scott@vtx-cpd.com

Replying to Rachel C. 15/07/2026 - 16:44

Thanks Rachel, I completely agree. I still think faecal testing has an important role, particularly early in the work-up to exclude parasites and other infectious causes before moving on to more invasive or expensive investigations such as ultrasound or endoscopy. I don’t think this paper suggests we should stop doing faecal testing, but rather that we need to be much more cautious about how we interpret bacterial PCR results. Simply detecting organisms like Clostridium perfringens or E. coli doesn’t necessarily mean they are causing the diarrhoea, and using those results alone to justify antibiotics is probably not appropriate. For me, it’s a useful reminder to interpret faecal PCR in the context of the whole clinical picture, rather than in isolation.

I hope you are well!

Scott 🙂

Replying to Silvana S. 22/07/2026 - 09:55

Hi Silvana,

Thank you for your excellent question. I hope you are doing well.

This is exactly the sort of case where I think we need to step back and think about what is driving the diabetes rather than simply treating the blood glucose.

Hyperthyroidism is one of the recognised causes of insulin resistance, and the new AAHA guidelines list uncontrolled hyperthyroidism as an important concurrent disease that should be identified before selecting an SGLT2 inhibitor. They recommend screening cats over seven years of age for hyperthyroidism and generally favour insulin in cats with significant concurrent disease or where metabolic stability is uncertain.

If the cat is otherwise bright, eating well, well hydrated, has no ketosis, and is genuinely stable, I don’t think there is necessarily an urgent need to stop Senvelgo immediately. However, I would focus aggressively on getting the hyperthyroidism under control and monitor the diabetic response very closely. There is certainly be a possibility that improving the hyperthyroidism will reduce insulin resistance and substantially improve diabetic control.

My concern would be that ongoing weight loss and polyphagia make it difficult to know how much of the clinical picture is due to persistent diabetes versus uncontrolled hyperthyroidism. If those signs persist despite improving thyroid control, or if ketones become a concern, I would have a fairly low threshold for transitioning to insulin.

That said, I don’t think we necessarily need years of direct experience before carefully applying these drugs outside the original label population. It seems to me that they can be extremely valuable in selected cases that are not completely stable or entirely conventional, provided we understand the risks, monitor closely and have informed owners.

Interestingly, a recently published case series explored the use of velagliflozin in non ideal diabetic cats with concurrent diseases. While hyperthyroidism was not included, the authors successfully managed cats with conditions such as chronic kidney disease and hypersomatotropism, in some cases using combination therapy and intensive CGM and ketone monitoring. Their experience suggests that, in carefully selected patients with close monitoring and informed owner consent, there may be scope to use SGLT2 inhibitors outside the original label recommendations.

My own experience has probably reinforced that view. I have used these drugs successfully in several patients that would not have been considered ideal candidates in the original clinical trials. One cat, had IRIS stage 3 chronic kidney disease, significant biliary disease, was receiving corticosteroids and multiple medications for CKD, and still responded remarkably well to treatment. I have also used an SGLT2 inhibitor successfully in a cat with progressive FIP receiving corticosteroids, and in another cat with severe non regenerative immune mediated anaemia that was being treated with cyclosporine and prednisolone. All three of those cases responded very well, despite being far from straightforward.

Obviously these are anecdotal experiences rather than evidence, and I certainly would not advocate indiscriminate off label use. However, they have given me confidence that with careful case selection, very close monitoring, particularly of ketones during the early treatment period, and clear communication with owners, these drugs may have a broader role than we initially thought.

So, in your case, I certainly wouldn’t dismiss Senvelgo simply because the cat has hyperthyroidism. I would be inclined to treat the hyperthyroidism aggressively, monitor the diabetes and ketones closely, and then reassess how the cat is doing clinically over the following few weeks. If the clinical picture improves, I think it is entirely reasonable to continue. If not, then transitioning to insulin would be my next step.

I hope that helps.

Scott 🙂

Case Reports J Feline Med Surg 2026 Feb;28(2):1098612X251414198. doi: 10.1177/1098612X251414198. Epub 2026 Jan 3.
SGLT2 inhibitor therapy in diabetic cats: first clinical experiences with non-ideal candidates
Achilles Vanneste 1, Emma Van Heuckelom 1, Dagmar Vannieuwenhuyse 1, Charlotte De Voogt 1, Sylvie Daminet 1
Affiliations Expand
PMID: 41482870 PMCID: PMC12929899 DOI: 10.1177/1098612X251414198

Replying to Lucy Bennett 11/07/2026 - 22:49

Hi Lucy,

Firstly, don’t apologise at all. It is really lovely to hear from you!

