scott@vtx-cpd.com
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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 🙂
Here is Laura’s full response again:
Should Senvelgo be given on the morning of sedation, or withheld?
Senvelgo should be given as normal on the morning of the sedation, as there should be no increased risk of hypoglycaemia etc with procedures, and the patient will benefit from avoiding hyperglycaemia during the GA/sedation. There is a minor difference of maximal plasma concentration when given with or without food, but this is not deemed clinically relevant and thus we would not worry about giving it on an empty stomach.
Bear in mind when you look this up, it says to withhold it, we strongly disagree and this advice to withhold does not come from medics or boehringer, withholding would greatly increase the risk of hyperglycaemia and hence a EKA ; we need to remember that this drug lasts > 24 hours, and thus withholding it just increases the risk of hypergly and does not help you interpret the BG the day of sedation anyways.
What blood glucose monitoring would you recommend pre- and during the procedure?
The glucose will be normal throughout if Senvelgo is administered, as there is no insulin admin, there is no risk of hypo, and as the Senvelgo will keep the glucose below the renal threshold, like every day with Senvelgo, the BG will be normal. What would be ideal is to monitor the BG and ketones; prior to starting, perioperatively and before discharge – although I would expect it to be entirely in the normal range throughout, especially if your ketones are <2.5 at the start.Are there any sedation agents you would particularly avoid? (For example, concerns about medetomidine’s insulin antagonism in insulin-managed diabetics and whether that would still be relevant for a cat on Senvelgo.)
No again no need to avoid specific medications, or sedations, provided this cat is stable on Senvelgo and is ketone negative 🙂 We avoid medetomidine in insulin treated cats as it causes mild transient hyperglycaemia which would affect insulin control on the day of the sedation, which adds risk to an insulin dependent diabetic.Hi Emma,
I’ve spoken to Laura, and she very kindly replied with the following information. This is certainly contrary to what I had understood about the drug, so I’ve definitely learned something here. Thank you so much for the brilliant question. I’d very much go with what Laura is recommending in this case — she’s without doubt one of the most experienced clinicians in the UK using Senvelgo at the moment, and there’s clearly lots to take away from her guidance. Here’s what she shared:
Should Senvelgo be given on the morning of sedation, or withheld?
Senvelgo should be given as normal on the morning of sedation. There’s no increased risk of hypoglycaemia during sedation or anaesthesia, and the patient will benefit from avoiding hyperglycaemia during the procedure. Although there’s a minor difference in peak plasma concentration when given with or without food, this isn’t considered clinically relevant — so even on an empty stomach, it’s fine to give.
It’s worth noting that although some sources suggest withholding the drug, this advice does not come from medical endocrinologists or from Boehringer. In fact, they strongly disagree with withholding it. Doing so increases the risk of hyperglycaemia and could precipitate an EKA (euglycaemic ketoacidosis). Since the drug has a duration of action >24 hours, withholding it doesn’t really assist in interpreting BG on the day either — it just adds risk.
What blood glucose monitoring would you recommend pre- and during the procedure?
If Senvelgo is given as normal, the glucose levels should remain within the normal range throughout, as the drug keeps glucose below the renal threshold and there’s no insulin involved, so the risk of hypoglycaemia is negligible. Ideally, BG and ketones should be checked before sedation, during the procedure, and again before discharge — but assuming ketones are <2.5 at the outset, everything should stay within normal limits.
Are there any sedation agents you would particularly avoid?
There’s no need to avoid any particular sedatives, provided the patient is stable on Senvelgo and is ketone-negative. The usual caution around medetomidine in insulin-treated diabetics doesn’t apply here — the transient hyperglycaemia it causes would only be a concern in patients where insulin dosing is affected. In this case, there’s no insulin on board, so that effect isn’t clinically significant.
Thanks again for raising such a great clinical question — it’s really helped clarify things, and I know I’ll be adjusting my own approach in the future based on this.
Scott
Replying to Jane Sedgewick 21/04/2025 - 12:31
Maybe we should do the study!
Just a thought!
