scott@vtx-cpd.com
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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 🙂
Replying to Laura S. 11/01/2026 - 15:47
Hey Laura!
In dogs, I tend to use Vivomixx or Visbiome more often than many of the veterinary-labelled formulations. The evidence base for probiotics in general is quite variable and, as you say, a bit all over the place, but the human-grade, high-potency multi-strain products are at least consistent in terms of CFU delivery and strain stability.
In terms of dosing psyllium in dogs, I usually start at around ½–1 teaspoon per 10 kg once daily, mixed well into food, and I introduce it gradually over a few days to minimise bloating or transient stool worsening. I then titrate based on stool response rather than aiming for a fixed “target” dose. For larger dogs this often ends up being a few teaspoons daily, but I prefer to creep up slowly rather than start high.
In chronic cases, my bias towards Vivomixx/Visbiome is largely influenced by the Rossi et al. PLOS One 2014 paper comparing probiotic VSL#3 strains with prednisone plus metronidazole in dogs with idiopathic IBD. While it was a small, open-label study, it was quite striking that the probiotic group showed improvements not just in clinical scores and histology, but also in regulatory immune markers such as FoxP3 and TGF-β, along with partial normalisation of dysbiosis, particularly increases in Faecalibacterium. That immunomodulatory signal is something we simply do not see consistently with many veterinary probiotics.
So in practice, for chronic enteropathy or IBD-type cases, I am often using these products as part of a longer-term strategy rather than just as a short-term “add-on”. In more acute or mild cases, I think the choice of probiotic probably matters less, and consistency and owner compliance are more important than the specific brand.
As with fibre, though, I try to frame probiotics as supportive rather than curative, and if stools remain abnormal despite diet, fibre, and probiotic support, that is usually my cue to escalate the work-up rather than keep layering supplements on top.
Scott 🙂
Replying to Lesley M. 11/01/2026 - 08:50
Hey Lesley.
I hope you are well.
In terms of how I use psyllium, for most acute or subacute large-bowel cases I will use a plain psyllium husk powder, human-grade is fine. As a rough guide, I will often start at around ½–1 teaspoon per 10 kg once daily, mixed well into food, and then adjust based on stool response. I am careful not to introduce it too quickly, and usually advise owners to start at half that dose for the first 2–3 days to reduce the risk of bloating or worsening stool quality, then build up if tolerated.
I agree with you on pumpkin, I have had mixed results. Some dogs respond nicely, others not at all, and the variability in fibre content makes it harder to dose consistently. Psyllium feels more predictable and easier to titrate.
Where I differ slightly from what you have said is that while I mostly use psyllium short term in acute colitis or intermittent soft stools, I do use it longer term in selected dogs. There is a nice paper in BMC Veterinary Research (2021) looking at police working dogs with chronic idiopathic large-bowel diarrhoea, where daily psyllium supplementation led to improved stool consistency, reduced defecation frequency, and even weight gain, with benefits persisting after stopping supplementation in many dogs. That has made me more comfortable using it longer term in dogs with stress- or work-associated colitis, or chronic large-bowel signs where diagnostics are otherwise unremarkable.
For mild intermittent soft stools, I would agree with you, psyllium can act a bit like a stabiliser rather than a cure. I will often use it alongside diet and probiotics as a first-line, low-risk option, especially when owners want to avoid medication. If stools normalise and stay normal, great. If not, that is usually my signal to stop leaning on fibre and look harder for an underlying dietary intolerance, enteropathy, or other cause.
So I probably see psyllium as a short-term adjunct in acute large-bowel diarrhoea, a trial option in mild intermittent soft stools, and a longer-term tool in selected chronic or stress-associated large-bowel cases, especially active or working dogs.
Used deliberately, titrated slowly, and reviewed regularly, rather than as a default or permanent sticking plaster.
Really good discussion, it has been interesting to see how fibre has quietly crept back into the evidence base after being a bit overlooked for years.
Scott 🙂
Replying to Laura S. 20/01/2026 - 14:48
I did always think it ‘felt’ better with a new needle… but that was clearly me feeling better and not the patient! 🙂
The saving the planet take on things was interesting too… I suppose we need to be thinking in that way more. The environmental impact of healthcare must be huge!
Scott 🙂
Replying to Svetlana D. 22/01/2026 - 13:36
Haha!
Love all of these! Great suggestions! There are some words that I just give up trying to pronounce and just make a joke about not being able to say them during presentations!
I hope you are well.
Scott 🙂
Replying to Fiona D. 23/01/2026 - 15:02
Fiona!
