scott@vtx-cpd.com
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Replying to Sarah Keir 25/08/2025 - 15:27
Hey Sarah!
Thanks so much for your reply.
Following the most recent biopsy, I’ve opted for a preventative strategy focused on stabilising ALT and mitigating long-term hepatic damage. In terms of management, I’ve added:
Zinc supplementation at 8–10 mg/kg/day of elemental zinc, divided BID, to limit further copper uptake and enhance hepatic sequestration. We’ll monitor serum zinc to guide dosing and avoid toxicity.
Vitamin E at 10 IU/kg/day (capped at 400 IU), aiming to provide antioxidant and anti-fibrotic support.
Liver-specific diet: transitioning to Purina Liver Support (HP), primarily for its reduced copper content. I appreciated your point about protein levels, I’ve flagged this to the owners to monitor condition score and muscle mass. Fortunately, Anchor is in excellent condition and the food is well tolerated so far.
Continuing supportive therapies: Denamarin, ursodiol, vitamin B12 injections, taurine, and probiotics.
We’re planning to recheck ALT, AST, ALP, GGT, B12, and serum zinc 12 weeks after all changes are in place.
The owners were understandably a bit hesitant about corticosteroids for now, especially given how well Anchor looks clinically. That said, I’ve left the door open to revisit a steroid trial if ALT remains persistently elevated or if clinical signs evolve.
Hope all is well with you otherwise!
Scott 🙂
Replying to Jacquin M. 24/08/2025 - 16:17
Hey Jacquin,
Thanks for sharing! Are you able to share the liver values and what the pre and post bile acids are? I would be interested to see if you are able to share them.
Hope you have a lovely weekend.
Scott 🙂
Replying to Julia Biernat 29/08/2025 - 09:53
Hey Julia!
I agree too! An interesting finding though.
I hope you are enjoying the course.
Scott 🙂
Replying to Sarah Keir 25/08/2025 - 15:32
Me too!
It is another interesting ‘cat thing’!
Scott 🙂
Hi Tori,
Zenrelia is available here in Canada where I practice, though I haven’t had any dogs come to me on it yet so I don’t have firsthand experience. The early trial data are certainly encouraging in terms of speed of effect, safety, and the convenience of once-daily dosing. I’d be really interested to hear your initial impressions and thoughts now that it’s available in the UK.
Scott 🙂
Replying to Laura S. 23/08/2025 - 20:29
No problem!
I will definitely check secondary coagulation factors before surgical liver biopsy, but not with FNA’s.
Would love to hear if other do differently!
Scott 🙂
Hey Felipe!
Thanks you for sharing another brilliant video!
Scott 🙂
Replying to Laura S. 17/08/2025 - 17:34
Hi Laura,
Thank you for these brilliant questions.
Yes, you are exactly right that severe dental and periodontal disease can be a source of systemic inflammation, and it is not unusual to see concurrent mild to moderate ALT or ALP elevations on pre-anesthetic bloodwork. In many cases, these enzymes normalise after the dental disease is addressed, sometimes with adjunctive hepatic support like Denamarin. So, in that sense, proceeding with the dental procedure can indeed be both therapeutic and diagnostic. The caveat, as you noted, is the anesthetic risk if there is concurrent, undiagnosed liver disease. The pragmatic approach with limited finances is to weigh welfare benefit against risk: if the enzymes are only mildly to moderately raised, the patient is otherwise stable, and the dental disease is severe and painful, then addressing the dental disease is a reasonable decision with informed owner consent. If the liver values are markedly elevated, synthetic function is impaired (low albumin, low urea, low cholesterol, abnormal clotting times), or the patient is systemically unwell, then I would be much more cautious.
This is supported by a growing body of evidence linking periodontal infection to distant organ changes in the liver, kidneys, and heart. Colin Harvey’s 2022 review (Vet Clin Small Anim, 52:121–137) summarises that bacteremia is common in dogs with periodontal infection, that stress indicators such as CRP and serum amyloid A increase with severity of periodontal disease, and that histopathological liver changes are more severe in dogs with advanced periodontal pathology.
