scott@vtx-cpd.com
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Replying to Lesley M. 30/05/2026 - 22:43
Hi Lesley,
Thanks for the update.
To answer your main question first, in an ideal world I would absolutely like to have a bone marrow aspirate and core biopsy because it is really the only way to confidently distinguish PIMA from some of the other causes of severe non regenerative anaemia. That said, in the real world I don’t think it is always essential, particularly if the owners are reluctant and the results are unlikely to significantly alter what you are going to do.
In this case, if the owners told me they were happy to pursue immunosuppression regardless of the marrow findings, then I would be reasonably comfortable continuing treatment without a biopsy. The procedure itself is generally very well tolerated and I would not consider it particularly painful compared with many of the things we routinely do, but it is still an anaesthetic or heavy sedation procedure in a severely anaemic dog and there is always some risk and stress involved.
The bigger question I ask myself is whether the result would genuinely change management. If the answer is no, then I think it is entirely reasonable to continue treating presumptively.
The serial PCVs are interesting. Going from 34% post transfusion on the 20th to 21% on the 29th is obviously disappointing, but not necessarily unexpected. Remember that the transfused red cells are only buying you time while the marrow hopefully starts producing its own cells. The fact that she has fallen back down does not necessarily mean treatment has failed. What I would really like to know is whether there is any evidence of emerging regeneration on blood smear review or repeat reticulocyte counts compared with the original sample.
One thing I would say is that we are still very early in the disease course. She is only about 10 days from the transfusion and only around two weeks into immunosuppressive treatment. Based on the PIMA literature, I would not expect many dogs to have shown a convincing response yet. In the Assenmacher study the median time to a regenerative response was 29 days, and some dogs took substantially longer than that. I think we have to be careful not to judge the success or failure of treatment too early.
To be honest, my biggest concern from what you’ve written is not the haematocrit, it is the owners. Unfortunately many of the dogs that do poorly in the published studies are not necessarily the dogs that cannot respond, but the dogs whose owners understandably run out of emotional, financial or practical tolerance before the marrow has had time to recover.
The panting, PU/PD and lethargy are exactly the things that make these cases difficult. From the owner’s perspective they see a dog that was anaemic, then receives treatment, and now appears miserable because of the steroids. Meanwhile the haematocrit has dropped again, which understandably makes them feel nothing is working.
If it were my case, I would probably spend more time setting expectations than changing medications right now. I would explain that the next two to four weeks are really the critical period. If she can remain stable enough to get through that window, then we have a much better chance of knowing whether she is going to respond.
I think adding cyclosporine is entirely reasonable given the mycophenolate intolerance. Most of these dogs ultimately end up requiring combination immunosuppression anyway, and cyclosporine is probably my preferred second line choice in this situation.
If she proves refractory, there are a couple of additional options worth keeping in mind. There is a recent case report by Yuki and colleagues describing two dogs with confirmed PIMA that failed to respond adequately despite prednisolone and conventional immunosuppressive therapy. Both subsequently achieved complete remission following the addition of oclacitinib. Obviously this is only a two case report, so I would not jump to it early, but it is an interesting rescue option if she continues to struggle despite prednisolone and cyclosporine (Yuki et al., 2023).
For the really refractory cases, I have also seen darbepoetin used occasionally as an adjunct. The evidence is limited and it is not addressing the underlying immune mediated process, but in selected dogs that are proving difficult to get regenerative, particularly where owners are committed and repeated transfusions are becoming problematic, it is something I would at least have on the list of possible rescue therapies. I certainly would not be reaching for it yet, but I would keep it in the back of my mind if we find ourselves several weeks down the line with persistent severe non regenerative anaemia.
Keep me posted. I’d genuinely be interested to hear how she gets on.
Best wishes,
Scott
Replying to Silvana S. 11/06/2026 - 10:54
Hi Silvana,
Thank you so much for taking the time to write such detailed feedback!
