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scott@vtx-cpd.com

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Viewing 15 posts - 1 through 15 (of 2,314 total)
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  • scott@vtx-cpd.com
    Keymaster

    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 🙂

    scott@vtx-cpd.com
    Keymaster

    Hey Felipe!

    Thanks you for sharing another brilliant video!

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster

    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 🙂

    scott@vtx-cpd.com
    Keymaster

    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 🙂

    scott@vtx-cpd.com
    Keymaster

    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 🙂

    scott@vtx-cpd.com
    Keymaster

    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 🙂

    scott@vtx-cpd.com
    Keymaster

    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 🙂

    scott@vtx-cpd.com
    Keymaster

    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 🙂

    scott@vtx-cpd.com
    Keymaster

    Replying to Kerry Doolin 22/08/2025 - 01:09

    Thank you Kerry!

    So interesting. Thanks for sharing the links.

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster

    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 🙂

    scott@vtx-cpd.com
    Keymaster

    Replying to Aileen D. 20/08/2025 - 16:00

    Aileen!!!!

    Love this. They really are a game changer, and usually managed very well by owners too.

    Is there a brad of tube you like? I really hope you have enjoyed the course. Any feedback you have regarding the course/content would be much appreciated.

    Thank you again for your support.

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster

    Replying to Aileen D. 20/08/2025 - 16:15

    Hello Aileen!

    Lovely to see you here! Thanks so much for sharing the article… you know you have made it when you make the Glasgow papers! Very cool case.

    I will make sure that Kerry and Neus see this question and we will get back to you ASAP.

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster

    Replying to Shannon Thorell 13/08/2025 - 21:13

    Thanks Shannon.

    Please le us know if there are any other topics/content you would like to see/hear!

    Have a lovely weekend.

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster

    Replying to Sarah Keir 14/08/2025 - 09:34

    Hi Sarah,

    Great point! Thankfully that is one complication we are spared in small animal medicine. In people with cirrhosis, portal hypertension leads to development of oesophageal and gastric varices which can rupture and cause catastrophic haematemesis, often fatal even with intervention.

    In dogs and cats, while we do certainly see portal hypertension, the sequelae are quite different. Instead of varices, we are more likely to see acquired portosystemic shunts, ascites, or hypertensive gastropathy. The mucosal congestion from portal hypertension can contribute to erosions or low grade bleeding, but the dramatic variceal haemorrhage so characteristic of humans is not a recognised clinical problem in veterinary patients.

    Thanks again,

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster

    Replying to Sarah Keir 14/08/2025 - 09:37

    Thanks Sarah, totally agree, DCM is a real consideration at this stage and something we’ll need to keep on the radar going forward, I must admit I often forget this sort of thing!. Look forward to your thoughts on the liver side when you’re back.

    Best,

    Scott 🙂

Viewing 15 posts - 1 through 15 (of 2,314 total)