scott@vtx-cpd.com
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Replying to Steph Sorrell 02/06/2025 - 09:24
Thanks Steph!
Scott 🙂
Thanks Mark.
Your go-to combination of buprenorphine, gabapentin, and meloxicam is very similar to what many of us reach for in the first instance, and there’s sound rationale behind each. That said, it’s worth keeping in mind that while these medications are commonly used and make intuitive sense in painful inflammatory bladder conditions, none of them have been robustly studied for non-obstructive FIC in terms of efficacy beyond placebo.
In fact, a recent consensus summary (authored by the amazing Sam Taylor) highlights that analgesics such as NSAIDs, opioids, gabapentinoids, and even frunevetmab (anti-NGF monoclonal antibody) have not yet been formally evaluated in clinical trials for this indication. That doesn’t mean they shouldn’t be used—pain management is absolutely recommended—but it does mean we need to weigh their potential benefits against the stress of administration, especially when oral dosing is difficult or negatively affects cat behaviour. Gabapentin is helpful in many cats, but we have to be honest that in some cases, the stress of medicating may actually worsen the condition by increasing perceived threat and reducing control.
Other drugs like prednisolone, pentosan polysulfate, and glycosaminoglycans have not shown significant benefit in blinded studies, although both placebo and treatment groups often improve—possibly related to better home care, handling, or reduced threat perception (e.g. giving meds in a treat or encouraging owner-cat bonding). These behavioural and environmental influences may explain why MEMO (multimodal environmental modification) consistently shows better long-term results than medications alone.
Trazodone is one I’ve seen used selectively in cats that are extremely hypervigilant or live in high-arousal home environments, but I rarely use it personally.
Amitriptyline and fluoxetine remain options in refractory or relapsing cases, particularly if there’s concurrent urine spraying or clear evidence of chronic stress or anxiety. However, these should ideally be started with behavioural guidance and close follow-up. Fluoxetine has been associated with urinary retention in some reports, and any use for behavioural modification should always accompany MEMO, not replace it.
I am not a huge fan of subcutaneous fluids in these cases. There’s no evidence it improves outcome, but it may make sense on a case-by-case basis. I wouldn’t do it routinely unless there’s a clear clinical rationale.
I’ll also make sure Sam sees this!
Consensus guideline link: https://journals.sagepub.com/doi/10.1177/1098612X241309176
Scott 🙂
Replying to Mark Laloo 28/05/2025 - 18:12
Thanks Mark!
I agree. I rarely use ketamine for sedation now.
Alfaxalone is a very useful drug!
Scott 🙂
Hi Mark,
Thanks so much for the questions.
For FMT in cats, the core principles mirror canine protocols, though feline-specific studies are limited. Donors should ideally be healthy indoor-only cats with no history of GI disease, recent antimicrobials, or ongoing medication. Screening typically includes CBC/biochem, faecal float, Giardia ELISA, and a full PCR panel for infectious enteropathogens. Some centres pool donor faeces, but single-donor protocols tend to be preferred for traceability and consistency.
Material is usually fresh (processed and administered within 6 hours), though frozen samples (stored at –80°C with 10% glycerol) can be used in some settings. Most transplants are delivered via retention enema under light sedation, though oral and nasoesophageal approaches are being explored. A typical course involves 1–3 treatments depending on response. To be honest I will actually GA my feline transplant patients due to the higher risk of aspirating the transplanted material than dogs.
It’s also worth flagging a recent feline case series in JFMS (Lee et al., 2025; DOI: 10.1177/1098612X251337274), which describes adverse events in nine cats undergoing FMT. These included lethargy, vomiting, diarrhea, inappetence, weight loss, and transient GI pain. Events were managed with antimicrobials, antiemetics, and supportive care. Importantly, 8/9 cats still showed positive clinical response (7 complete, 1 partial), highlighting both the potential and the need for caution.
For a great recent review of both FMT and probiotics in small animals, including practical donor selection and preparation advice, you might also find this helpful:
https://www.advancesinsmallanimalcare.com/article/S2666-450X(24)00006-3/fulltext
On the probiotic front, Vivomixx, Visbiome, and Sivomixx probably represent the most evidence-based blends in terms of documented strain content, viability, and peer-reviewed outcomes—particularly in dogs, though feline data is building. Visbiome Vet has the most strain-specific research and independent verification of capsule content. Fortiflora is still widely used and palatable, but contains only one strain and less independent efficacy data.
I’ll also make sure Steph sees your comment, I’d be really interested in her thoughts.