It’s particularly useful to hear your perspective as someone working in general practice and who has actually completed the course. One of the things I’m struggling with is whether the pancreas should stay within the GI course, so it’s really interesting to hear that you found value in having those sessions included, even if they weren’t an exhaustive deep dive into pancreatic disease.
Iām also pleased to hear that the overall session length felt about right. That’s always a difficult balance to strike.
Your suggestion about replacing (or shortening) the feeding tube lecture and using that time for clinical case discussions is a really interesting idea. Applying the concepts from across the course to real life cases is something I think would add a lot of value, and it’s certainly something I’ll consider as part of the redesign.
It’s also reassuring to hear that you don’t see any major omissions, and your comments regarding faecal microbiota transplantation echo some of my own thoughts about where it currently sits in day-to-day primary care practice.
One other question, if you don’t mind: do you feel the course was pitched at the right level? Did you find it challenging enough, and did you come away with enough genuinely new information that changed or influenced your clinical practice? That’s something I’m particularly keen to improve as I update the content.
Thanks again for your help and for completing the course in the first place. I’ll make sure you’re entered into the prize draw!
All the best,
Scott š
Hi Silvana,
Yeah, this is really interesting. I’ve actually been aware of this drug for a while, but to be quite honest I haven’t seen it used commercially where I’m working in Canada, so I haven’t had any firsthand experience with it.
Your post has definitely made me think about it again though. I actually wonder why it hasn’t taken off more widely. I suppose part of the reason is that many of us are very comfortable using darbepoetin. We use darbepoetin quite a lot in our CKD patients, and I suspect we continue to reach for it because it’s familiar and we’ve generally had good success with it.
That said, the mechanism behind molidustat is fascinating. It belongs to a newer class of drugs called hypoxia-inducible factor prolyl hydroxylase inhibitors (HIF-PHIs). Rather than supplying exogenous erythropoietin, these drugs work by inhibiting HIF-prolyl hydroxylase enzymes, which stabilizes hypoxia-inducible factor (HIF). This leads to increased endogenous erythropoietin production, along with effects on iron metabolism, including reduced hepcidin concentrations and improved intestinal iron absorption and transport. In theory, this may produce a more physiologic stimulation of erythropoiesis while also addressing some of the iron dysregulation that contributes to anaemia in CKD patients.
The early efficacy data are certainly encouraging. In the pilot study that supported conditional FDA approval, around 50% of cats achieved either a 4% absolute increase in haematocrit or a 25% increase from baseline by day 28. By day 56, approximately 75% of cats had achieved a clinically meaningful response. The most common adverse event was vomiting, and notably hypertension and seizures were not reported in the study population. A subset of cats was followed for an additional eight weeks and maintained their increased haematocrits while also gaining weight and maintaining stable blood pressure.
One thing I find particularly interesting is that HIF-PHIs may offer advantages in cats that are ESA-resistant or hyporesponsive. Because they also improve iron homeostasis and downregulate hepcidin, they may potentially help address some of the inflammatory and iron-restricted components of CKD-associated anaemia. If larger studies continue to show no worsening of hypertension, they may eventually prove especially useful in cats with concurrent CKD and systemic hypertension.
That said, I don’t think we can say it has been shown to be better than darbepoetin at this stage. As far as I’m aware, there are no head-to-head studies comparing molidustat directly with darbepoetin in cats with CKD-associated anaemia. The advantages are currently more theoretical and practical than proven: oral administration, endogenous erythropoietin stimulation, effects on iron regulation, and conditional approval specifically for feline CKD-associated anaemia.
The safety data are also worth considering. In laboratory studies involving healthy cats, higher doses resulted in significant erythrocytosis/polycythaemia, with some cats removed from the studies after haematocrits exceeded 60%. Clinical findings included abnormal mucous membrane colour, prolonged capillary refill time, tachycardia, and evidence of increased blood viscosity. Histopathologic findings included vascular congestion and thrombotic lesions affecting multiple organs, changes that were attributed to the drug’s pharmacologic effect of stimulating erythropoiesis. Other findings included mild increases in creatinine, potassium, vomiting, and occasional elevations in liver enzymes. Most of these effects were observed at doses higher than those intended clinically, but they certainly reinforce the need for careful monitoring.