Welcome. How lovely to see you here and thank you for joining us. What an interesting role. That will be a big change from general practice!
I hope the course is helpful. Make sure to ask lots of questions!
Scott 🙂
Replying to Laura S. 20/01/2026 - 14:00
Hi Laura,
I hate having to watch myself back! 🙂 Just to reassure you (and to avoid any confusion), when I mentioned metronidazole in the context of xylitol toxicity, I was not suggesting this as a standard or routine component of xylitol management. I was specifically referring to what was reported in the published case report you’ve cited (Schmid & Hovda, J Med Toxicol 2016), and simply describing the treatment protocol that was used successfully in that individual dog.
That paper is one of the few detailed reports of survival following severe xylitol toxicity with hypoglycaemia, acute hepatic failure, and coagulopathy, and metronidazole was included as part of a broader supportive care strategy alongside dextrose, vitamin K, FFP, NAC, and SAMe. My intention on that slide was to highlight what has been reported in the literature, rather than to imply that metronidazole should be routinely added in all xylitol cases.
In practice, as we discussed, management of xylitol toxicity is centred on rapid control of hypoglycaemia, aggressive supportive care, monitoring and treatment of coagulopathy, and hepatic support with NAC and SAMe. Use of metronidazole is very much case dependent and generally only considered in dogs with severe hepatic compromise where there is concern about endotoxemia or bacterial translocation — not as a blanket recommendation.
I hope that helps!
Scott 🙂
Replying to Lesley M. 11/01/2026 - 08:40
Thanks Lesley!
I hope all is well your end!
I think that’s a great point, particularly around the fact that hospitalisation doesn’t automatically have to mean antibiotics. There’s a lot we can do for these dogs in hospital that can make a real difference, fluid support, analgesia, antiemetics, nutritional support, and time, without necessarily reaching straight for antimicrobials.
I suppose it also depends how we define “sick”. Dogs that are starting to tick boxes for sepsis, changes in heart rate, temperature, respiratory rate, or white blood cell count, are a very different group and are clearly appropriate antibiotic candidates. That’s an important distinction, and one that can sometimes get lost when we talk about stewardship in broad terms.
I completely agree that the “sick” end of the AHDS/HGE spectrum feels different, and it’s understandable that antibiotics have historically been used there. That said, your point about pain relief and antiemetics being under-recognised is really important. These dogs can clearly be uncomfortable, and addressing pain, nausea and hydration probably has a far bigger impact on how they feel (and how quickly they improve) than we sometimes acknowledge.
There’s also some interesting emerging discussion around faecal microbiota transplantation, even in more acute cases, as a way of supporting gut recovery without the collateral damage associated with antibiotics. It’s not something most of us have ready access to, but it does challenge the idea that “sicker” automatically equals “needs antibiotics”.
Your stepwise approach, supportive care first, analgesia, antiemetics, fenbendazole where appropriate, feels very pragmatic and probably does exactly what you describe: buys time while many of these cases self-resolve.
Thanks again! Your experience is so valuable and we appreciate you sharing!
Scott 🙂
Replying to Rosie Marshall 18/01/2026 - 17:28
Rosie!
Lovely to hear from you. I hope all is well. COVID… now that is a whole can of worms! How interesting you did the vaccinations! I did wonder if needle type might have an influence? That might be the next study… are there certain manufacturers that produce better needles?
Scott 🙂
Replying to Annet Krabbenborg 18/01/2026 - 20:15
I always did it and felt better for it… but it seems it makes little difference!
I think all it does it make the people giving the injection feel a little better! 🙂
I think it is interesting from an environmental perspective there is so much medical waste in the world and we should not further contribute to this if it is not necessary for patient welfare!
Scott 🙂
Replying to Annet Krabbenborg 18/01/2026 - 22:17
I just wish they would make something similar for dogs! 🙂
Replying to Annet Krabbenborg 18/01/2026 - 22:17
I agree, most do!
I was speaking to the Purina rep. about it recently and they said if the cats don’t like it, it is worth persisting. They suggest leaving fresh stuff down for 5-7 days even if they don’t take to it on day one. Some cats will go for it after a few days supposedly.
They gave us some free sample boxes, so this is relatively easy to ask owner to do, I can imagine a more challenging sell if owners are paying for it? I suppose the moral of the story is, if they have a whole box they should persist!
Scott 🙂
Replying to Laura S. 13/01/2026 - 13:34
Hi Laura,
The forum is always open for you! I hope you are well.