Looking at the overall picture, I actually think there are probably two separate questions here. The first is whether this dog has AHDS, and the second is whether there is concurrent gastrointestinal obstruction or another structural disease process.

Clinically, there are certainly lots of features that fit AHDS. The acute onset of haemorrhagic diarrhoea, the haemoconcentration, the dehydration, the rapid progression and the very flat demeanour are all consistent. The falling albumin and total protein are also entirely compatible with acute intestinal protein loss. I wouldn’t call this protein losing enteropathy as a primary diagnosis. Rather, I would describe it as protein loss secondary to severe intestinal disease. Protein losing enteropathy simply tells us that protein is being lost through the gastrointestinal tract. It is a mechanism rather than a disease itself. AHDS absolutely can cause marked enteric protein loss, so in this situation I would say the patient has AHDS with secondary protein loss rather than primary PLE.

You’re also absolutely right about the calcium. Once albumin falls, total calcium commonly falls with it because a significant proportion of calcium is protein bound. Unless the ionised calcium is low or there are compatible clinical signs, I generally don’t become overly concerned by a mildly reduced total calcium in this situation.

The chemistry otherwise doesn’t really raise any major red flags for me. The normal renal parameters despite significant dehydration suggest you caught the patient reasonably early. Liver enzymes are unremarkable. Pancreatic lipase isn’t supportive of pancreatitis, although as always we interpret that alongside the clinical picture rather than in isolation.

The heart rate actually catches my attention more than anything else. A heart rate of around 60 bpm in a flat, dehydrated, painful little Cavapoo is certainly not what I would expect. Coupled with the progressive hypothermia and increasing respiratory rate, I agree with you that I’d be increasingly worried about evolving systemic inflammatory response syndrome. Dogs developing sepsis or severe inflammatory disease don’t always mount the textbook tachycardic response, particularly as they become more decompensated.

As for Addison’s disease, I don’t think you made the wrong decision. It should always sit somewhere on the differential list for acute gastrointestinal disease, but with a normal potassium, no obvious electrolyte pattern to support it and another very plausible diagnosis, I don’t think I would have prioritised a cortisol either. If the case wasn’t progressing as expected, or if the bloodwork became less convincing for AHDS, then absolutely I would revisit it.

The ultrasound is the really interesting part.

Looking at your images, I can completely understand why you were concerned. Those hyperechoic rounded structures with clean distal acoustic shadowing certainly give the impression of luminal foreign material. If I’d been scanning the dog in real time, I suspect I would have been thinking exactly the same thing.

The difficulty is that static images only tell part of the story. What I would really want to know is whether those structures moved independently, whether they maintained their appearance from different imaging planes, whether they remained within the gastric lumen throughout the examination and whether they produced consistent clean acoustic shadowing from every angle. Sometimes compacted ingesta, mineralised material or even gas interfaces can produce surprisingly convincing appearances on still images.

The other thing that stands out is the amount of fluid within the stomach. If the dog genuinely hadn’t eaten since Thursday evening, I would expect the stomach to be relatively empty unless there was ongoing fluid accumulation or delayed gastric emptying. That immediately makes me wonder whether there is gastric outflow dysfunction or ileus.

Could AHDS alone produce that? Absolutely. Severe inflammatory ileus is well recognised in these patients. You can see delayed gastric emptying, fluid filled stomachs and diffusely fluid distended bowel secondary to inflammatory ileus rather than mechanical obstruction.

Equally, however, you cannot confidently distinguish inflammatory ileus from an early mechanical obstruction on a single ultrasound examination if you can’t identify the pylorus and proximal duodenum. That’s exactly why I think referral was the right decision.

I also completely agree with your hesitation about metoclopramide. If I genuinely believed there was a possibility of a mechanical obstruction or gastric outflow obstruction, I would avoid using a prokinetic until I’d excluded that. Once you’re comfortable there isn’t a foreign body, then metoclopramide becomes much more attractive if you think you’re dealing with inflammatory ileus.