The current conditional approval specifies administration at 5 mg/kg orally once daily for up to 28 days, followed by a mandatory treatment break of at least seven days. Weekly haematocrit monitoring beginning around day 14 is recommended to ensure the haematocrit does not exceed the upper reference limit, and treatment should be discontinued if polycythaemia develops.
Your post has definitely made me reconsider it, and I think it’s something worth keeping a close eye on. I’d actually be interested in speaking with our inventory manager to see whether it’s available to us, because I do think it could be worth bringing a bottle in and trying it in some selected patients.
I’m already thinking of a handful of CKD cats that are currently receiving darbepoetin where this might represent a reasonable alternative. It would be fascinating to hear from anyone who has used it in practice and how their patients have responded.
Best wishes,
Scott š
Replying to Silvana S. 14/06/2026 - 09:49
Hi Silvana,
The radiologist actually came to a similar conclusion regarding the lungs, describing a mild bronchial pattern that could certainly fit with chronic bronchitis, although they felt age-related change couldn’t be completely excluded.
The rib changes you mentioned were one of the things I looked at closely as well, but there was no evidence of an aggressive rib lesion or neoplastic process reported.
The incidental finding I was hinting at was actually much more subtle (and much stranger!). The radiologist identified multiple thin linear metallic opacities in the cranial abdomen, most consistent with migrating barbecue bristle foreign bodies.
To be fair, they’re quite difficult to spot on the images, so if you’re struggling to see them you’re definitely not alone. š If people are interested, I can try re-uploading the images with some annotations or adjusted contrast to help highlight where they are.
Thanks for having a go at it!
Scott š
Replying to Sara Prior 13/06/2026 - 19:06
Hi Sarah,
That small round opacity caught the radiologist’s eye as well, but it was ultimately interpreted as most likely an end-on vessel rather than a true pulmonary or hepatic lesion.
The incidental finding I was actually hinting at was elsewhere in the image. There are multiple thin linear metallic opacities in the cranial abdomen, which the radiologist felt were most consistent with migrating barbecue bristle foreign bodies.
To be fair, they are quite difficult to see, so if you’re struggling to spot them, don’t feel bad. š If there’s interest, I can try re-uploading the images with some annotations/highlighting to make them easier to identify.
It’s one of those findings that’s easy to miss initially because your attention naturally gets drawn to the thorax and the reason the radiographs were taken in the first place.
Scott š
Hi Lesley,
How are you?
Thanks for sending this through. PIMA is definitely one of those diagnoses that most of us don’t encounter very often, and I think it is easy to assume the prognosis is poor when you first see these dogs because they often present with such profound anaemia and seem frustratingly slow to respond to treatment.
Looking at the information you’ve provided, I think PIMA is certainly a reasonable concern. The anaemia is severe, with an HCT of only 16% and haemoglobin of 4.8 g/dL, but the reticulocyte count is only 26 Ć 10ā¹/L, which is clearly non regenerative. In a dog with classical IMHA and a haematocrit this low, I would generally expect to see a much stronger regenerative response unless we had caught the disease very early. The lack of regeneration despite severe anaemia is one of the key findings that pushes me toward considering PIMA.
The pathologist’s comments are helpful and largely reflect our current understanding of the disease. In classical IMHA, antibodies target mature circulating red blood cells, resulting in haemolysis, spherocytosis, agglutination and a strong regenerative response. In PIMA, the immune system appears to target erythroid precursors within the bone marrow instead. As a result, the marrow is unable to effectively release mature red cells despite profound anaemia. Many of these dogs have little or no evidence of peripheral haemolysis, and some will be Coombs positive while others are not.
