scott@vtx-cpd.com
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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. 😊 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 🙂
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. 😊 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 🙂
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 × 10⁹/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 (2004–2013). Journal of the American Veterinary Medical Association. 2019;255(3):366–376.
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):1205–1211.
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 you’ve 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 I’ve 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?
I’ve 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 🙂
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 Cushing’s 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 “quiet” 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 🙂
Replying to Lucy Bennett 02/05/2026 - 13:48
Hi Lucy 🙂
It’s really nice to meet you and congratulations on William that’s such a special time even if returning to clinical work in small steps can feel a bit strange at first. It sounds like you’ve 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 you’re 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. You’re 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 🙂
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. I’d be really interested to hear what your team makes of it after journal club.
Scott 🙂
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 🙂
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 🙂
Replying to Felipe M. 23/04/2026 - 22:22
Felipe!
This is so interesting, thank you for sharing.
Scott 🙂
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 🙂
Replying to Mirja S. 16/04/2026 - 14:34
Hi Mirja,
These are great questions!
I think the “sneezy, snotty” geriatric cats are cases I certainly see a lot. It’s often that cycle of an initial infectious trigger—something bacterial or viral like herpesvirus—which then leads into this ongoing cycle of inflammation that just perpetuates itself.
At the root of many of these cases, there’s an underlying inflammatory process, often something like a chronic lymphoplasmacytic rhinitis. Because of that, many of them are actually steroid responsive.
If you’re reluctant to use steroids (which is completely reasonable, especially with CKD and age in the background), I’m also not a huge fan of repeated antibiotic trials—but a short course (e.g. a couple of weeks of doxycycline) can be reasonable if you’re 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 I’d 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
I’m 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 that’s not pursued.
In terms of maropitant:
Systemically, it can help with appetite and nausea, but it’s 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 benefit—but 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, I’d 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:
I’ve never used it for this indication, and I’m 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.
It’s 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 🙂
Replying to Laura S. 14/04/2026 - 19:41
Hi Laura,
That all makes complete sense, and I think what you’re describing is probably a very common driver for why people are reaching for Libres early, that understandable concern about missing hypoglycaemia at home, especially if there has been a bad prior experience in the practice. Those cases do tend to shape behaviour quite strongly.
I think the intention behind it is absolutely reasonable, but I’m not sure the Libre fully solves that problem in the early phase. In a newly diagnosed patient starting insulin, the variability is so high and the physiology is still settling, so even if you have continuous data, it does not necessarily translate into safer or more actionable decision making in those first few days. You can end up with a lot of data that looks reassuring or concerning without it actually reflecting what is truly happening in real time, particularly given the lag and early inaccuracy we talked about.
The scenario you describe with the ketotic but otherwise stable cat is a really interesting one. In that context, I do think a Libre can have some value in terms of trend monitoring and reducing handling, but I completely agree with you that it can feel like quite a significant expense for what is essentially additional reassurance rather than something that is clearly changing management. Especially if the patient is otherwise stable, on fluids, and you are already monitoring clinically and with intermittent blood glucose checks.
What you said about how you used to manage these cases is also really important, because that approach was always based on identifying general trends rather than exact numbers, and I think that principle still holds. Once you have seen a nadir and a rise, you have a reasonable sense of how that patient is responding in that moment, but as you pointed out, the day to day variability is substantial. The Fleeman and Rand paper really highlights that nicely, with quite a high proportion of cases where you would make a completely different dosing decision the next day despite identical conditions. So even what we consider structured curves are only ever a snapshot of a very dynamic system.
I think where that leaves us is that both curves and Libres have limitations, and neither should be over interpreted in isolation. In those early stages, particularly in newly diagnosed diabetics, I still think the priority is cautious insulin initiation, some targeted blood glucose monitoring, and close attention to the clinical picture rather than trying to achieve precision through dense data collection.
Where I do think Libres come into their own is a bit later, once things are more stable and you are trying to fine tune control or understand patterns in the home environment. That is where the additional data becomes much more meaningful and can genuinely guide decision making.
So overall I don’t think your instinct is off at all. Using a Libre for reassurance in those early cases is understandable, but it is probably not adding as much clinical value as it feels like it should, and in some cases may give a false sense of precision.
Never straightforward!
Scott 🙂
Replying to Silvana S. 13/04/2026 - 21:06
No problem!
Thank you for all of the brilliant interaction and questions.
I hope you are having a brilliant week.
Scott 🙂
Replying to Silvana S. 12/04/2026 - 10:00
Hi Silvana, great questions!
With active bleeding into the thorax, the CRT is not always increased. It can be, particularly if the dog is hypovolaemic and progressing toward shock, but early on it may still be normal. Remember that CRT is quite a crude parameter and can be influenced by stress, peripheral vasoconstriction, and examiner variation. In some dogs with haemothorax, especially if the bleeding is slower or partially contained, you may just see mild tachycardia and vague signs rather than obvious shock. So I would interpret CRT alongside heart rate, pulse quality, mentation, and lactate if available, rather than relying on it in isolation.
For rodenticide or other coagulopathies, you might see petechiae or ecchymoses, but not always. Petechiae are more typically associated with platelet disorders, whereas rodenticide toxicity tends to cause deficiencies in clotting factors, so you are often dealing with larger volume bleeding rather than pinpoint haemorrhages. In practice, dogs with rodenticide toxicity may present with cavitary bleeding such as haemothorax or heamoabdomen, and sometimes you will see external signs like bruising, bleeding from venipuncture sites, or epistaxis, but the oral exam can be completely unremarkable.
In a busy consult, the most useful clinical clues tend to be a combination of nonspecific signs like lethargy and hyporexia, plus cardiorespiratory changes such as tachypnea, increased effort, or muffled heart sounds. If something feels off, a quick point of care ultrasound is probably the highest yield next step, as it will very quickly tell you if there is pleural fluid present and help guide your next decisions.
I hope that helps!
Scott 🙂
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