scott@vtx-cpd.com
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Replying to Jane Sedgewick 22/04/2025 - 20:03
Hello!
I hope you are well.
I agree, I think the main concern here is that trazodone could blunt the adrenal response enough to complicate interpretation either way. It could potentially make it harder to diagnose hypoadrenocorticism if the basal or post-ACTH cortisol is artificially low, but equally it could dampen the exaggerated response we might expect in a patient with Cushing’s, making a definitive diagnosis more difficult.
It is probably rare that we would need to use trazodone in these cases, but it is definitely worth remembering to avoid anxiolytic or sedative medications around the time of adrenal function testing whenever possible, just to minimise the risk of muddying the results.
Thank you again for sharing your thoughts and experience.
Scott 🙂
Replying to Janette B. 22/04/2025 - 14:32
Hey, no worries at all and thanks so much for getting back to me! That is really helpful to know, it is great to hear you are seeing such a clear benefit with the transversus abdominis plane blocks. I am not sure I have ever actually heard the words quadratus lumborum out loud before, let alone used it myself! 😅 Sounds like a really interesting option though, especially for the more painful cases. Thanks again for sharing your experience!
Scott 🙂
Times flies!
Thank you for all of the amazing knowledge that you have shared so far Helen!
Scott 🙂
Replying to Helen S. 22/04/2025 - 12:49
Hey pal!
Thank you so much for sharing!
Have a wonderful week everyone!
Scott 🙂
Thank you for being brilliant!
Scott 🙂
Replying to Jane Sedgewick 21/04/2025 - 14:14
Hi Jane,
Thanks so much for your messages.
Your point about regional variation is fascinating. I agree it would be very interesting to look at more closely. I had not made the connection with “Derbyshire neck” before, but it makes complete sense to wonder about environmental or historical iodine factors influencing thyroid disease patterns. It would be really interesting to explore whether historical iodine deficiency could have left any lasting regional patterns in feline hyperthyroidism prevalence. If you are able to gather any broad figures from PDSA cases, that would be fantastic and could provide a really useful starting point for looking into this further.
On the monitoring side, regarding TSH, I do not recommend measuring it at every monitoring visit. If the TT4 is within the expected therapeutic range, typically in the mid to lower half of the reference range, and the cat is clinically well, then TSH does not usually add much additional value. Similarly, if the TT4 is low-normal and clinical signs have resolved, I would not routinely check TSH. However, TSH becomes particularly useful when the TT4 is in the low-normal range but clinical signs are persisting, or when there is concern that concurrent non-thyroidal illness could be artificially lowering the TT4 concentration. In these situations, measuring TSH can help differentiate between true resolution of hyperthyroidism and ongoing disease that is being masked by other factors.
If the TSH is suppressed, that would suggest that hyperthyroidism is still active despite the TT4 appearing low-normal. If the TSH is detectable or elevated, that would point more towards true resolution or iatrogenic hypothyroidism. It is important to note that TSH is not sensitive enough to be used for initial diagnosis of hyperthyroidism and must always be interpreted alongside TT4 or fT4 results. It also is not a standard part of every monitoring check unless clinical signs or bloodwork suggest it would add useful information.
In your current case, where the TT4 is low-normal but the cat is still showing clinical signs, measuring a TSH would definitely be valuable. It could really help clarify whether you are looking at persistent hyperthyroidism that is being masked by illness, early iatrogenic hypothyroidism, or whether another concurrent disease process is responsible for the ongoing signs.
Please do let me know if you would like to chat through your case in more detail, I would be very happy to. And thank you again for raising such thoughtful and practical points.
Best wishes,
Scott
Replying to Jane Sedgewick 21/04/2025 - 12:12
Hi Jane,
In terms of what I am personally seeing, interestingly, I am seeing more diabetes insipidus (DI), particularly partial or complete central diabetes insipidus (CDI), than psychogenic polydipsia (PP) in my current caseload. That could certainly reflect the type of cases being referred to me, but even in broader general populations, I think true CDI is perhaps a little more common than we have traditionally assumed, especially now that we are using DDAVP trials more routinely and are better able to identify partial forms that may previously have gone undiagnosed. That said, psychogenic polydipsia is still very much out there, and I would agree that there seems to be a trend toward increased cases in more anxious, highly attached post-pandemic dogs, particularly among designer crosses like cockapoos, cavapoos, and similar breeds.