On antibiotics, we are certainly moving toward more judicious use, but in the context of suspected biliary or acute hepatobiliary disease, amoxicillin–clavulanic acid is usually the more appropriate first-line choice. It provides broader coverage for common biliary pathogens, including beta-lactamase–producing organisms, which are not uncommon in these cases. Plain amoxicillin may be reasonable in selected, lower-risk situations, but in acute liver or biliary presentations, particularly where ascending infection or neutrophilic cholangitis is suspected, I would generally favour amoxicillin–clavulanate. Practical considerations such as IV availability can influence initial drug selection, but where possible, amoxicillin–clavulanate remains the empiric antibiotic of choice pending culture and sensitivity results.
In the specific context of neutrophilic cholangitis and cholangiohepatitis, acute disease in both dogs and cats is characterised by neutrophilic periportal and intrahepatic bile duct inflammation, with neutrophils present within bile duct walls and lumina. The distribution and severity of inflammation can vary considerably both within and between cases, and in some patients the inflammatory infiltrate extends into the hepatic parenchyma, resulting in cholangiohepatitis. Broad-spectrum antimicrobial therapy remains the cornerstone of treatment, particularly when bactibilia is confirmed. Amoxicillin–clavulanate is a sensible initial empirical choice in these cases. Because antimicrobial resistance is relatively common in biliary isolates, aerobic and anaerobic culture and sensitivity testing is strongly recommended whenever possible. Current recommendations suggest treatment courses of six to eight weeks, but in practice this should be guided by response to therapy, using serial ultrasound, serum liver enzyme activities, and bilirubin concentrations. If biochemical abnormalities or gall bladder changes persist or worsen despite appropriate antibiotics, prompt repeat cholecystocentesis should be considered to rule out antimicrobial resistance.
Regarding the gall bladder case and Denamarin, this is a really common point of debate. Your referral centre colleagues are technically correct in that there is no strong evidence that Denamarin directly treats primary gall bladder disease or alters outcomes in conditions such as biliary sludge or mucoceles. Where I think Denamarin still has a role is in supporting the liver around the gall bladder. Gall bladder disease almost never exists in isolation, there is usually secondary hepatocellular stress from inflammation, cholestasis, endotoxin exposure, or impaired bile flow. In that context, antioxidant and hepatoprotective support with SAMe and silybin is biologically plausible and, in my view, reasonable. I would not frame it as treating the gall bladder itself, but rather as supportive therapy for secondary hepatic injury.
Where did I make the metronidazole and xylitol comments? Just so I can check the context before I answer.
I hope that makes sense.
Scott 🙂
Replying to Laura S. 28/12/2025 - 15:39
Hi Laura,
The pressure to get patients home quickly, balance costs, and still make safe decisions absolutely influences real-time judgement, whether we like it or not. In your case, the concern about pyrexia suppressing appetite versus an early surgical complication is entirely reasonable, and I can completely see why a single NSAID dose felt like a pragmatic way to help clarify the picture.
The fact that he went straight to the food bowl once home does suggest that stress, hospitalisation, or mild post-op discomfort may well have been bigger contributors than anything more sinister. Hindsight is always generous, but I agree with your conclusion that in a similar case, holding off and reassessing may be just as reasonable, particularly if demeanour remains good.
Thanks for sharing the outcome!
Scott 🙂
Replying to Annet Krabbenborg 27/12/2025 - 15:25
Hi Annet,
That’s a great question, and I’m glad you’re finding the discussions useful.
In terms of duration, I’ve so far used capromorelin continuously for several months in a small number of cats, particularly those with CKD and progressive sarcopenia, without running into obvious tolerance or safety issues. In the published study it was used for 55 days, so we’re obviously extrapolating beyond the evidence base when we go longer term, but clinically I’ve found it can be helpful to think of it less as a short “kick-start” and more as ongoing supportive therapy in carefully selected patients.
That said, I don’t automatically plan it as lifelong treatment for every case. I usually reassess at 4–8 weeks, looking at weight trajectory, muscle condition, appetite, quality of life, and owner perception. If there’s a clear benefit, I’m comfortable continuing, sometimes with short breaks or dose adjustments, and if there’s no meaningful improvement, I stop it. Cost and owner expectations also factor into that decision.
I think the key is being clear that this is aimed at supporting body condition and quality of life, rather than reversing the underlying disease process. Used with that mindset, longer-term use can make sense in cachectic or sarcopenic patients where options are otherwise limited.
Really pleased you’re enjoying being a member, and thanks for joining in the discussion!
I hope life in practice is treating you well.
Scott 🙂
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