Scott 🙂
Replying to Jane Sedgewick 21/04/2025 - 12:31
Hi Jane,
Thanks so much for bringing this up.
The session was recorded relatively recently, within the last couple of years. After reading your feedback, I went back and checked my slides. I had written “35 years,” but that was directly lifted from Ettinger, and in hindsight, it really should have read “over 35 years.” I missed the word “over,” which may have made that part of the lecture unclear, so apologies for any confusion there.
As I mentioned during the session, the reported prevalence of feline hyperthyroidism has certainly increased over time, but it is extremely variable depending on the study and region. For a bit of broader context: although the first feline goitre was described post-mortem in 1964 (Lucke, cited in Peterson, 2012), a retrospective review of 7,000 postmortems at the Animal Medical Center between 1970 and 1984 found an average of only 1.9 cases of goitre per year before 1977 (Peterson et al, 1994, cited in Peterson, 2012). This suggested that the disease was either novel or very rare at that time.
Since then, there has been an increase in the reported prevalence of hyperthyroidism in several countries. For instance, in Germany, the prevalence increased by 10% over 17 years, and in North America, it increased by 2% over 20 years. In addition, prevalence varies considerably across different countries, with studies reporting 21% in Ireland among cats over 10 years old, 20% in Poland, 3.9% in Hong Kong, 2.4–3% in the UK, and 7% in South Africa. In all of these studies, age has consistently been identified as a major risk factor for the development of hyperthyroidism. However, it is important to note that prevalence rates may be influenced by the study populations, with some studies only including geriatric cats (potentially inflating prevalence estimates) and others being based solely on cases seen at specialist veterinary hospitals, which may not fully represent the general feline population.
Specifically regarding Spain, in 2005 a study compared the cumulative annual incidence of hyperthyroidism in cats over 9 years of age in Spanish referral hospitals to those in the UK. It found a markedly lower incidence in Spain (1.53%) compared with the UK (11.92%), although only 27% of geriatric cats were evaluated for hyperthyroidism during the study period, which was a major limitation. Later, a 2015 study reported a 10% prevalence of hyperthyroidism in Spanish cats, increasing to 14% in cats over 13 years old. This brought the prevalence figures in Spain closer to those of other European countries, although that study also had a relatively small sample size (207 cats) and found that 10% of cats diagnosed as hyperthyroid based on TT4 levels did not yet show clinical signs, reinforcing the importance of regular screening even in asymptomatic older cats.
More recently, a large cross-sectional study published at the end of 2024 looked at 27,888 cats in Spain (Pérez Domínguez et al, 2024) and found an overall hyperthyroidism prevalence of 6.2% (95% CI 5.9–6.5%), rising to 7.9% (95% CI 7.2–8.8%) among cats older than 10 years. Interestingly, prevalence varied between 2.7% and 6.9% depending on the region, again highlighting how heterogeneous the distribution can be.
As you pointed out, it is possible that the incidence could be changing again more recently, but we are still lacking very recent UK-specific data to confirm whether there is a true shift in prevalence.
Thanks again for your comment.
Best wishes,
Scott 🙂
Replying to Amy G. 07/04/2025 - 16:04
Hi Amy,
Thanks so much for your questions and I’m really glad to hear you’re enjoying the course!Here are some thoughts:
1) Cystoisospora Positive Results
Yes, Idexx now reporting cystoisospora alongside giardia is both helpful and sometimes a little confusing. In most cases, cystoisospora (formerly known as Isospora) is considered an incidental finding in adult animals. They tend to be asymptomatic carriers unless immunocompromised or heavily parasitized.
In young animals, or those with clinical signs (especially diarrhea), cystoisospora can cause disease and may need treatment (e.g., with sulfadimethoxine or ponazuril).
Your approach is spot on: if symptoms have resolved with treating the giardia alone, no need to treat the cystoisospora. If symptoms persist, or if you have a high burden of cystoisospora on recheck, then it’s appropriate to target it specifically.That said, even if not treating the cystoisospora specifically, I would definitely load them up with a good probiotic (like Visbiome) and fibre (such as psyllium husk). This supports gut health, modulates the microbiome, and can help promote clearance and recovery.
