scott@vtx-cpd.com

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 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 🙂