One other thing I’d mention is that foreign bodies and AHDS are not mutually exclusive. A foreign body can certainly produce haemorrhagic diarrhoea through severe mucosal injury, and conversely a dog with AHDS may have incidental gastric contents that complicate interpretation. So I don’t think the presence of bloody diarrhoea excludes obstruction at all.

Overall, I actually think your clinical reasoning was excellent. You recognised that the patient wasn’t following the straightforward AHDS script, you identified an imaging finding that made you uncomfortable, you appreciated the uncertainty, and rather than forcing the case into one diagnosis you referred it. That’s exactly what I would hope someone would do.

Please let me know what the referral centre found. I’m genuinely interested to hear how this one turns out.

Scott 🙂

Replying to Emma Riley 25/06/2026 - 21:09

Thank you for joining!

I will make sure Liz sees this… she is best positioned to answer!

Hope you are well.

Scott 🙂

Replying to Sara Prior 17/06/2026 - 21:38

The biggest question was what to do about it!

We did nothing! I hope it does not cause the dog any issues, but I suppose there is a possibility of abscess formation?

Scott

Replying to Hannah B. 18/06/2026 - 15:38

Hi Hannah,

Great to hear from you. I hope you are well.

I think the uptake of FMT in practice is still quite variable. I am doing it a lot in my referral practice and have found it to be a very useful adjunctive therapy in selected cases, but I am also seeing it being taken up more and more in general practice. I do think it is very achievable in a first-opinion setting if there is a sensible donor screening process in place. In my experience, the procedure itself is not technically challenging; the more important aspect is donor selection and screening.

In terms of oral versus rectal administration, there are studies using both routes, but no veterinary study has directly compared oral versus rectal FMT efficacy in dogs and cats. The guidelines state that FMT has been administered orally and by rectal enema in companion animals, but that rectal enema remains the most common route in the published veterinary literature. So at the moment I would not say one is definitely better than the other.

I think the use of oral FMT largely depends on availability. Oral FMT is attractive where a reliable commercial product is available. I have recently started using the oral product from AnimalBiome here in Canada (https://www.animalbiome.com/), but they do not currently ship to the UK, and I am not aware of any UK-based veterinary companies producing an oral FMT product at present. Because of this, rectal administration is likely to remain the most practical option for many clinicians in the UK.

For rectal FMT, the amount used varies quite a bit between studies, so there is no single evidence-based dose. In published studies and the guidelines, common ranges are roughly 2.5–7 g donor faeces/kg body weight, diluted with sterile saline to a slurry that will pass through the catheter. The Companion Animal FMT Consortium members commonly use 10–20 mL/kg of slurry for medium-to-large dogs, and 5–10 mL/kg for small dogs and cats. In practice, I tend to think in terms of making a slurry that is concentrated enough not to leak everywhere, but liquid enough to pass through the catheter with gentle pressure.

A very practical starting point would be to use a carefully screened healthy donor, collect freshly voided faeces if possible, process it promptly, mix with sterile 0.9% saline, filter it through gauze, cheesecloth, or a sieve to remove hair and grass, then administer rectally using a catheter-tip syringe and a soft red rubber catheter. Some studies have used 12 Fr red rubber catheters, and a Foley catheter has also been described in cats. I would not overcomplicate the equipment at the start.

Regarding sedation, I think this is very patient-dependent. One thing I would emphasise is that the procedure itself is not technically challenging. There are clinicians who perform FMT in dogs completely unsedated. I have one patient where we simply give butorphanol and perform the procedure without any issues. For most of my other patients, we use some form of sedation. For smaller patients and particularly cats, I tend to favour general anaesthesia so that the airway is protected and the procedure is less stressful for everyone involved. The guidelines also state that sedation is usually not necessary, but should be considered for anxious, aggressive, intolerant patients, or patients that cannot retain the transplant.

So in short: yes, it is feasible and I think it is becoming increasingly common in both referral and general practice; no, we do not yet know whether oral or rectal administration is superior in dogs; start with rectal administration if you do not have access to a validated oral product; use a screened donor; aim for around 2.5–7 g/kg faeces diluted to a workable slurry; administer with a soft red rubber catheter and catheter-tip syringe; and sedate only as needed for the individual patient.

I hope you are enjoying the course. Any feedback would be much appreciated, and I’d be very interested to hear if you decide to try FMT in practice and how you get on.

Scott 🙂