In terms of signalment, CDI typically affects young to middle-aged dogs, often presenting between six months and six years of age, although some cases of partial CDI may present later. Large-breed dogs do appear to be slightly overrepresented, with breeds like Labradors, German Shepherds, and Dobermans cropping up a little more often, but it can certainly occur in mixed breeds as well. In the majority of cases, CDI is idiopathic. Secondary causes such as head trauma, neoplasia affecting the hypothalamic-pituitary axis, or severe inflammatory disease of the CNS are seen less commonly, and when they do occur, there are often accompanying neurologic signs.
You are absolutely right that the population you are seeing, for example a PDSA caseload, can have a big impact on how often you encounter these conditions, and I think your observations from practice are spot on. It is really interesting how these patterns shift depending on the setting.
It is also worth noting that the literature is very sparse when it comes to psychogenic polydipsia. There are very few robust studies available, and much of what we know is extrapolated from case series or anecdotal reports. Definitely another area that would be well worth publishing in if someone had a suitable case series or a structured approach to diagnosis and management.
I am very grateful for your engagement.
Best,
Scott 🙂
Replying to Rachel H. 26/04/2025 - 16:02
No problem!
Let me know if you have any other questions!
Scott 🙂
Replying to Rachel H. 20/04/2025 - 15:43
Hello, thank you so much for your message and I’m really glad to hear you are enjoying the course so far!
That’s a great question and you are right that several medications can influence thyroid testing results. However, when it comes specifically to causing an increase in TSH, sulfonamides are the clearest and most direct cause among the options listed.
Here’s why:
Sulfonamides (especially potentiated sulfas like trimethoprim-sulfa) directly inhibit thyroid hormone synthesis. This leads to low T4 and T3 levels, which in turn causes the pituitary to respond by increasing TSH. So the sulfonamides both lower thyroid hormone and trigger a compensatory TSH rise.
Prednisolone typically causes suppression of TSH (and sometimes free T4 as well), not an increase.
Carprofen generally has minimal or no direct effect on TSH or thyroid hormones.
Potassium bromide can occasionally be associated with low T4 levels, but it does not consistently cause a TSH increase and the effect is much less direct compared to sulfonamides.
So while it is true that several drugs can affect thyroid testing, sulfonamides are the one in this list that cause a clear and predictable increase in TSH through a true hypothyroid-like effect.
Hope this helps clear it up and please feel free to reach out with any more questions!
Have a lovely weekend!
Scott 🙂
Replying to Rachel C. 25/04/2025 - 16:47
Hi Rachel,
Glad that was helpful!
When it comes to second line immunosuppressives, I tend to avoid azathioprine in most cases now, mainly because of the narrow therapeutic window, delayed onset of action, and potential for hepatotoxicity and bone marrow suppression. It can still be considered in certain situations, usually in larger dogs where cost is a limiting factor and close monitoring is possible, but it’s not my first choice.
In practice, I tend to go for mycophenolate mofetil in dogs, especially when I’m aiming to taper steroids or dealing with more severe disease. It has a faster onset than azathioprine and a better safety profile overall, with gastrointestinal side effects being the most common issue, though often manageable.
I prefer ciclosporin in cats and smaller dogs. It’s generally well tolerated and effective, but cost becomes a major barrier in large breed dogs, which limits its practicality in those cases.
I rarely use leflunomide, but it’s an option I might consider in more refractory or unusual cases.
Best,
Scott
Replying to Liz Bode 23/04/2025 - 21:03
Fancy seeing you here!
Scott 🙂
Replying to Spela Bavcar 21/04/2025 - 23:00
Spela!
Lovely to see you here!
Thank you so much for being brilliant!
Scott 🙂
Replying to Felipe M. 21/04/2025 - 08:31
Thank you so much Felipe!
We are very lucky to have you join us!
Scott 🙂
Replying to Liz Bode 23/04/2025 - 21:11
Haha!
It would not have surprised me if it was just something I had never heard of!!!!
Scott 🙂
Replying to Katherine Howie 23/04/2025 - 11:43
Thanks so much for sharing, Kath. Really appreciate the tip about monitoring caudal vena cava compressibility, that’s such a handy one to keep in mind! Great point too about adjusting fluid balance reassessments depending on the patient’s losses.
Scott 🙂
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