2) Folate and Cobalamin Monitoring
Good questions here too. In general:
After starting cobalamin or folate supplementation, if clinical response is good, I often recheck blood levels in 6–8 weeks.
If levels have normalized and symptoms are resolved, you can consider stopping supplementation.
Some patients, especially those with severe ileal disease or chronic enteropathies, will need long-term supplementation.
After stopping, I would only recheck cobalamin if clinical signs recur, unless it was a really severe initial deficiency, in which case one follow-up test a few months later can be reassuring.
High cobalamin levels from supplementation are not a clinical concern. It is water-soluble, so excess is simply excreted. Persistently high endogenous cobalamin (without supplementation) could in theory be a marker of certain neoplasias, but that is not relevant when we are supplementing. No need to worry about high serum cobalamin caused by supplementation.
Several studies in human patients with hypocobalaminemia suggest that supplementation with oral cobalamin might be as effective as parenteral administration. A study that included 51 dogs showed that serum cobalamin concentrations increased significantly and normocobalaminemia was achieved in all hypocobalaminemic dogs with chronic enteropathy after daily oral cobalamin supplementation for at least 3 weeks (range 20–202 days). However, similar to this study, another investigation by the same research group showed that supranormal serum cobalamin concentrations were achieved in only about half of the dogs. The dogs in this study reached normal serum cobalamin concentrations within 4 weeks of receiving oral cobalamin, but a hypercobalaminemic state was reached after 12 weeks of oral cobalamin supplementation in about two-thirds of these dogs. In addition, other recent studies suggest that daily oral cobalamin supplementation is effective to normalize the serum cobalamin status in dogs with chronic inflammatory enteropathy (CIE) and also to maintain normal cobalamin status in dogs with hereditary cobalamin malabsorption that had previously been supplemented with parenteral hydroxocobalamin. Thus, oral cobalamin supplementation is a simple, noninvasive, and pain-free alternative to weekly subcutaneous injections of either cyanocobalamin or hydroxocobalamin. An alternative pathway of intestinal cobalamin absorption beyond receptor-mediated transport in the ileum is a possible explanation why oral cobalamin supplementation might be effective in spite of a defective receptor-mediated uptake into enterocytes. This has also been reported in people. However, expression levels of the ileal cobalamin-intrinsic factor receptor in dogs with chronic enteropathies have not been investigated.
3) Fenbendazole Duration for Giardia
There is a bit of variation here depending on protocol:
The typical course is 5 days (at 50 mg/kg once daily), regardless of whether symptoms resolve earlier.
Even if clinical signs resolve in a couple of days, it is important to complete the full 5-day course to maximize efficacy and reduce recurrence.
In refractory cases, some protocols extend treatment up to 7–10 days or combine fenbendazole with metronidazole, but for most cases 5 days is sufficient.
Best,
Scott 🙂
Hi Emma,
This is a really interesting question.
In terms of fasting and blood glucose monitoring, I would still recommend a shorter fasting period if possible, around six to eight hours rather than the traditional twelve, to minimize the risk of dehydration or ketone production, given the ongoing glucose loss through the kidneys. Baseline blood glucose should absolutely be checked pre-sedation, and regular monitoring during the procedure (every 30 to 60 minutes depending on the length and depth of sedation) is advisable. True hypoglycaemia is rare in Senvelgo-treated patients compared to those on insulin, but they can be vulnerable to dehydration and ketogenesis, so ketone monitoring would also be sensible if practical.
When it comes to medication handling on the day of sedation, based on both human recommendations and cautious extrapolation to cats, SGLT2 inhibitors are typically withheld on the day of surgery or sedation to reduce the risk of complications such as dehydration or diabetic ketoacidosis. Therefore, I would recommend skipping the Senvelgo dose on the morning of sedation and resuming it once the patient is eating and drinking normally again post-procedure.