Hepatic disease specifically has been linked with periodontal infection in two studies that found a correlation between increasing severity of gingivitis and periodontitis and increasingly severe microscopic changes in hepatic tissue (Pavlica et al. J Vet Dent 2008;25:97–105; DeBowes et al. J Vet Dent 1996;13:57–60). The liver is also the site of production of acute-phase proteins such as CRP and amyloid A, which increase with systemic inflammation and can be measured in serum, further reinforcing the systemic link between oral and hepatic health.
Yes, you are correct. In anorexic cats, it is not unusual to see mild hyperbilirubinemia, often related to cholestasis that develops secondary to reduced bile flow with fasting and dehydration. This is usually mild, transient, and resolves with rehydration and restoration of adequate caloric intake. Of course, one always has to be mindful of the possibility of true hepatobiliary disease in cats, but mild bilirubin elevation in an otherwise straightforward anorexic or dehydrated patient can often be explained by stasis.
From a safety point of view, I do not routinely run secondary coagulation parameters before performing FNAs of the liver. The most important thing is to ensure that the patient has an adequate platelet count, since platelets are the main determinant of whether a clinically significant bleed is likely. The relationship between liver disease and coagulation abnormalities is complex, because the liver produces both pro-coagulant and anti-coagulant factors, so standard clotting times do not correlate perfectly with bleeding risk. For this reason, I do not think they provide a reliable measure of safety in most cases. The key consideration is to establish that there is no obvious severe bleeding tendency, and I would only be especially cautious if there was evidence of more advanced hepatic dysfunction or distortion.
In practice, I have not encountered clinically significant haemorrhage from liver FNAs, whereas the risk with biopsy is considerably higher. So overall, FNAs are safe, routine coagulation profiles are not always essential, and the main thing is to ensure there is an adequate platelet count and the patient is clinically stable.
I hope that helps. Let me know if you have any other questions!
Scott 🙂
Replying to Laura S. 17/08/2025 - 13:12
Hey Laura!
Lovely to hear from you! Be brave next time! 🙂
The BBQ bristles caught my eye too! the stomach appearance was indeed due to the distribution of the homogeneous fluid/soft tissue opaque material and gas. This changed depending on the view.
I hope you are having a good weekend so far!
Scott 🙂
Replying to Elizabeth Murch 16/08/2025 - 13:13
Hey Elizabeth!
We are so lucky to have two specialist radiologists where I work! Makes my job a lot easier and means I can share these lovely reports/conclusions.
I am glad this was helpful. Let me know if you have any other questions.
Scott 🙂
Replying to Sarah Keir 14/08/2025 - 09:28
Hi Sarah,
I hope you are having a great start to your weekend!
That is a really interesting thought. NAC’s mucolytic effect comes from its ability to cleave disulfide bonds in mucoproteins, reducing the viscosity of secretions, and that is why it is used in respiratory medicine as a nebulised treatment in humans. To date there is no published evidence in veterinary medicine, or in human hepatology (that I can find), to support the use of NAC as a mucolytic in the biliary tract. When we use NAC in hepatobiliary cases, it is primarily for its antioxidant properties and role as a glutathione precursor, not for mucus breakdown. The way it works in the airways is by direct local contact with secretions at high concentration, which is difficult to replicate in the biliary system because systemically administered NAC is unlikely to reach the gallbladder in sufficient local concentration to act as a mucolytic.
For patients with early mucinous hyperplasia, the approaches that currently have the best rationale are monitoring with serial ultrasound, addressing any concurrent endocrinopathies such as hypothyroidism or hyperadrenocorticism, and in some cases using ursodeoxycholic acid to improve bile flow and reduce stasis. Do you agree? What is your approach when you find this sort of thing during your ultrasound scans?
