scott@vtx-cpd.com

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 Rosanna Vaughan 02/03/2026 - 12:36

No problem!

Let me know if there is anything else I can do.

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 🙂