Scott 🙂
Replying to Mark Laloo 28/05/2025 - 17:44
Hi Mark,
Thanks so much for your thoughtful response. I completely agree that having a standardised approach helps immensely with both consistency and team confidence.
The use of subcutaneous insulin alongside IV insulin in DKA isn’t well supported by current evidence, and most guidelines still recommend against it during the acute phase. The concern is that SC absorption is unreliable in dehydrated or vasoconstricted patients, and combining routes can complicate interpretation of response and titration. That said, I’ve also heard of it being used in transition phases, or when IV access becomes a limitation—but like you, I prefer to wait until hydration has been restored and enteral intake has resumed before switching over.
On the topic of alternative approaches, there are two small studies worth noting: the 2013 JVECC study by Marshall et al. (DOI: 10.1111/vec.12038) looked at IM glargine (with or without SC glargine) in 15 cats with DKA. All survived to discharge with a median hospital stay of 4 days. A later randomized trial by Gallagher et al. in 2014 (JVECC, DOI: 10.1111/vec.12269) compared IM/SC insulin to a CRI of regular insulin. The SC/IM group had significantly faster resolution of ketonemia and acidosis, and shorter hospitalization. Small numbers, but potentially practice-informing in the right setting.
I completely agree that electrolyte management is often the most challenging and dynamic part of these cases. I’d love to hear more about how your team handles potassium and phosphate adjustments—do you work from a fixed supplementation chart or tailor it dynamically?
Euglycaemic DKA has become such a hot topic in human endocrinology with SGLT2 inhibitors. How were you monitoring for it in those cats, and what approach did you take once it was identified?
I’ll also make sure Rodolfo sees this—it’ll be really interesting to hear his take too.
Thanks again for a great discussion.
Scott 🙂
Hi Kath,
Thanks for posting. Such a great case to spark discussion. In these scenarios, I always find the biggest challenge is how we prioritise interventions and manage the balance between risk and benefit. How aggressive should we be with fluid resuscitation? When and how do we give analgesia safely? And how much do we try to correct before heading to surgery?
Curious to hear how you prioritise.
Scott 🙂
Hi Christina,
Thanks so much for sharing—what a tough case. I think Josep’s nailed this one and has covered all the key angles better than I could, so I’ll defer to him here!
Scott 🙂
Replying to Rachel H. 29/05/2025 - 15:18
No problem!
Let me know if there is anything else I can do to help.
Have an amazing weekend.
Scott 🙂
Replying to Raquel M. 27/05/2025 - 14:31
Thanks so much, Raquel.
Really insightful reflections
I think one of the key points you touch on is perception. Librela is often seen as safer than NSAIDs, especially among clients and some GPs, which can understandably shape prescribing behaviour. But I’d argue we’re simply more familiar with NSAIDs. We have decades of data on long-term effects, we know what adverse events tend to look like, and we’ve developed fairly robust strategies for monitoring and mitigation. Librela, by contrast, is still relatively new, and some of the serious concerns, while rare, are only becoming visible through post-marketing data and case-level reporting. So while neither drug class is risk-free, our comfort level and experience with NSAIDs is definitely more established.
Your point about reassessing clinical response over time is such an important one. I’ve also seen dogs on repeat Librela doses where it wasn’t entirely clear what the ongoing benefit was, and I do think it can be easy for monthly injections to become routine without always re-evaluating outcome. Regular follow-ups and clearer criteria for success would go a long way here, especially in the absence of objective pain scoring tools being used consistently.
Regarding neurological side effects, yes, there’s growing interest in this area, especially since the FDA included neurological signs like ataxia and seizures in their 2024 safety update. The Zoetis review still classifies these as “very rare,” but there’s certainly enough signal to warrant caution. To your neurologist’s point, bedinvetmab is not expected to cross the blood–brain barrier under normal conditions, but in cases of compromised barrier integrity (such as inflammation, trauma, or certain neurodegenerative diseases), we can’t be completely certain. The neurologist I work with now will avoid using Librela entirely in cases of inflammatory brain or spinal disease for exactly that reason. So I think your concern about potential misdiagnosis is well-placed, especially in settings without access to advanced imaging.
For now, I’d say careful neuro exams, a clear indication of OA based on physical exam (or ideally imaging), and caution in any dog with neurological history are all justified.
Thanks again!
