scott@vtx-cpd.com
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Replying to Christina Frigast 23/04/2025 - 09:02
Hi Christina,
Thank you so much for sharing this case and for your thoughtful reflections. What a difficult and emotional situation to manage, and I think you handled it really well given the information available at each step. It is completely appropriate to bring this topic up here, and I am really glad you did because it raises some very important points about the early recognition and management of occult hemorrhage.
In cases like this, where we have a strong mechanism of injury, clinical signs that are not fully explained by initial imaging, and a persistent tachycardia despite otherwise reassuring parameters, I would absolutely be thinking about early occult hemorrhage. As you highlighted, it can be very challenging because PCV often lags behind active bleeding by several hours, and initial AFAST/TFAST scans can be negative if the bleeding rate is slow, intermittent, or if blood is initially sequestered within tissue planes like the retroperitoneal space or mesentery. Serial focused imaging, careful hemodynamic monitoring, and early suspicion are really the key tools at our disposal. You did all of these things really well.
In terms of specific treatments to slow or stop internal bleeding in these scenarios, there is no perfect medical option unfortunately. Some clinicians will consider the use of antifibrinolytics such as tranexamic acid, especially if there is a suspicion of ongoing hemorrhage but surgical control is not immediately possible or is being planned. The evidence for tranexamic acid in veterinary trauma is still limited, but extrapolating from human trauma protocols like CRASH 2, it is something worth considering at a dose of around 10 to 20 mg/kg IV over 10 minutes. That said, tranexamic acid will not stop major vessel bleeding or extensive retroperitoneal hemorrhage; it is more about stabilizing microvascular hemorrhage and slowing clot breakdown.
Regarding blood transfusions, yes, in cases like this where I have a high suspicion of occult bleeding, I am more inclined to plan early for transfusion even before the PCV drops significantly. Indicators that might push me toward early transfusion planning would include persistent tachycardia despite fluids, a rising lactate or failure of lactate to clear, signs of hypoperfusion such as low urine output or falling blood pressure, and certainly any positive AFAST or free fluid detection. Early crossmatching and blood typing, and even preemptive ordering of blood products if resources allow, can be really helpful.
You did absolutely the right thing by monitoring closely, repeating imaging, adjusting your management when clinical signs changed, and recognizing when surgical exploration was needed. Unfortunately, retroperitoneal bleeding can be very difficult to detect and manage medically, and even with early transfusion, the outcome might not have changed in this case given the extent of internal trauma.
It is such a sad outcome but I think you should be reassured that your clinical judgment was spot on and that you gave her every reasonable chance. Thank you again for sharing this, it is an excellent and important question and absolutely worth discussing.
All the very best,
Scott
Hi Christina,
Thanks so much for your really thoughtful question. It is a great one, and not an easy area to manage, especially when no clear underlying cause for the hypoalbuminemia can be found.
In general, my approach would be to start by trying to identify or exclude common causes if possible. Even if no obvious GI, liver, or renal disease is evident, I usually revisit the possibilities carefully. For GI losses, I look for more subtle signs such as hypocobalaminemia, low cholesterol, or changes on ultrasound. For liver function, I check synthetic markers including glucose, cholesterol, BUN, and coagulation times. For renal causes, I always recommend checking a UPC ratio even if azotaemia is not present. I also keep in mind that systemic inflammation, sepsis, neoplasia, heatstroke, or endocrine diseases such as Addison’s can contribute to significant hypoalbuminemia through vascular leakage and altered hepatic synthesis. If no clear cause is found, I often categorize it as critical illness-related hypoalbuminemia secondary to systemic inflammation and endothelial dysfunction.
When peripheral edema or ascites is present, if it is mild to moderate, I tend to focus first on treating the underlying disease, optimizing nutrition, and providing cautious fluid therapy. If edema or ascites is severe or causing respiratory compromise, I would typically intervene, often with therapeutic abdominocentesis to relieve pressure and, if possible, plasma or albumin support.
In terms of plasma transfusions, plasma is generally much more useful for addressing clotting factor deficiencies than for meaningfully replacing albumin. Very large volumes, around 20 to 25 mL/kg, are needed to make any meaningful increase in albumin levels, and even then, studies show plasma can sometimes dilute albumin rather than improve it in critically ill patients.
When considering albumin therapy, ideally I would use canine-specific albumin where available. It is safe, effective, and carries a much lower risk of hypersensitivity reactions compared to human albumin products. If canine albumin is not available, human serum albumin can be considered, but it carries significant risk of both immediate type I hypersensitivity reactions and delayed type III hypersensitivity reactions, including serious complications such as vasculitis, glomerulonephritis, and in some cases death. Critically ill dogs do seem somewhat protected against acute reactions compared to healthy dogs, but they still develop antibodies against human albumin weeks after exposure. It is critical that clients are informed about these risks before human serum albumin is administered. Diluting it to a 5 percent solution and giving it as a slow infusion appears safer than rapid 25 percent infusions, but it does not eliminate the risk entirely.
