scott@vtx-cpd.com
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Replying to Silvana S. 06/04/2026 - 09:56
Hey.
At my hospital I still see a lot of enrofloxacin being used as a first line antibiotic for many liver cases, which is interesting given what we are seeing in the data. I think part of it comes from a perception that these are “serious” infections and therefore need a “stronger” antibiotic up front, but this paper really challenges that idea. When you look at the actual isolates, with E. coli and Enterococcus dominating, and the relatively low resistance rates to amoxicillin clavulanate, it makes a good case for starting more simply and more rationally.
I completely agree with your point about ascending infections and the overlap with enteric flora, and we see the same variability in dogs as well, including the occasional unexpected isolate. But in most cases, starting with amoxiclav while you wait for culture seems both clinically appropriate and a better stewardship decision.
Scott 🙂
Replying to Silvana S. 06/04/2026 - 10:07
We are now looking in to the practicalities of getting one of these systems in to try.
Looking quite expensive so far! I will keep you posted. This is the system we are looking at:
Scott 🙂
Replying to Silvana S. 06/04/2026 - 10:14
I agree!
I must admit, I don’t have a huge amount of knowledge or experience with radiation therapy.
I am also surprised by what can be achieved with one dose!
Scott 🙂
Replying to Liz Bode 03/04/2026 - 18:15
Thanks Liz.
Really helpful!
Scott 🙂
Replying to Sophie L. 29/03/2026 - 16:56
Hi Sophie, great question and I am really glad you are enjoying the course.
I do not recommend routine use of fresh frozen plasma for all liver biopsy cases. In most dogs with chronic hepatitis, coagulation testing does not reliably predict bleeding risk, and there is very limited evidence that prophylactic plasma actually reduces the risk of post biopsy haemorrhage.
I tend to reserve FFP for cases where there is a clearly increased bleeding risk, such as marked prolongation of PT or aPTT, significant thrombocytopenia, low fibrinogen, or clinically relevant anaemia. It may also be considered in patients with known or suspected clotting factor deficiencies or in those undergoing more invasive procedures where bleeding risk is higher.
In many cases, careful patient selection, appropriate biopsy technique, and close post procedural monitoring are more important than routine plasma administration.
So in short, targeted rather than routine use is the approach I would recommend.
Scott 🙂
Replying to Liz Bode 29/03/2026 - 19:35
I literally had no idea this was even a thing until I saw this paper!
Scott 🙂
Replying to Liz Bode 29/03/2026 - 19:36
Thanks Liz!
So not a firm no in cats?
Scott
Replying to Hayley G. 25/03/2026 - 11:20
Hayley!!!!
Welcome! So lovely to see you here! Please let us know how you are enjoying the course. I really hope you find it helpful.
Have a lovely week.
Scott 🙂
Replying to Emma Johnstone 25/03/2026 - 11:45
I agree!
Super interesting! My biggest worry is cost. It is a shame that radiation is such an expensive intervention!
Scott 🙂
Replying to Emma Johnstone 25/03/2026 - 12:04
Hi Emma,
That definitely mirrors my experience as well, I think most of us have had those cases where you’re standing there waiting for something to happen and instead you just end up with a very peaceful, very sedated cat.
The oral dexmedetomidine paper is really interesting! A 5 out of 6 success rate is hard to ignore, even if it’s only a handful of cases. In that series they used 20 µg/kg orally and achieved emesis in most cats, but importantly all of them still became moderately to profoundly sedated, so it’s not really avoiding that aspect, just changing the route. I haven’t personally used oral dexmedetomidine yet, so I can’t speak from direct experience, but it’s definitely something I’m watching with interest.
In terms of whether oral medetomidine would behave similarly, I think it’s biologically plausible. We know from older sedation studies that oral alpha 2 agonists in cats can be absorbed well enough to cause quite marked sedation and even some vomiting, so the mechanism is clearly there. The challenge is probably consistency and predictability rather than whether it can work at all. With IM dosing we have a much clearer expectation of onset and effect, whereas oral or transmucosal routes may be a bit more variable.
My slight hesitation at the moment is that loss of control over timing. If it works, great, but if it doesn’t you may have delayed charcoal or other decontamination steps while waiting to see if anything happens. In a straightforward, cooperative cat I would probably still default to IM medetomidine at an effective dose to maximise the chance of emesis and then move on fairly quickly if nothing happens.