So while in theory NAC’s mucolytic property is attractive, there is no evidence base at present to support its use for preventing or managing mucinous hyperplasia or mucocele development. I would still view NAC as valuable in sick animals that cannot tolerate oral medication, particularly for its hepatoprotective and antioxidant effects, but not as a gallbladder mucolytic. In patients with early mucinous changes I would focus on ursodiol and careful monitoring, and reserve NAC for those that are systemically unwell or unable to take SAMe.
Thanks again for sharing such interesting thoughts!
Scott 🙂
Hey Helen!
I hope you are well. Welcome to the course. We really appreciate your support and for choosing vtx!
Let us know if you have any other questions, or even feedback/suggestions for the course.
Have a great weekend.
Scott 🙂
Thanks Tori.
Interesting questions. Even I remember seeing lots of these cases when I worked at the PDSA many years ago!
Overrepresented in Rottweilers?
Scott 🙂
Replying to Kerry Doolin 22/08/2025 - 01:09
Thank you Kerry!
So interesting. Thanks for sharing the links.
Scott 🙂
Hi Aileen,
Based on her presentation and rapid full recovery, Border Collie Collapse (BCC) remains the most likely diagnosis.
Storm’s episode, featuring generalized ataxia, altered mentation, heavy panting, and congested mucous membranes, would understandably signal potential heat stroke, particularly with a recorded temperature of 40.3 °C. Initiating cooling measures and monitoring were the right steps. Yet, when you consider the moderate environmental temperature (muggy ~18 °C), the short exercise duration, and her swift return to normal, the features don’t align with typical exertional hyperthermia. Instead, they mirror what we know of BCC, a condition that tends to be triggered more by mental arousal and excitement than by heat or the length of exercise.
Distinguishing between early heat-related illness and BCC at initial presentation can be very challenging—both can present similarly, and early hyperthermia is common in both. Treating cautiously as a heat-related emergency is entirely appropriate in the acute setting. Over time, however, the pattern becomes clearer: BCC episodes are often reproducible, self-limiting, and occur within very specific contexts, with rapid recovery and no lasting neurological or systemic compromise. Detailed history remains your most powerful diagnostic tool.
You mentioned prior, milder wobbliness—these could very well have been partial expressions of BCC. Consistent context, lack of progression, and normal inter-episode exams reinforce BCC. Dogs affected by BCC typically do well in structured settings, such as agility, where arousal is managed and activities are controlled.
Regarding investigations: there remains no commercially available genetic test for BCC in Border Collies. The available DNM1/EIC test, offered by Laboklin and others—is specific to Labrador-type collapse and is not applicable to Border Collies. Laboklin’s genetic panel for Border Collies includes tests for conditions like CEA, MDR1, Sensory Neuropathy, and Trapped Neutrophil Syndrome, but does not cover BCC.
Research by Norton et al. (2021) in Genes (Basel) illuminates the genetic complexity of BCC. With a heritability estimate (h²SNP) of 49–61%, BCC is driven by thousands of genetic variants—ranging from small to large effect—across multiple loci on chromosomes 1, 6, 11, 20, and 28. This underscores that BCC is a highly heritable yet polygenic disorder, rather than a simple Mendelian entity. (Norton EM et al., 2021 Nov 29;12(12):1927) This complex nature explains why we don’t yet have a single-gene test.
Dr. Susan Taylor and collaborators have made significant contributions in this area. She was a professor at the University of Saskatchewan’s Western College of Veterinary Medicine, focusing on neurological and athletic canine disorders—including BCC. Their work includes standardized exercise studies, metabolic panels, video and questionnaire analyses, and ongoing DNA sample collection. Remarkably, none of the classic metabolic causes or the dynamin-1 mutation (seen in Labrador EIC) have been implicated in BCC, reinforcing its distinct and complex pathophysiology. You can read more on her profile here:
https://wcvm.usask.ca/departments/sacs/sacs-people/susan-taylor.php
Cardiac evaluation? Though Storm’s exam was normal, a Holter monitor—particularly during exertion or high arousal—could be prudent to rule out intermittent arrhythmias, even if these are unlikely given the BCC pattern.
I am interested to see what others have to say!
Warm regards,
Scott 🙂
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