One thing I would say is that I would still want to be careful before fully committing to the diagnosis without bone marrow evaluation. The mild microcytosis and occasional spherocytes are not particularly convincing for IMHA, but they do remind us that chronic blood loss remains a differential. As your pathologist mentions, chronic gastrointestinal bleeding can eventually become non regenerative once iron deficiency develops. That is usually something worth excluding if it has not already been investigated.
The paper that I find most useful when discussing prognosis is the Michigan State University study by Assenmacher and colleagues, which evaluated 66 dogs with PIMA. The median haematocrit in that population was only 13%, remarkably similar to what you’re seeing here. Many dogs were just as severely affected as this patient at diagnosis. Despite that, 83% of dogs eventually developed a regenerative response and approximately 60% achieved remission. Median survival time for the entire cohort was 913 days, which is around 2.5 years. That is considerably better than many clinicians expect when they first encounter these cases (Assenmacher et al., 2019).
What I think is particularly important from that study is the timeline. These dogs rarely respond quickly. The median time to a regenerative response was 29 days, and some dogs took more than 100 days to respond. Median time to remission was approximately 59 days. In other words, many dogs are still profoundly anaemic several weeks after diagnosis despite appropriate immunosuppressive therapy. This is often where clinicians and owners start to lose confidence in the treatment plan, when in reality the dog may simply not have had enough time yet to respond.
The authors actually commented that a substantial proportion of deaths and euthanasias occurred because treatment was perceived to have failed before a regenerative response had a chance to occur. That is probably one of the most clinically useful messages from the paper. Owners need to understand from the outset that this is often a marathon rather than a sprint.
The need for transfusion support is also very common. Over 90% of dogs in the study received packed red cell transfusions, with many requiring multiple transfusions. Some dogs received as many as ten transfusions before eventually responding. Therefore the fact that she has already needed a blood transfusion does not concern me particularly and would be entirely consistent with the published experience.
In terms of treatment, prednisolone remains the foundation of therapy. Most clinicians will add a second immunosuppressive agent, particularly in severe cases. Historically azathioprine, cyclosporine and mycophenolate have all been used. Unfortunately, gastrointestinal toxicity is one of the more common reasons we end up abandoning mycophenolate. If that happens, cyclosporine would probably be my next choice. Some clinicians will also use a combination of prednisolone and cyclosporine from the outset in more severe cases.
An interesting recent publication by Yuki and colleagues described two dogs with confirmed PIMA that failed to respond adequately despite treatment with prednisolone and conventional immunosuppressive agents. Oclacitinib was added to the protocol and both dogs subsequently achieved complete remission. The proposed mechanism is inhibition of JAK1 mediated cytokine signalling involved in immune dysregulation. Obviously this is only a two case report and far from definitive evidence, but it does suggest that oclacitinib may become an option for refractory cases in the future (Yuki et al., 2023).
Another point that has increasingly changed my management of these patients is thrombosis risk. Historically we have thought of thromboembolism primarily as an IMHA problem, but the PIMA data suggest that thromboembolic disease may also be important in these dogs. In the Assenmacher study, confirmed thromboembolic events occurred in 14% of cases and were associated with dramatically shorter survival times. Dogs that developed thrombosis had a median survival time of only 54 days compared with over 1,300 days for dogs that did not. Pulmonary thromboembolism, portal vein thrombosis and splenic vein thrombosis were all documented.
For that reason, unless there is a contraindication, I generally think seriously about thromboprophylaxis in these patients, particularly those receiving high dose steroids, requiring repeated transfusions or showing evidence of hypercoagulability.
One reassuring finding from the literature is that bone marrow fibrosis, which often sounds alarming when reported, was not associated with a significantly worse prognosis. Nearly half the dogs in the Michigan State study had evidence of collagen myelofibrosis on marrow biopsy, yet many still achieved remission and long term survival. Therefore if fibrosis is reported on the marrow evaluation, I would not automatically assume the prognosis is poor.
Overall, my feeling would be that if bone marrow findings support PIMA, I would describe the prognosis as guarded but certainly not hopeless. The next few weeks are often the most difficult period because the dog remains dependent on transfusion support while waiting for the immunosuppressive therapy to work. However, if she can be supported through that period, there is a realistic possibility of achieving remission and a good long term outcome based on the available literature.
