scott@vtx-cpd.com

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 🙂

Hi Rosanna, great question!

I hope all is going well with you!

Emesis in cats is always a calculated gamble rather than a “go-to” intervention, and I think most of us now frame it as one option within a wider decontamination strategy rather than a default step. Success rates are variable, sedation is almost guaranteed with α2-agonists, and timing and toxin type matter.

Medetomidine/dexmedetomidine are probably the most evidence-supported options we currently have. Older studies suggested reasonable success with dexmedetomidine around 7 µg/kg IM, but more recent work suggests that this is often sub-emetic and primarily sedating. The 2025 JFMS prospective study looking at medetomidine doses found the best balance of efficacy and side effects at 20 µg/kg IM, with a median time to emesis of ~5 minutes and no clear benefit to higher doses beyond increased sedation. Your experience with 10 µg/kg IM resulting in “just a sleepy cat” fits very well with that data.

There’s also increasing interest in oral/transmucosal α2-agonists. While the recent JFMS case series using oral dexmedetomidine (20 µg/kg) focused specifically on emesis, it’s worth remembering that the concept of oral α2-agonists in cats isn’t new. A JAVMA study back in 2000 demonstrated that orally administered α2-agonists (in combination with ketamine) reliably produced marked sedation, with vomiting and hypersalivation being the main adverse effects and relatively mild physiological disturbance. That older work supports the biological plausibility of oral/transmucosal dexmedetomidine causing both sedation and emesis, even if the modern application is more targeted.

Hydromorphone is a reasonable alternative, with success rates around 70–75% in experimental settings and typically less profound sedation, but it’s less commonly stocked in general practice and still not reliably emetic.

Neurological signs and “should we induce?”: This is the hardest part, and I don’t think there’s a single right answer. The traditional contraindication to emesis in patients with neurological signs is really about airway protection and aspiration risk, not the presence of neurological signs per se. The complicating factor in cats is that α2-agonists will cause sedation anyway, so you’re essentially deciding whether controlled, anticipated sedation with close monitoring is acceptable versus foregoing emesis altogether.

In a cat that is already ataxic or mydriatic but still alert, responsive, normocardic, and able to maintain posture, I think it’s reasonable to consider emesis if:

The ingestion is potentially life-threatening (eg, chocolate, acetaminophen, lilies),

The timing is plausible for gastric decontamination,

You can provide close monitoring, rapid reversal (atipamezole), and oxygen if needed.

That said, the cannabis/chocolate case you describe is exactly where uncertainty bites. Unknown dose, unknown chocolate type, and a potentially long ingestion window all reduce the likelihood that emesis will meaningfully change outcome. In those situations, I’m increasingly inclined to prioritise early activated charcoal (with or without repeated dosing) once the cat is stable, rather than persisting with repeated emesis attempts that delay charcoal and add sedation.

Take home:

If attempting emesis with medetomidine, 20 µg/kg IM seems to be the sweet spot.

Expect sedation; plan for reversal and monitoring.

Neurological signs don’t automatically rule out emesis, but they should raise the threshold and shorten the leash on how long you try before moving on.

If emesis doesn’t occur quickly, I stop and move to charcoal/supportive care rather than escalating doses.

Out of interest, do you have other drugs available? Do you have dexmedetomidine in your practice?

I hope that helps.

Scott 🙂