scott@vtx-cpd.com
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Replying to Emma Holt 16/05/2025 - 21:52
No problem!
There is clearly some difference of opinion here! I am going to some talks on this later in the year too so will keep you updated with what the smart people (not me!) are saying!
Hope all is well with you.
Scott 🙂
Replying to Emma Holt 16/05/2025 - 21:52
No problem!
There is clearly some difference of opinion here! I am going to some talks on this later in the year too so will keep you updated with what the smart people (not me!) are saying!
Hope all is well with you.
Scott 🙂
Replying to Jen Rowland 14/05/2025 - 22:22
Hey Jen.
Thanks for the question. Love the profile picture! Very Wildlife on One! This is not a paper I am familiar with, but will make sure Liz sees the question!
Hope you are enjoying the course.
Scott 🙂
Replying to Christina G. 15/05/2025 - 11:57
I am sure Liz will give extra points for bravery and having a go!
Scott 🙂
Replying to Anna M. 13/05/2025 - 09:27
Hi Anna,
Thanks so much for your kind words, and I’m really glad to hear you’re enjoying the course.
Great question regarding the use of a thyroid diet in cats with hyperthyroidism. In general, I don’t recommend combining the iodine-restricted diet (like Hill’s y/d) with oral antithyroid medications such as methimazole. The rationale is that the diet works by limiting iodine availability, which is essential for thyroid hormone synthesis, while methimazole works by inhibiting the enzyme that helps produce thyroid hormone. If both are used together, it becomes difficult to assess response, and more importantly, if the cat is still producing any thyroid hormone, even in small amounts, the dietary restriction can drive the thyroid gland to become more efficient at extracting any available iodine, potentially leading to overstimulation of remaining thyroid tissue.
Because of this, if I recommend a thyroid diet, it’s typically as a standalone option, and only when strict dietary control is possible, meaning no access to other foods, treats, or flavoured medications that might contain iodine. It is a particularly useful choice for cats who are not good candidates for oral medication due to side effects or administration challenges, or when owners prefer a non-pharmaceutical approach and can reliably control the cat’s entire diet.
That said, there are occasional exceptions. For instance, I might briefly overlap the diet and medication during a transition period or in a palliative context where full control is not the goal, but that is relatively uncommon and always tailored to the individual case.
I hope that helps.
Best regards,
Scott 🙂
Replying to Anna M. 13/05/2025 - 09:31
Hi Anna,
The connection between hypothyroidism and fructosamine lies in how thyroid hormone levels influence protein metabolism, particularly albumin turnover. Fructosamine reflects the average blood glucose over the preceding two to three weeks by measuring the degree of glycation of circulating proteins, especially albumin. In hypothyroid dogs, there is a reduction in protein turnover, including albumin, which can result in artificially elevated fructosamine levels that do not accurately reflect glycaemic control. This can make it appear as though a diabetic dog is poorly regulated when, in fact, glucose levels may be acceptable.
So in dogs with concurrent hypothyroidism and diabetes, fructosamine may overestimate average blood glucose, particularly if the hypothyroidism is not well controlled. For monitoring these patients, I generally recommend placing greater emphasis on home blood glucose curves or using continuous glucose monitoring if available, as these provide real-time data that are not influenced by protein metabolism. It’s also important to ensure that the hypothyroidism is well managed and that T4 levels are within the therapeutic range before placing much weight on fructosamine values. If fructosamine is used, it should be interpreted cautiously and in the context of clinical signs, body weight trends, and serial blood glucose data, rather than in isolation.
I hope this helps clarify the connection, and I’d be happy to discuss further if helpful. Let me know how you are getting on with the course.
Best regards,
Scott 🙂
Thank you for sharing!
Gracias por compartir!
Is that translation correct?!
Scott 🙂
Replying to Helen S. 12/05/2025 - 12:07
I love the nail sketch so much!!!!!!!!!!!
I feel like Andy and I have conversations like this almost every day!
Scott 🙂
Replying to Aaron H. 11/05/2025 - 16:50
Welcome Aaron!