I’d be very interested to know whether a marrow aspirate or core biopsy has been performed and, if so, what the findings were. That would probably be the most important piece of information in refining both diagnosis and prognosis.
Best wishes,
Scott
References
Assenmacher TD, Jutkowitz LA, Koenigshof AM, Lucidi CDA, Scott MA. Clinical features of precursor targeted immune mediated anemia in dogs: 66 cases (2004ā2013). Journal of the American Veterinary Medical Association. 2019;255(3):366ā376.
Yuki M, Taira H, Narita M, Inden T, Yokota S, Naito E, Maeda S. Complete remission of two canine cases with precursor targeted immune mediated anemia after combination therapy with prednisolone, cyclosporine and oclacitinib. Open Veterinary Journal. 2023;13(9):1205ā1211.
Replying to Raquel M. 10/05/2026 - 14:22
Hi,
Thanks so much for sharing this. Suga sounds like a really interesting case, and honestly it sounds like youāve done an excellent job managing him given the limitations of access on island. Catching hypoglycemia on that first visit, especially in a dog that was not overtly crashing clinically, is incredibly valuable and exactly why these cases can be so easy to miss initially. I completely agree that sometimes the glucose result is so low relative to how the dog appears that you almost feel obligated to double check it before believing it.
It also sounds very reasonable to continue with prednisone if he is clinically stable and the owners are comfortable. I think many of these cases end up being a balance between ideal management and what is realistically accessible both financially and geographically. Diazoxide can work extremely well clinically, but Iāve also found the cost can become a major limiting factor very quickly, particularly for larger dogs or long term management. I suspect that is one of the major reasons it remains underutilized despite how effective it can be in some patients. Palladia is definitely interesting as well, although we still do not have especially robust prospective data for it yet.
I think you handled the referral discussion appropriately too. Even if owners ultimately decide not to pursue CT or surgery, it is still important they understand those options exist, particularly given the survival differences reported in the paper. In your setting especially, there are obviously additional logistical hurdles beyond what many owners face on the mainland. Where would you send for CT?
Iāve had good experiences with CGMs overall. I do think they can be very helpful in selected patients, particularly diabetic cats where in hospital curves are often stressful and misleading, but sensor quality, placement, and owner compliance all make a huge difference. I probably find them more useful for trends and pattern recognition than for making decisions based on single absolute numbers. Interestingly, they can be less accurate a lower levels.
Really appreciate you sharing the case!
Scott š
Replying to Emma Holt 18/05/2026 - 21:20
Hi,
I think that is probably a big part of it, honestly. We are imaging patients much earlier and much more frequently now, especially older dogs undergoing staging CTs or workups for unrelated problems, so we are likely identifying many of these lesions at a much earlier stage in their biological progression than we historically would have. Years ago, many of these masses probably only came to attention once they were large enough to cause clinical signs, vascular invasion, or obvious endocrine disease.
I completely agree with your approach as well. I still think these cases need to be individualized and interpreted in the context of the whole patient. Why we are imaging the patient in the first place really matters, because the context can be very different depending on whether the adrenal gland is truly suspected to be clinically relevant versus being an incidental finding during imaging for something unrelated.
I suppose one of the more common reasons we specifically evaluate the adrenal glands clinically is concern for hyperadrenocorticism, but as you know, in many of those patients we are actually seeing bilateral adrenal enlargement associated with pituitary dependent disease rather than a unilateral adrenal mass. Overall, it is still less common that we identify a unilateral adrenal lesion that then becomes the major focus of the case.
I always have a fairly detailed discussion with owners about how far they would realistically want to pursue things diagnostically and therapeutically. I do think assessment for functionality is important, although I would generally only be pursuing Cushingās testing if there are compatible clinical signs or supportive clinicopathologic changes. Investigation for pheochromocytoma can obviously be much more challenging, but that definitely remains an important differential consideration as well.
