scott@vtx-cpd.com
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Replying to Riley D. 05/03/2026 - 17:16
Hi Riley,
This is a really great question!!!!!
You are absolutely right about the physiology behind IGF1 testing. For IGF1 concentrations to increase in hypersomatotropism there must be adequate circulating insulin, because insulin upregulates hepatic growth hormone receptors and allows growth hormone to stimulate IGF1 production. In untreated diabetic cats that are markedly insulin deficient, IGF1 can therefore be falsely low even if hypersomatotropism is present. This is why historically we have recommended measuring IGF1 after the cat has been receiving exogenous insulin for a period of time, usually a few weeks, so that hepatic IGF1 production has normalised.
The use of SGLT2 inhibitors as first line therapy complicates that model a little. Because these drugs reduce hyperglycaemia through renal glucose loss rather than through insulin signalling, some cats may remain relatively insulin deficient. In those situations a single IGF1 measurement performed before insulin exposure could theoretically underestimate IGF1 and give a false negative result. So your instinct is correct that interpretation becomes more difficult if the cat has never received insulin.
In practice there are a few points that help. First, many cats with hypersomatotropism are not truly insulin deficient, they are insulin resistant, and they often still have measurable endogenous insulin secretion. In those cats IGF1 may still rise despite the absence of exogenous insulin. Second, the test is most clinically useful in cats showing insulin resistance or progressive difficulty controlling glycaemia, which is less common in cats that remain well controlled long term on SGLT2 inhibitors.
In a cat like the one you describe, where there were some physical features raising suspicion and you tested before starting treatment, I think that was a perfectly reasonable decision. If the IGF1 had been clearly elevated it would have been very informative. If it comes back negative or borderline, however, I would interpret that cautiously rather than assuming hypersomatotropism has been excluded. If clinical suspicion remains, repeating IGF1 later, particularly if the cat ever receives insulin or develops evidence of insulin resistance, is a sensible approach.
The other important practical point is that a cat doing well for 18 months on an SGLT2 inhibitor with stable clinical signs and good glycaemic control is much less likely to have clinically significant hypersomatotropism driving their diabetes, so the long term clinical course in your case is quite reassuring.
I hope that helps!
Scott 🙂
Replying to Lia Petcu 11/03/2026 - 03:10
Hey Lia!
That is really interesting! Do you run a session for dog donation? Where are you working at the moment? Do you store the blood in house? What a great initiative!
Scott 🙂
Replying to Rosie Marshall 09/03/2026 - 16:40
Rosie.
I spoke to one of the ECC specialists at Glasgow Vets Now and another ECC specialist in Australia. Neither of them are doing this practically and have not heard of anyone doing it at the moment.
Theoretically TXA is emetogenic but I am not aware of people using it this way in practice currently.
I hope that helps.
Scott 🙂
Replying to Lia Petcu 09/03/2026 - 12:59
Hello Lia!
Thank for the reply! I think they are so helpful in so many patients. The complication rate is quite low, but it is important to know the things that can go wrong.
The only downside of these tubes for me is that they are not as easy to send home still in place. I like oesophageal feeding tubes in many of my patients as I can send patients home with them. Owners seem to manage these very well at home.
Do you place many oesophageal feeding tubes?
Scott 🙂
Replying to Raquel M. 07/03/2026 - 17:24
Posting about it now!
Scott 🙂
Replying to Lesley M. 01/03/2026 - 09:04
Thanks Lesley, that’s a really helpful perspective, especially from first opinion where you’re seeing so many of these cases in day-to-day practice. I think what you say about the balance between theoretical risk and the reality of improving quality of life for older dogs is really important. In many of these patients we are dealing with advanced degenerative disease and limited time horizons anyway, so a treatment that allows them to move comfortably for those months or years can make a huge difference for both the dog and the owner.