Thinking about sedation protocols, medetomidine is often used cautiously in diabetic patients because of its insulin-inhibitory effects and potential to cause transient hyperglycaemia. However, in a Senvelgo-treated cat, this concern is somewhat less pronounced because blood glucose control is managed independently of insulin secretion. That said, any major shifts in glucose can still be problematic, so I would advocate for using low-dose medetomidine with a plan for reversal using atipamezole, or considering alternative protocols based on the cat’s cardiovascular status. Opioids such as buprenorphine, benzodiazepines like midazolam, and agents like alfaxalone are all safe and useful adjuncts in this context, given their minimal impact on glucose metabolism.
Of course, there are many factors that can affect glucose control around sedation, including stress, fasting, the type of sedation used, and underlying disease. These patients, particularly those on Senvelgo, often still retain some background endogenous insulin secretion. It is not typically an absolute insulin deficiency, which can offer a degree of metabolic flexibility. I would argue that as long as we are monitoring carefully, any abnormalities can be identified early and corrected appropriately, reducing the overall risk.
Finally, to make sure we cover all bases, I am also reaching out to Laura Bree, who spoke at our recent CPD event and has extensive clinical experience with Senvelgo, to get her perspective on best practices for sedation in these patients. I would love to hear what the drug company had to say as well, so please do share their advice when you have it.
In summary, I would recommend a shorter fasting period, omission of the Senvelgo dose on the morning of sedation, careful peri-procedural blood glucose (and ketone) monitoring, low-dose or reversible sedation protocols where appropriate, and a general emphasis on hydration monitoring. I would love to hear what the drug company advice was!
Scott 🙂
Replying to Caitlin M. 19/04/2025 - 14:33
Hi,
Great to meet you!
I’m sure this course will fit in really well with the emergency work you’re doing now. Really looking forward to working with you over the next little while.
Best,
Scott 🙂
Hi Georgia,
Yeah, it’s such an interesting discussion. I think I’m not uncomfortable with the idea of using insect protein. There’s definitely a sustainability piece to it as well. As long as we can demonstrate clear nutritional value, I think it really opens up that broader conversation about protein sources in animal food and how different cultures view them.
You know, we would generally find the idea of horse meat pretty unacceptable in the UK, whereas it’s considered quite normal in parts of Europe like Germany. Even something like kangaroo is very popular here, but it’s not necessarily something everyone in Canada would find palatable. And then, of course, there are places where dog meat is still consumed, which really highlights how subjective and culturally dependent these attitudes are.
I think it’s a fascinating wider discussion about what is considered “acceptable” protein, and insect protein feels like a logical, sustainable evolution.
Scott 🙂
Replying to Helen S. 14/04/2025 - 13:59
Thank you so much for sharing this Helen.
Have a lovely weekend.
Scott 🙂
Replying to Liz Bode 14/04/2025 - 21:10
Interesting!
Is torso-caudal a typo or is it an anatomical location I have not heard of.
Both are possible! 🙂
Scott x
Replying to Katy S. 14/04/2025 - 23:03
Hi Katy,
It’s so lovely to see someone from Glasgow on the course! I’m Glaswegian born and bred myself. I live and work in Canada now, but I’m actually coming back to Glasgow for a visit in just a few weeks, I can’t wait!
I completely understand that feeling you described, even with lots of experience, emergencies can still get the adrenaline going. I’m really looking forward to working with you through the course and helping make those situations feel a bit more manageable.
Best,
Scott 🙂
Replying to Rachel Gordon 14/04/2025 - 17:43
Hi Rachel,
It’s great to meet you! I love the North East, my very first job was at the PDSA in Gateshead. Good old days!
It sounds like you have a full (and very lively!) household. I’m really looking forward to working with you through the course, I’m sure everything will come back to you quickly. Emergency vetting definitely has a way of staying with you once you’ve done it!
Best,
Scott 🙂
Replying to Jane Sedgewick 15/04/2025 - 13:22
Hi Jane,
Lovely to see you at radiography rounds.
You are absolutely right that significant polyuria can lead to medullary washout, and this is an important consideration when interpreting the results of any water deprivation test or DDAVP trial. The rationale for recommending a DDAVP trial first (rather than starting with a formal water deprivation) is primarily related to safety and practicality:
In a patient with true CDI, the response to DDAVP is often quite striking even if there has been some degree of washout — typically you will still see a clear reduction in water intake and an increase in USG over the 3 to 5 day trial.