I think ultimately many of these cases still come down to careful monitoring and serial reimaging, particularly in patients where surgery is not something the owners would realistically pursue. At the same time, I do think this paper shifts my level of concern about assuming that a small lesion is biologically āquietā simply because of size alone.
Really interesting topic overall, and I suspect our recommendations will continue to evolve quite a bit over the next few years as more data emerges.
Scott š
Replying to Lucy Bennett 02/05/2026 - 13:48
Hi Lucy š
Itās really nice to meet you and congratulations on William thatās such a special time even if returning to clinical work in small steps can feel a bit strange at first. It sounds like youāve already done a huge amount with your imaging certificate so the instinct to revisit and strengthen those disease pattern links makes a lot of sense and will pay off quickly once youāre back seeing cases regularly.
That Frenchie sounds like a genuinely frustrating case and honestly the kind that tests everyone especially when you inherit it partway through and finances are tight. Youāre thinking about it in exactly the right way though. The vomiting versus regurgitation distinction is key but can get very blurred in real life particularly once a case has been going on for a week. Owners often describe a mix because repeated vomiting can lead to oesophageal irritation and secondary regurgitation or vice versa. The timing clue you mentioned is helpful but not absolute as regurgitation is often soon after eating or drinking but not always especially if there is oesophageal dysfunction or intermittent obstruction.
I think Frenchies in particular are always really challenging in this space. Even when you are specifically looking for something like a hiatal hernia it can be very frustrating because you will not always see it on standard imaging and even on CT it can be missed if it is intermittent. Sometimes you do need something dynamic like a fluoroscopic swallow study to really demonstrate what is happening in real time. Alongside that I think it is always important to step back and assess how much the BOAS component is contributing because the upper airway and reflux cycle in these dogs can be a big driver of ongoing clinical signs.
In terms of differentials I would still keep things broad. Gastrointestinal causes like partial foreign body pyloric outflow obstruction or severe gastritis remain possible even with previous imaging as these can be subtle or evolving. Pancreatitis is always worth keeping in mind in this breed. Oesophageal disease becomes more relevant with the regurgitation component so reflux esophagitis intermittent hiatal hernia or other functional oesophageal disorders all fit within the picture.
From a practical standpoint I tend to approach these cases like other chronic GI patients as well. A GI panel including cobalamin and folate can be useful to build a bigger picture and endoscopy is often indicated if things are not resolving. A lot of these dogs will have some degree of inflammatory disease within the stomach or intestines so if nothing structural is identified and they are not improving then a steroid trial can be reasonable alongside the fundamentals like dietary modification and good supportive care. At the same time I would still continue antiemetic support if vomiting is part of the picture and tailor that based on response.
The lack of response to maropitant and supportive care does make me lean a bit more toward an ongoing structural or functional issue rather than simple gastritis but cases like this often end up being multifactorial which is why they can feel so difficult.
Really glad to have you on the course and I hope the first KIT day back felt like a good step rather than an overwhelming one.
Keep the questions coming!
Scott š
Replying to Lucy Bennett 02/05/2026 - 16:08
That sounds like a great journal club paper, Lucy. It is one of those studies that is immediately practice-relevant because it challenges a rule many of us have probably carried for years: sharp object equals no emesis. I still think there needs to be a lot of case selection here, especially witnessed ingestion, asymptomatic dog, likely gastric location and a sensible discussion with the owner about uncertainty, but it is reassuring to see that emesis was successful in a good proportion of cases and no complications were recorded in that group. Iād be really interested to hear what your team makes of it after journal club.
Scott š
Replying to Sophie L. 03/05/2026 - 15:07
Hi Sophie,
In general, placing a urinary catheter with a closed collection system can be helpful from an infection control perspective in suspected or confirmed leptospirosis cases, particularly in dogs that are polyuric or difficult to manage in terms of urine containment. It allows you to minimise environmental contamination and reduces the risk of staff exposure, which is especially relevant in busy hospital settings where maintaining control of urine can be challenging.