Your comment about feeling a bit less gung ho starting new cases resonates with me as well. It seems like many people have shifted slightly in that direction over the past year, not necessarily abandoning the drug, but being a bit more deliberate about which patients we start and how we frame the discussion with owners. I also think it’s interesting that you mention exploring other adjuncts like amantadine more often, as it feels like some of those older analgesic strategies are coming back into the conversation again.
The neurological and incontinence changes you mention are the sort of things that I find difficult to interpret as well. In very elderly dogs it can be challenging to know whether we are seeing a drug effect, progression of underlying disease, or simply the natural trajectory of ageing. Your lab’s “euro turn” is exactly the kind of scenario where attribution becomes tricky.
And I completely agree with your final point about NSAIDs. The example of idiosyncratic carprofen hepatopathy in Labradors is a good reminder that even drugs we’ve used for decades and consider very familiar can still have rare but serious adverse events. In that sense, perhaps Librela is just being scrutinised more closely because it’s newer and used so widely.
It will be interesting to see how the pharmacovigilance data evolves over the next few years as reporting improves. Thanks again for sharing your experience, it’s really valuable to hear how colleagues are navigating this in practice.
Scott 🙂
Replying to Rosie Marshall 05/03/2026 - 10:13
Hi Rosanna,
It definitely makes animals feel sick, but I am not aware iof it being used specifically for thhis purpose in practice.
In dogs it works surprisingly well. Several studies looking at IV tranexamic acid have shown emesis in the majority of dogs (around 85–90%), often within a couple of minutes, which is why people have started discussing it as an alternative to apomorphine in places where that’s hard to obtain.
Cats are a very different story though. The evidence base there is extremely thin. There are a few reports and small experimental studies suggesting that tranexamic acid can induce vomiting in cats, but the numbers are tiny and the work hasn’t really been replicated much in clinical practice. One small experimental study reported emesis in about 90% of cats using escalating doses up to around 40 mg/kg, but that was in a very controlled setting with healthy animals and only ten cats.
More broadly, it doesn’t seem to be widely used in practice at the moment, and most of the established feline emesis protocols still rely on alpha-2 agonists such as medetomidine, dexmedetomidine or xylazine, simply because we have much more experience with them and they tend to work reasonably predictably.
My suspicion is that TXA keeps coming up because it works so well in dogs and it’s a drug that many hospitals already stock for haemorrhage control, so people are naturally wondering whether it might have a role in cats too. But at the moment I’d probably put it in the “interesting but still a bit experimental” category for feline patients.
Out of curiosity I’ve actually contacted a couple of ECC colleagues, including one from Vets Now, to ask what they’re currently doing in practice. If I hear anything useful or if anyone is using it more routinely I’ll let you know.
Scott 🙂
Replying to Rosanna Vaughan 02/03/2026 - 12:36
No problem!
Let me know if there is anything else I can do.
Scott 🙂
Replying to Raquel M. 07/03/2026 - 17:24
I did!!!!
Thanks for flagging! I need to read it properly and I will do a post on it!
I hope you are well.
Scott 🙂
Replying to Laura S. 06/01/2026 - 13:48
I popped through an invitation for a free place on the BOAS day!
Hope you can make it!
Scott 🙂
Replying to Silvana S. 28/02/2026 - 15:45
No problem!
I will get that set up for you.
Enjoy the rest of your weekend.
Scott 🙂
Emma this is such a difficult situation!
Can you share the histopathology report with me?
An eight year old Labrador with histologically confirmed end stage cirrhosis but currently stable blood parameters and a good quality of life is in that grey zone where we want to protect them but also avoid destabilising something that is, for now, compensated. The fact that her liver enzymes, albumin, urea and glucose are all within reference range suggests she is functionally coping despite the architectural change, which is encouraging. The weight loss is concerning but not unexpected in advanced chronic liver disease and may reflect reduced metabolic reserve rather than acute deterioration.