That said, I can absolutely see a role for it in certain cases! Interested to hear others experience.
Scott 🙂
Replying to Emma Johnstone 25/03/2026 - 15:11
Hi Emma!
Thank you for ending through the histopathology! Really helpful!
What stands out most is just how advanced and diffuse the architectural change is. There is marked parenchymal collapse with widespread fibrosis and a strong ductular reaction alongside multifocal nodular hepatocellular hyperplasia which is essentially the liver trying to regenerate in the face of chronic injury. That combination fits very well with what you described surgically and explains the “cow kidney” appearance. This is very much an end stage remodelling process rather than an active aggressive inflammatory disease at this point.
The really important nuance for me is that inflammation is actually minimal within the sections. There are only low level lymphocytes and plasma cells with very limited interface activity and hepatocellular necrosis. That makes an ongoing immune mediated hepatitis much less convincing as a current driver even if something like that may have initiated the process earlier in the disease course. Similarly the copper is low grade and not associated with injury so it is very unlikely to be clinically relevant here.
So I think your instinct is right that we are dealing with the aftermath of something chronic rather than something actively smouldering. At this stage the liver is structurally very abnormal but functionally still compensating which is why her bloods and clinical signs are relatively reassuring.
That said determining an immune pathogenesis in cases like this is genuinely difficult particularly once we are looking at end stage change where the initiating lesion has effectively been lost in the remodelling. In some situations you can consider a therapeutic trial of immunosuppression as both a treatment and a diagnostic tool. Solidifying a diagnosis of immune hepatitis may rely in part on assessing response to treatment. There is quite a bit of variability in how people approach this and at present there is no true standard of care protocol. That said clinicians have reported success using corticosteroids alone or in combination with other agents such as azathioprine cyclosporine or mycophenolate depending on tolerance and response. In a case like this I would only consider that route if there were stronger indicators of ongoing inflammatory activity or clinical deterioration that could not otherwise be explained.
In terms of progression these cases can be quite variable. Some will remain surprisingly stable for a period of time until they reach a tipping point and then decompensate with ascites portal hypertension or hepatic encephalopathy. Others can tick along for longer than expected if they maintain adequate functional reserve. The ongoing weight loss is probably the earliest sign that metabolic capacity is limited even if the standard parameters still look okay.
I also completely understand the owner’s hesitation around adding medications. In a case like this I tend to reframe that conversation slightly because we are no longer trying to prevent injury but to support what function remains. There is generally good tolerance for things like SAMe silybin combinations or ursodeoxycholic acid if there is any concern about cholestasis and sometimes those can be introduced gently if the owner is open to it. But equally if she is bright and eating and they are cautious I do not think it is unreasonable to move slowly.
On the vaccination question this histopath actually makes me a bit more comfortable rather than less. There is no strong evidence of an active immune driven process that we would worry about exacerbating. Given the low exposure risk you described I would still feel very comfortable deferring leptospirosis if that aligns with the owner’s preference. If you did decide to vaccinate I would not consider this liver pathology an absolute contraindication but I would approach it cautiously as we discussed before.
I hope that helps!
Scott 🙂
Replying to scott@vtx-cpd.com 17/03/2026 - 20:27
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 🙂
***This was a great reply from Lesley, I am posting again so it is not lost***
Thankyou for this, thought provoking as always and we will discuss it at our next clinical governance meeting on Wednesday purely because you have brought it to mind!
I think librella is great and I have had very few side effects noted. Maybe the odd incontinence case and possibly deterioration in neurological function but these dogs are generally old and a few more months or years pain free is worth the lottery to me. My own ancient lab was on it and did end with a weird euro turn but his days had been numbered for about 18 months. I have not seen the acute deterioration in elbow cases.
That being said I am definitely less gung ho about starting new cases due to the reports and general feeling towards librella and would be more inclined to explore other less commonly used drugs like amantadine. We would be very very reluctant to start younger dogs on it unless there was really no other option and I do slightly get the fear if I do start a new case on it but in general they do well and I think the risk:benefit is definitely still in favour of benefit and it lets old dogs have a better quality of life while they’re here which is our goal.
(I am in first opinion practice and do consults only for info so I have alot of librella cases. Less now than last year I would say though!)
I have also just been listening to the toxins webinar and the non-dose dependant idiosyncratic liver failure due to nsaids (carprofen) in (mostly) labradors perhaps proves nothing is truly safe!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 🙂
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