That said, it would not be inappropriate to place a catheter, but I would not do this routinely. If the patient is stable and manageable, good barrier nursing with appropriate PPE and cleaning protocols is usually sufficient. I would often prioritise taking these patients outside more frequently so they are not urinating throughout the hospital environment, which can be a simple and effective way to reduce contamination risk.
If the patient is oliguric or anuric, then catheter placement becomes more appropriate from a monitoring perspective, as you want to accurately assess urine output. It can also be useful in more critical or recumbent patients where containment is otherwise difficult.
One important consideration is that urinary catheter placement does carry a risk of increasing urinary tract infections, particularly if left in place for longer periods, so that risk has to be balanced against the infection control benefits.
So overall, catheterisation is a reasonable option in selected cases, but not something I would consider routine if you are able to manage the patient safely with good nursing care and hygiene practices.
Glad you are enjoying the course, and keep the questions coming.
Scott š
Replying to Mirja S. 21/04/2026 - 15:41
No problem!
Let me know if you have any other questions. I hope you are having a lovely weekend.
Scott š
Replying to Felipe M. 23/04/2026 - 22:22
Felipe!
This is so interesting, thank you for sharing.
Scott š
Hey Rosie!
So lovely to hear from you. I hope all is well with you. Great question!
I will make sure Felipe sees this question and we will get back to you.
Schnauzer by any chance?!
Scott š
Replying to Mirja S. 16/04/2026 - 14:34
Hi Mirja,
These are great questions!
I think the āsneezy, snottyā geriatric cats are cases I certainly see a lot. Itās often that cycle of an initial infectious triggerāsomething bacterial or viral like herpesvirusāwhich then leads into this ongoing cycle of inflammation that just perpetuates itself.
At the root of many of these cases, thereās an underlying inflammatory process, often something like a chronic lymphoplasmacytic rhinitis. Because of that, many of them are actually steroid responsive.
If youāre reluctant to use steroids (which is completely reasonable, especially with CKD and age in the background), Iām also not a huge fan of repeated antibiotic trialsābut a short course (e.g. a couple of weeks of doxycycline) can be reasonable if youāre concerned about secondary bacterial involvement.
That said, I think in most of these cats, any infection at this stage is secondary rather than primary, and the main issue is inflammatory/immune dysregulation within the nasal passages.
If you want to avoid steroids, the main alternative Iād consider would be cyclosporine, targeting that underlying inflammatory component.
In terms of other options and diagnostics:
Lysine: no longer strongly recommended based on current evidence, though still sometimes used
Iām generally not a fan of superficial nasal swabs in these casesYou could consider a deeper nasal or nasopharyngeal swab for a full respiratory PCR panel (including herpesvirus) if you felt it would change management
From an investigation standpoint, more definitive options would include advanced imaging and guided nasal biopsies, although in many of these patients thatās not pursued.
In terms of maropitant:
Systemically, it can help with appetite and nausea, but itās not really a primary respiratory treatment
There has been some more recent evidence suggesting intranasal maropitant may not be as effective as previously thought, which is a bit disappointing (though studied in a slightly different population).Anecdotally, some cats seem to benefitābut that may partly be due to the act of instilling something into the nose, giving mild topical or flushing relief.
Supportive care still plays a role:
Nebulisation is a good option.
You could consider topical/intranasal steroids if trying to avoid systemic effects
That said, systemic steroids are generally more reliably effective when needed.So practically, Iād approach these as chronic, manageable inflammatory conditions, using trial-based therapy depending on what the owner is comfortable with.
On Cartrophen (pentosan polysulfate) and tracheal collapse:
Iāve never used it for this indication, and Iām not aware of any good evidence supporting it. The rationale is likely extrapolated from cartilage support, but this would be considered anecdotal rather than established.
Itās not something I would describe as a recognised or evidence-based treatment for tracheal collapse.
Thank you so much for your questions and thank you for joining the course and supporting vtx!
Scott š
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