Scott 🙂
Replying to Sybil Dryburgh 25/05/2025 - 23:23
Hi Sybil,
Haha, I honestly thought you were just making a very passionate point with those capital letters and I was completely here for it! And I totally agree, when you’re 48 hours post-op and they’re still not eating, NSAIDs can sometimes be the thing that turns the corner, especially when everything else feels a bit underwhelming.
Thanks for mentioning erythromycin. There’s a really helpful recent multicenter study out of WA looking at prokinetic use in hospitalized dogs, and it shows a clear shift toward erythromycin or dual metoclopramide/erythromycin therapy between 2018 and 2023. Interestingly, erythromycin alone or in combination became more common over time, and while efficacy wasn’t the primary endpoint, its increasing use suggests clinicians found it clinically helpful. No significant adverse effects were recorded, though obviously prospective studies would be ideal.
Erythromycin acts via motilin receptor stimulation in dogs (partly via 5-HT3 cholinergic pathways), and at low doses (0.5–1.0 mg/kg PO or IV) mimics the migrating motor complex (MMC) pattern, aiding coordinated gastric emptying. High doses (10–30 mg/kg), though, can actually trigger retrograde peristalsis, so careful dosing is crucial. I still default to 1 mg/kg IV q8h or oral where I can get it. Azithromycin is starting to crop up in the literature too, showing similar effects in manometric studies and possibly fewer antimicrobial resistance concerns long term.
On the metoclopramide front, I also wanted to share a study I came across recently by Wilson, Evans, and Mauer (Vet Anaesth Analg. 2006), which compared low and high dose metoclopramide infusions in dogs under GA. The high dose group—bolus 1 mg/kg IV followed by 1 mg/kg/hr CRI—had a 54% reduction in the relative risk of gastroesophageal reflux compared to placebo. That’s a huge difference, and it’s got me thinking more about dose escalation in critical GI cases.
I’ll admit, I’ve rarely gone above 2 mg/kg/day in my own patients, but I did try 4 mg/kg/day (CRI) in one recent regurg-heavy ileus case where erythromycin wasn’t available. It actually seemed to help. Silverstein and Hopper mention doses up to 7–8 mg/kg/day in their critical care book, though I’m still trying to find the primary reference. I’d be really curious to hear if anyone else has pushed the dose higher. Was it effective, and did you run into any neuro signs or other issues?
Anyway, always love chatting GI motility. It’s one of those areas where a few subtle tweaks can make a huge difference to outcomes.
Scott 🙂
References
Teo EF, Sharp CR, Boyd CJ, Chee W. Use of erythromycin and metoclopramide in hospitalized dogs: a multicenter historical cohort study. Front Vet Sci. 2024;11:1206335. doi:10.3389/fvets.2024.1206335Wilson DV, Evans AT, Mauer WA. Evaluation of the effect of metoclopramide on the incidence of gastroesophageal reflux in anesthetized dogs. Vet Anaesth Analg. 2006;33(5):336–44
Mann FA, et al. Small Animal Critical Care Medicine. 2nd ed. Elsevier; 2015.
Replying to Jane Sedgewick 25/05/2025 - 14:54
Hi Jane,
Really interesting to hear that. Your audit findings are very much in line with what this new paper and others are pointing to. I must admit I often start around 1.5 mg/kg myself, based on the Sieber-Ruckstuhl et al. (JVIM, 2019) study which showed excellent electrolyte control with that starting dose. In fact, most dogs in that study ended up needing further dose reductions down to a median of 1.1 mg/kg to maintain stability over time, especially once they were past the initial stabilisation window.
It aligns nicely with the Vincent et al. (JVIM, 2021) trial too, which compared 1.1 mg/kg and 2.2 mg/kg and found no difference in electrolyte control, but much more biochemical evidence of overtreatment, including suppressed renin activity and lower urine specific gravity, in the standard-dose group. I do think we’ve probably been overtreating some dogs for a long time, largely out of convention.
Like you, we’ve also seen plenty of patients do well on extended intervals, 5 or 6 weeks for cost reasons in some cases, and even the ones with fairly inconsistent compliance seem surprisingly stable once they’ve had time to equilibrate. It does make you wonder how much of our rigid scheduling is about pharmacology versus calendar logic.
And yes, once they’re through that initial adjustment period, they really do just get on with things. Most of our long-term Addisonian dogs seem to die with the condition, not from it.
Thanks again for sharing!
Scott 🙂
Replying to Alys J. 25/05/2025 - 12:48
Hi Alys,
Thanks for your message.