If plasma or albumin products are not available, alternative strategies include early aggressive enteral nutrition to provide the building blocks needed for hepatic albumin synthesis and judicious use of isotonic fluids to maintain perfusion while avoiding overload. If ascites is causing respiratory compromise, therapeutic abdominocentesis can be very helpful.
For dosing guidance, to estimate the albumin deficit, the following formula is useful: Dose of albumin in grams equals ten multiplied by the difference between two and the patient’s albumin in grams per deciliter, multiplied by bodyweight in kilograms, multiplied by 0.3. The general goal is to raise albumin to at least two grams per deciliter where possible. Any albumin administered will initially replenish the interstitial albumin pool before serum albumin levels rise, which makes targeting specific goals a bit challenging and highlights the importance of clinical monitoring.
In summary, I would consider albumin supplementation particularly if the albumin concentration is less than 1.5 grams per deciliter with clinical signs of oedema or effusion. I focus on treating any underlying disease, prefer using species-specific albumin if available, use human serum albumin cautiously only when necessary, and understand that plasma alone is not an efficient method for albumin replacement unless there are concurrent coagulation abnormalities. Supportive care, close monitoring, and clear communication with the owner are key parts of managing these complex cases.
All the best,
Scott :
Replying to Christina Frigast 23/04/2025 - 08:34
Hi Christina,
Thank you so much for sharing that case. What an excellent and very real-world example of how tricky and subtle sepsis can be early on. I completely agree with you: one of the biggest challenges is that many of these patients do not “look septic” at first, especially when their initial vitals are relatively stable and clinical signs are non-specific.
I think you did absolutely the right thing in this case. Recognizing that something was not adding up, reassessing as the patient evolved, and making the call to refer when you did likely made a real difference to his chances. It is so easy in hindsight to spot the patterns, but in the moment it is incredibly hard, especially when juggling many patients and limited diagnostics OOH.
I also found the paper a really helpful reminder that sepsis is a spectrum, not a binary state, and that it can develop quite insidiously before tipping into a more recognizable critical illness. I love that you are using the experience to reflect and build on your already very strong clinical instincts. That is the most important thing.
Was the patient on antibiotics when you first saw him? It would be really interesting to hear more about that aspect too.
I will also pass this case on to Kerry and Neus for their comments. I think it would be a really great one for us all to learn from and discuss a bit more.
Thank you again for taking the time to share, and I am really glad he made it to ICU. Fingers crossed he continues to do well.
All the best,
Scott
Replying to Jane Sedgewick 22/04/2025 - 20:07
Jane, have you ever used trazodone in cats for this purpose?
I recently came across an interesting study published in Journal of Feline Medicine and Surgery (Tucker et al, 2024) looking at the sedative properties of oral trazodone, gabapentin, and their combination in healthy cats. They evaluated 21 cats and found that trazodone alone at 5 mg/kg, or the combination of trazodone 5 mg/kg plus gabapentin 10 mg/kg, produced significant sedation compared to placebo. Gabapentin alone at 10 mg/kg did not achieve significant sedation in this group. The combination seemed to produce the most profound effect, and there were no obvious side effects reported.
It made me wonder whether trazodone might have a role alongside or instead of gabapentin in certain cases, especially for cats that do not respond as well to gabapentin alone. I have not used trazodone routinely in cats for this indication myself, but would be interested to know if you or anyone else has any experience with it, and whether you think it could be a useful option.
Would love to hear your thoughts.
Scott 🙂
Replying to Jane Sedgewick 22/04/2025 - 20:07
Hello!
Thank you, I completely agree, this definitely fits with my experience as well. Gabapentin has been such a helpful tool for improving the vet visit experience for stressed cats.
You raise a really good point about potential effects on blood parameters, particularly T4. Based on available studies, gabapentin does not appear to have a clinically significant impact on routine biochemistry, haematology, or total T4 measurements in cats when used as a single pre-visit dose. For example, van Haaften et al. (2017) demonstrated that a single 100 mg dose of gabapentin significantly reduced signs of fear and stress in healthy cats during transport and examination, without altering serum biochemistry results. Similarly, the recent study specifically investigating hyperthyroid cats did not report any measurable changes in blood parameters, including T4, although it is important to note that the primary outcomes were behavioural rather than biochemical.
However, sedation and reduced stress can theoretically influence other physiological parameters such as heart rate, blood pressure, and potentially glucose concentration. These changes are likely mild but are worth considering if interpreting results in borderline cases. At this point, no strong evidence suggests gabapentin interferes with T4 measurements in a clinically meaningful way when used appropriately.
