically with cortisol assays, it absolutely can cause suppression of the hypothalamic-pituitary-adrenal (HPA) axis through feedback inhibition, and five days may not have been long enough to avoid that. Recent data has added some nuance to our understanding here. A 2024 prospective study by Del Baldo et al. looked at HPA axis recovery in 20 client-owned dogs treated with intermediate-acting glucocorticoids like pred or methylpred. They found that while the median time to recovery was just three days, some dogs took much longer, and in one case, the HPA axis remained suppressed for over 18 weeks. That dog showed flat ACTH stim responses for months before eventually regaining a measurable post-stim cortisol. So even though most dogs bounce back quickly, there is significant variability, and a flat cortisol result five days post-pred cannot be considered definitively diagnostic.

The other major factor is the fact that she has never had electrolyte abnormalities. True primary hypoadrenocorticism almost always involves some degree of electrolyte derangement, either at diagnosis or over time. In contrast, dogs with atypical Addison’s have glucocorticoid deficiency only and retain normal sodium and potassium because their mineralocorticoid axis is intact. The fact that she’s needed her Zycortal dose reduced at every recheck, with normal electrolytes throughout, strongly suggests that she may not have any clinically relevant mineralocorticoid deficiency at all.

I think your current approach of continuing the Zycortal but gradually tapering it based on electrolyte monitoring is a very reasonable one. If you reach a dose that’s very low, for example below 0.5 mg/kg, and electrolytes are still normal, I’d absolutely consider a trial off Zycortal. You could skip the next injection, then recheck electrolytes at two to three weeks and again at four to five weeks to watch for any delayed shifts. If her sodium and potassium remain within normal limits and she’s clinically stable, it would support that she does not need mineralocorticoid supplementation.

If you wanted to go a step further, once she’s stable off Zycortal, you could consider repeating the ACTH stimulation test after a longer washout from higher-dose steroids. Including an endogenous ACTH measurement at that time would be helpful too. A truly Addisonian dog should have an elevated endogenous ACTH with a flat cortisol response, whereas a dog with prior suppression will typically have a low to low-normal ACTH as the pituitary axis reawakens.

If she does well off Zycortal, you can just continue low-dose prednisolone long-term and manage her as an atypical Addisonian, assuming her clinical signs remain controlled. Or, if the repeated testing points away from Addison’s altogether, you may even be able to wean her entirely.

You’re already handling this really thoughtfully, and I think you’re absolutely on the right track. Let me know how she gets on or if you want to chat further down the line.

Best,

Scott 🙂

Full reference:

Del Baldo F, Corsini A, Tardo AM, et al. Hypothalamic–pituitary–adrenal axis recovery after intermediate-acting glucocorticoid treatment in client-owned dogs. Journal of Veterinary Internal Medicine. 2024;38(2):942–950. doi:10.1111/jvim.16979

Replying to Samantha T. 07/05/2025 - 19:14

Welcome Sam!

Thank you for your brilliant contribution, and thank you for the cute kitten picture!

Scott 🙂