When I think about vaccination in cases like this I usually break it down into three considerations. First is exposure risk. How high is her genuine risk of encountering Leptospira based on geography, lifestyle, wildlife exposure and local prevalence. A rural, swimming, rodent chasing dog in a high incidence area is a very different scenario to a largely urban, low exposure patient. Second is immune competence. In advanced cirrhosis there can be immune dysregulation, but there is not strong evidence that vaccination meaningfully accelerates hepatic fibrosis or precipitates decompensation in a stable patient. Third is what would happen if she contracted leptospirosis. In a dog with severe pre existing cirrhosis, an acute leptospiral insult could be catastrophic, even if her baseline biochemistry looks acceptable today.
From a purely pathophysiological perspective, the inflammatory stimulus associated with a modern killed leptospira vaccine is typically transient and mild. We do not tend to see clinically significant hepatic injury from vaccination in stable chronic liver patients. That said, there is always a theoretical risk of transient systemic inflammation and in a dog with very limited hepatic reserve, even a small perturbation could tip them into decompensation, although this would be uncommon.
In cases like this I often individualise. If exposure risk is low, I would feel comfortable delaying or even omitting the leptospira component and documenting that discussion clearly with the owner. If exposure risk is moderate to high, I would lean towards vaccinating but doing so thoughtfully. That might mean ensuring she is clinically very stable at the time, no intercurrent illness, good hydration, and perhaps scheduling it on a day when the owners can monitor her closely for 24 to 48 hours. I would not routinely premedicate unless there is a history of vaccine reaction.
You also raise an important point about a possible immune mediated component to the liver disease. In true immune mediated hepatitis, particularly if immunosuppressive therapy is being used, we might be more cautious. But in established end stage cirrhosis without active inflammatory markers and without immunosuppression, the risk profile is a little different.
Ultimately this becomes a shared decision making conversation with the owner about realistic exposure risk versus theoretical vaccine risk. There is no single right answer, but I would not consider vaccination absolutely contraindicated purely on the basis of stable end stage cirrhosis. I would just approach it carefully and document the rationale.
I hope that helps a little! What treatment is the patient on at the moment?
Scott 🙂
Hello!
I hope you are well.
https://www.sciencedirect.com/science/article/pii/S2666450X24000063?via%3Dihub
These are my favourite guidelines for this, and honestly they’re one of the best single “how-to” resources we currently have in small animal medicine:
Winston JA et al. Clinical Guidelines for Fecal Microbiota Transplantation in Companion Animals (2024) (Advances in Small Animal Care; doi: 10.1016/j.yasa.2024.06.006). The paper is very practical and walks you through donor selection/screening, product prep (fresh vs frozen, dilutions, filtering, glycerol), and patient prep/administration options. It also has accompanying video content hosted on the journal site, which is genuinely useful for the practical workflow side.
A couple of quick, cat-specific pearls that are directly aligned with those guidelines (and often answer the common practical questions):
Donor selection/screening is the whole game in cats (TT foetus PCR, FeLV/FIV status, parasite screening, avoiding raw-fed donors, avoiding recent antibiotics, etc.).
Use fresh feces when you can, process promptly, and if you freeze product, avoid refreezing after thaw.
Volume matters in cats—vomiting/regurgitation risk can be volume-dependent, so most people aim for smaller volumes and good retention rather than “big volume delivery.”
If you tell me what you’re treating the cat for (acute diarrhoea vs chronic enteropathy vs suspected dysbiosis, and whether immunosuppressed / comorbidities), I can help with the case generally if you like!
Scott 🙂
Replying to Silvana S. 21/02/2026 - 19:52
Hi Silvana,
I think that’s a very fair position. A lot of us have taken exactly the same approach. Even if we’ve never personally seen enrofloxacin-associated retinal degeneration, the reports are certainly memorable enough to make you pause, especially when there are reasonable alternatives available.
Marbofloxacin is a very sensible choice and, in most cases where a fluoroquinolone is indicated, it does the job perfectly well without that lingering concern in the back of your mind. I completely understand the “I’d rather be cautious” mindset, particularly in cats where we already feel like we’re walking a pharmacological tightrope at times.
Thanks for sharing your thoughts.
Scott 🙂
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