Regarding Bonqat (pregabalin), it is an interesting option. From a cascade standpoint, it would technically be preferred over human gabapentin products now that an approved veterinary pregabalin exists. Clinical experience with pregabalin in cats, however, is still relatively limited. A few studies have investigated its use:
Benito et al. (2022) conducted a study evaluating the pharmacokinetics, safety, and tolerability of pregabalin in healthy cats. They found it was generally well tolerated at doses around 5 mg/kg PO but noted dose-dependent sedation as the most common side effect.
Gruen et al. (2021) evaluated pregabalin for acute anxiety and fear responses in cats in a laboratory model. The study showed that pregabalin reduced stress-related behaviours compared to placebo, suggesting anxiolytic potential similar to gabapentin.
However, to date, there are no published head-to-head comparison studies between pregabalin and gabapentin in cats for vet visit stress, sedation, or procedural compliance. Extrapolation from human medicine suggests pregabalin might have a faster onset and potentially stronger anxiolytic effect than gabapentin, but clinical evidence in cats is still emerging.
Cost is also an important consideration, and while pregabalin may offer some advantages in terms of pharmacodynamics, the practical difference compared to gabapentin for most routine cases is still unclear based on the current evidence. Gabapentin remains much more widely used in practice at this stage.
I would be really interested to hear if anyone has already incorporated Bonqat routinely and how they feel it compares in terms of efficacy, ease of administration, and owner feedback.
I must admit, it is not really a drug I have used!
Scott 🙂
Replying to Jane Sedgewick 22/04/2025 - 20:03
Hello!
I hope you are well.
I agree, I think the main concern here is that trazodone could blunt the adrenal response enough to complicate interpretation either way. It could potentially make it harder to diagnose hypoadrenocorticism if the basal or post-ACTH cortisol is artificially low, but equally it could dampen the exaggerated response we might expect in a patient with Cushing’s, making a definitive diagnosis more difficult.
It is probably rare that we would need to use trazodone in these cases, but it is definitely worth remembering to avoid anxiolytic or sedative medications around the time of adrenal function testing whenever possible, just to minimise the risk of muddying the results.
Thank you again for sharing your thoughts and experience.
Scott 🙂
Replying to Janette B. 22/04/2025 - 14:32
Hey, no worries at all and thanks so much for getting back to me! That is really helpful to know, it is great to hear you are seeing such a clear benefit with the transversus abdominis plane blocks. I am not sure I have ever actually heard the words quadratus lumborum out loud before, let alone used it myself! 😅 Sounds like a really interesting option though, especially for the more painful cases. Thanks again for sharing your experience!
Scott 🙂
Replying to Helen S. 22/04/2025 - 12:49
Hey pal!
Thank you so much for sharing!
Have a wonderful week everyone!
Scott 🙂
Replying to Jane Sedgewick 21/04/2025 - 14:14
Hi Jane,
Thanks so much for your messages.
Your point about regional variation is fascinating. I agree it would be very interesting to look at more closely. I had not made the connection with “Derbyshire neck” before, but it makes complete sense to wonder about environmental or historical iodine factors influencing thyroid disease patterns. It would be really interesting to explore whether historical iodine deficiency could have left any lasting regional patterns in feline hyperthyroidism prevalence. If you are able to gather any broad figures from PDSA cases, that would be fantastic and could provide a really useful starting point for looking into this further.
On the monitoring side, regarding TSH, I do not recommend measuring it at every monitoring visit. If the TT4 is within the expected therapeutic range, typically in the mid to lower half of the reference range, and the cat is clinically well, then TSH does not usually add much additional value. Similarly, if the TT4 is low-normal and clinical signs have resolved, I would not routinely check TSH. However, TSH becomes particularly useful when the TT4 is in the low-normal range but clinical signs are persisting, or when there is concern that concurrent non-thyroidal illness could be artificially lowering the TT4 concentration. In these situations, measuring TSH can help differentiate between true resolution of hyperthyroidism and ongoing disease that is being masked by other factors.
If the TSH is suppressed, that would suggest that hyperthyroidism is still active despite the TT4 appearing low-normal. If the TSH is detectable or elevated, that would point more towards true resolution or iatrogenic hypothyroidism. It is important to note that TSH is not sensitive enough to be used for initial diagnosis of hyperthyroidism and must always be interpreted alongside TT4 or fT4 results. It also is not a standard part of every monitoring check unless clinical signs or bloodwork suggest it would add useful information.
In your current case, where the TT4 is low-normal but the cat is still showing clinical signs, measuring a TSH would definitely be valuable. It could really help clarify whether you are looking at persistent hyperthyroidism that is being masked by illness, early iatrogenic hypothyroidism, or whether another concurrent disease process is responsible for the ongoing signs.