We are very lucky to have you here.
Scott 🙂
Replying to Jane Sedgewick 06/05/2025 - 16:46
Hi Jane,
Great question! t’s something many of us are wrestling with as SDMA becomes a routine part of senior wellness panels. I completely agree, identifying early kidney changes is only worthwhile if we know what to do with that information, and the evidence on early intervention, particularly before azotaemia, is still catching up. IRIS Stage 1 CKD is now formally recognized and includes patients with persistent renal changes like proteinuria or elevated SDMA in the absence of azotaemia. While we don’t yet have large prospective studies showing that intervention in these cases extends lifespan, there is growing support for the idea that earlier detection allows us to modify risk factors and potentially slow progression. Interventions might include addressing proteinuria with ACE inhibitors or ARBs even before creatinine rises, ensuring optimal hydration (especially in older or low body condition dogs), and, in selected cases, adjusting diet to moderate phosphorus and protein intake, though timing of dietary change is still a debated topic.
That said, in real-world clinical practice, I rarely find myself asking for SDMA unless it’s already included in a panel. Most of the dogs I see already have obvious disease, and if they’re azotemic, then SDMA really adds little, its value as an early biomarker becomes moot.
But for earlier-stage cases, especially the older dog who “seems well” but turns up with a borderline USG and mildly elevated SDMA, it does prompt more thoughtful discussion. Ideally, I think SDMA is most useful when paired with urine findings and muscle condition score as part of a broader screening protocol. A persistently elevated SDMA across timepoints, particularly in the presence of proteinuria or low USG, is much more convincing than a single raised value. That layered context helps distinguish signal from noise and guides whether to start more frequent monitoring, recommend dietary changes, or even consider ACE inhibition pre-emptively.
Are you seeing more cases now where SDMA is elevated in isolation? How are you deciding when to act and when to wait?
I hope you are having a lovely weekend.
Scott 🙂
Replying to Katy S. 06/05/2025 - 16:01
Hi Katy,
That’s great to hear! It’s really common for thoracic POCUS to feel a bit daunting at first, especially beyond just screening for pericardial effusion, but it’s such a valuable tool once you get more familiar with it. Hopefully things will click quickly once you start scanning!
I hope you are enjoying the course!
Scott 🙂
Replying to Yvonne McGrotty 10/05/2025 - 16:40
I consider Britney to be a legend too… she is still in her 40’s!
Scott 🙂
Replying to naomi b. 10/05/2025 - 19:30
Hi Naomi,
Great to meet you! It’s brilliant to have you on board. Looking forward to learning together.
Best,
Scott 🙂
Replying to Jane Sedgewick 06/05/2025 - 20:07
Hey Jane.
I am really pleased you enjoyed the session. Yvonne is a bit of a legend!
I will make sure she sees this.
Scott 🙂
Replying to Jane Sedgewick 06/05/2025 - 16:40
Hi Jane,
Thanks so much for your take on the films.
You’re quite right that asthma seems like the least likely issue here. The final radiology report does not describe evidence of hyperinflation, and instead characterizes the pulmonary pattern as a moderate-to-severe unstructured interstitial to alveolar pattern, bilaterally symmetric and coalescing, particularly cranioventrally and caudodorsally. This distribution, along with mild pulmonary vessel dilation and moderate cardiomegaly, was interpreted as most consistent with left-sided congestive heart failure and cardiogenic pulmonary edema.
Like you, others flagged concerns about the stomach. The report describes it as containing a moderate amount of gas and a small amount of heterogeneous soft tissue opaque material, interpreted as normal ingesta, with no evidence of dilation or obstruction. So benign, per the radiologist, but I agree that without that context it does draw the eye.
The central abdomen is reported as having normal peritoneal serosal detail and no effusion, but I take your point. If we hadn’t had this radiologist’s read and were going strictly off our initial impressions, abdominal ultrasound would be entirely reasonable as a next step, especially given the age of the patient and nonspecific systemic signs.
Thanks again for jumping in despite being busy, and I’ll share updates as the case progresses.
Best,
Scott
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