In contrast, psychogenic polydipsia (PP) cases, even if partial medullary washout is present, are much less likely to show a significant response to DDAVP alone. If they do respond, the magnitude is often partial or inconsistent.
If there is an equivocal response, a formal modified water deprivation test (MWDT) can still be considered afterward to distinguish partial CDI, PP, or medullary washout as the primary driver.
You are quite correct that gradual water restriction or hospitalization can sometimes help “re-set” the medullary concentration gradient. In practice, a period of 3–5 days of progressive water restriction (stage 1 of the MWDT) is intended to partially restore the renal medullary gradient. This improves the diagnostic utility of the subsequent dehydration phase. That said, hospitalization carries risks (stress potentially exacerbating psychogenic drinking, logistical challenges) which is why starting with a DDAVP trial at home has become a popular, safer first step, particularly when hospital monitoring isn’t ideal.
In terms of background:
Distinguishing CDI from PP can be very challenging because disorders of AVP secretion are recognized even in psychogenic polydipsia (e.g., altered set-point for AVP release, exaggerated or subnormal AVP responses). The natural pulsatility and variability of AVP secretion, combined with chronic over- or underhydration, further complicate interpretation.
A modified water deprivation test (MWDT) is time-consuming, requires rapid access to blood and urine analysis (especially sodium and BUN), and demands close observation to prevent hypertonic dehydration.
The MWDT typically consists of a three-stage process:
Gradual water restriction over 3–5 days to re-establish medullary gradients.
Complete water deprivation with careful monitoring for weight loss or rising USG.
DDAVP administration if USG fails to rise, to assess the response directly.
Pets with partial CDI show slight urine concentration with dehydration and a further increase following DDAVP. Pets with PP typically concentrate urine during the water restriction phase. Pets with complete CDI or NDI fail to concentrate until (or unless) given DDAVP.
Importantly, a therapeutic trial of DDAVP remains a practical alternative for many patients:
A dramatic reduction in water intake and increase in USG during a 5–7 day DDAVP trial is highly suggestive of CDI.
Failure to respond points toward primary NDI or psychogenic polydipsia.
This approach avoids the risks of acute hypertonic dehydration associated with MWDT and can be performed at home, making it far more practical and owner-friendly.
While rare, a note of caution: in psychogenic polydipsia cases, DDAVP can occasionally cause dilutional hyponatremia, so monitoring is still advised.
You raise an excellent point about the limitations of relying on total calcium (tCa) alone.
A useful reference on this topic is:
Tørnqvist-Johnsen C, Schnabel T, Gow AG, et al. Investigation of the relationship between ionised and total calcium in dogs with ionised hypercalcaemia. J Small Anim Pract. 2020;61(4):247-252. doi:10.1111/jsap.13109.
In this study, over one third of dogs with confirmed ionised hypercalcaemia had total calcium within the normal reference range, and importantly, most of these dogs had normal serum albumin.This finding reinforces that early or modest ionized hypercalcemia (for example, due to malignancy or primary hyperparathyroidism) can be missed if relying only on total calcium values, even when albumin is normal.
So if clinical suspicion remains high (e.g., unexplained PU/PD, urolithiasis, azotaemia), it is worth pursuing ionized calcium testing if available, or at least repeating total calcium to monitor for evolution over time.
Thanks again for such excellent and thoughtful questions.
Best,
Scott 🙂
Thank you for sharing such a brilliant post, so much to think about with these patients! I love how you have highlighted the importance of considering potential complications before proceeding with interventions, it is something that can easily be overlooked in the rush of stabilising a critical patient.
Thank you for also sharing the link to the early warning system, I had not seen that before and it looks really helpful.
A couple of quick questions. Do you find yourself using the Kirby’s Rule of Twenty every day for these patients, or more selectively depending on the case?
Also, how often do you reassess fluid balance in these patients, do you tend to stick to every two to four hours, or does it depend on how unstable they are?
Thanks again.
Scott 🙂
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