Please do let me know if you would like to chat through your case in more detail, I would be very happy to. And thank you again for raising such thoughtful and practical points.
Best wishes,
Scott
Replying to Jane Sedgewick 21/04/2025 - 12:12
Hi Jane,
In terms of what I am personally seeing, interestingly, I am seeing more diabetes insipidus (DI), particularly partial or complete central diabetes insipidus (CDI), than psychogenic polydipsia (PP) in my current caseload. That could certainly reflect the type of cases being referred to me, but even in broader general populations, I think true CDI is perhaps a little more common than we have traditionally assumed, especially now that we are using DDAVP trials more routinely and are better able to identify partial forms that may previously have gone undiagnosed. That said, psychogenic polydipsia is still very much out there, and I would agree that there seems to be a trend toward increased cases in more anxious, highly attached post-pandemic dogs, particularly among designer crosses like cockapoos, cavapoos, and similar breeds.
In terms of signalment, CDI typically affects young to middle-aged dogs, often presenting between six months and six years of age, although some cases of partial CDI may present later. Large-breed dogs do appear to be slightly overrepresented, with breeds like Labradors, German Shepherds, and Dobermans cropping up a little more often, but it can certainly occur in mixed breeds as well. In the majority of cases, CDI is idiopathic. Secondary causes such as head trauma, neoplasia affecting the hypothalamic-pituitary axis, or severe inflammatory disease of the CNS are seen less commonly, and when they do occur, there are often accompanying neurologic signs.
You are absolutely right that the population you are seeing, for example a PDSA caseload, can have a big impact on how often you encounter these conditions, and I think your observations from practice are spot on. It is really interesting how these patterns shift depending on the setting.
It is also worth noting that the literature is very sparse when it comes to psychogenic polydipsia. There are very few robust studies available, and much of what we know is extrapolated from case series or anecdotal reports. Definitely another area that would be well worth publishing in if someone had a suitable case series or a structured approach to diagnosis and management.
I am very grateful for your engagement.
Best,
Scott 🙂
Replying to Rachel H. 26/04/2025 - 16:02
No problem!
Let me know if you have any other questions!
Scott 🙂
Replying to Rachel H. 20/04/2025 - 15:43
Hello, thank you so much for your message and I’m really glad to hear you are enjoying the course so far!
That’s a great question and you are right that several medications can influence thyroid testing results. However, when it comes specifically to causing an increase in TSH, sulfonamides are the clearest and most direct cause among the options listed.
Here’s why:
Sulfonamides (especially potentiated sulfas like trimethoprim-sulfa) directly inhibit thyroid hormone synthesis. This leads to low T4 and T3 levels, which in turn causes the pituitary to respond by increasing TSH. So the sulfonamides both lower thyroid hormone and trigger a compensatory TSH rise.
Prednisolone typically causes suppression of TSH (and sometimes free T4 as well), not an increase.
Carprofen generally has minimal or no direct effect on TSH or thyroid hormones.
Potassium bromide can occasionally be associated with low T4 levels, but it does not consistently cause a TSH increase and the effect is much less direct compared to sulfonamides.
So while it is true that several drugs can affect thyroid testing, sulfonamides are the one in this list that cause a clear and predictable increase in TSH through a true hypothyroid-like effect.
Hope this helps clear it up and please feel free to reach out with any more questions!
Have a lovely weekend!
Scott 🙂
Replying to Rachel C. 25/04/2025 - 16:47
Hi Rachel,
Glad that was helpful!
When it comes to second line immunosuppressives, I tend to avoid azathioprine in most cases now, mainly because of the narrow therapeutic window, delayed onset of action, and potential for hepatotoxicity and bone marrow suppression. It can still be considered in certain situations, usually in larger dogs where cost is a limiting factor and close monitoring is possible, but it’s not my first choice.
In practice, I tend to go for mycophenolate mofetil in dogs, especially when I’m aiming to taper steroids or dealing with more severe disease. It has a faster onset than azathioprine and a better safety profile overall, with gastrointestinal side effects being the most common issue, though often manageable.
I prefer ciclosporin in cats and smaller dogs. It’s generally well tolerated and effective, but cost becomes a major barrier in large breed dogs, which limits its practicality in those cases.
I rarely use leflunomide, but it’s an option I might consider in more refractory or unusual cases.
Best,
Scott
Replying to Liz Bode 23/04/2025 - 21:03
Fancy seeing you here!
Scott 🙂
Replying to Spela Bavcar 21/04/2025 - 23:00
Spela!
Lovely to see you here!
Thank you so much for being brilliant!
Scott 🙂
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