That’s a great question, and it’s one we’re all increasingly mindful of in light of antimicrobial stewardship guidance. First, how was the urine sample collected? If it was free-catch, that’s important context, especially in asymptomatic dogs. A recent JSAP study (Mandese et al., 2024) showed that significant bacteriuria was far more likely in male dogs, and not meaningfully reduced by cleansing prior to collection. This reinforces that we need to be cautious about interpreting bacteriuria on sediment alone in patients without urinary signs.
Subclinical bacteriuria is defined as the presence of bacteria in a properly collected urine sample (ideally via cystocentesis) with no clinical signs of urinary tract infection. Terminology like “occult UTI” or “infection” without symptoms should be avoided. While cytological detection of bacteria or pyuria can be supportive, studies have shown poor agreement with culture results and poor predictive value for actual infection (McGhie et al., 2014; O’Neil et al., 2013). So a positive sediment alone, especially in an otherwise well patient, doesn’t justify treatment.
The recent Frey et al. (JAVMA, 2024) study followed dogs with untreated subclinical bacteriuria and found that it was typically persistent but non-progressive. Only one dog developed pyelonephritis, and that dog had multiple comorbidities and urinary calculi. This aligns with ISCAID’s 2019 recommendations to avoid treatment for SB, even in the presence of pyuria or high CFU counts.
Similarly, Siu et al. (JAVMA, 2022) followed post-op spinal surgery patients with SB and showed no adverse consequences from delaying antibiotics until clinical signs emerged—again supporting a symptom-driven approach to treatment.
A broader 2019 review by Weese and colleagues reinforces that subclinical bacteriuria is relatively common in dogs (up to 12% in healthy individuals and higher in those with diabetes, obesity, or neurologic disease), but treatment is rarely indicated. Culture should only be performed if a result would change your management, otherwise it risks leading to unnecessary antibiotics.
In your case, no LUTS, weight loss as the presenting concern, and bacteria seen only on sediment, I’d lean toward monitoring rather than treating, unless cystocentesis culture confirms infection and other signs develop. I think it will also depend on what other parts of your investigation tell you.
I hope that helps! Have a lovely week.
Scott 🙂
Replying to Samantha L. 24/05/2025 - 22:46
Hi Samantha,
Lovely to hear from you, I hope you are enjoying the course.
Thanks so much for your thoughts, I really appreciated your perspective.
I agree, it’s definitely something that feels more psychological and individual than anything else. Like you, I hadn’t really given much conscious thought to the owner’s body condition in relation to how we approach weight discussions until I read this paper. But once you start reflecting on it, you can see how these subtle dynamics might play out in the background, especially when tensions rise or when an owner becomes defensive. It’s often in those moments that we start noticing more about the interaction and maybe even making unconscious attributions without realising.
I also completely agree that the owner’s attitude has a much bigger impact on our perception of their caregiving than their appearance. In any case, I think the paper is a useful reminder to stay self-aware and make sure our communication is always grounded in compassion, not assumptions. At the end of the day, it’s about doing what’s best for the pet and finding ways to support the owner in that without making it personal.
Thanks again for engaging with it.
Scott 🙂
Hi Laura,
Great question and I’m completely with you on the love for maropitant. It’s one of those game-changing drugs I’d now struggle to practise without.
I do use maropitant routinely in premeds (especially for opioids), and I’ve also used it in plenty of jaundiced or hepatopathy patients. The theoretical concern stems from the fact that maropitant is primarily cleared by hepatic metabolism (CYP3A), and plasma levels can be higher and clearance slower in dogs with moderate to severe liver disease. But in practice, short-term use—even in the face of elevated liver enzymes, hasn’t been shown to cause harm, and I’d consider it a reasonable choice if the clinical benefit is there (e.g. vomiting, nausea, perioperative antiemesis).
I think it’s also important to remember the difference between liver enzyme increases and true liver dysfunction. Maropitant is metabolised in the liver and should be used with caution in patients with hepatic disease—particularly when treating over longer periods. As it accumulates during a 14-day course due to metabolic saturation, careful monitoring of liver function and any adverse effects is sensible during extended use.
Really interesting question!
Warm wishes,
Scott 🙂
Replying to Jane Sedgewick 25/05/2025 - 14:25
Hi,
I don’t use it often either, but I agree it can be really helpful in those relapsing colitis cases where owners just need something practical they can do early. And totally with you on being confident it’s not NSAID-related before combining.
The evidence for sulfasalazine is definitely disappointing, and the human data is also a bit all over the place. It feels like one of those drugs that’s hung around more through tradition than strong trial data.
Have a great week!
Scott 🙂
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