scott@vtx-cpd.com
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Hello everyone.
My name is Scott. I am one of the founders of vtx and a European and RCVS Veterinary Specialist in Small Animal Internal Medicine. I am so excited that we have Neus and Kerry delivering the course ad I can get a chance to watch and learn rather than being the one behind the webinar!
I will be here on the discussion forum to help where I can. Make sure to use the discussion forum. Feel free to share any interesting cases too.
Thank you all again for your support and I hope you enjoy the course.
Scott 🙂
Replying to Emma Shepherd 03/02/2022 - 17:31
Totally agree Emma.
These cases definitely cause a lot of panic. For me I think we need to remember that these is a lot we can be doing before getting to the point of surgery to stabilise these patients.
Have a lovely weekend.
Scott 🙂
Replying to Lucie T. 04/02/2022 - 09:52
No problem!
Have you had the opportunity to try any of these techniques out?
Let me know if there were any particular procedures you were interested in and I can see if we can find some videos for you.
Scott 🙂
Replying to Hannah Sivills 01/02/2022 - 09:04
Hannah.
Lovely to hear from you! I hope you are safe and well.
I think it is a great idea to get this drug in… it is a game changer. You need to get it on special import:
We get it through these guys, once you have an account set up it should be quite easy!
Let me know how you get on.
Scott 🙂
Replying to Sybil Dryburgh 24/01/2022 - 22:46
This is literally my new favourite thing to do!!!!
I was so surprised to see how widely it is used as the standard of care in human medicine!
Scott 🙂
Replying to Sybil Dryburgh 24/01/2022 - 22:55
I thought it was interesting…
However, since I posted it, it has all kicked off in the Journal of Veterinary Internal Medicine! Something I do not say often. I have popped below a letter that was written to the journal in response to the article:
LETTER TO THE EDITOR
Letter regarding “A novel bone marrow-sparing treatment for primary erythrocytosis in a cat: Onion powder”
Food for thought instead of onion powder as a treatment for erythrocytosis in catsUrs Giger,Mary M. Christopher
First published: 22 October 2021 https://doi.org/10.1111/jvim.16301
Dear Editors,
The precise diagnosis of erythrocytosis/polycythemia can be challenging, and its management depends on the specific cause and severity.1-5 In a recent case report by Vasilatis et al in Journal of Veterinary Internal Medicine,6 a cat with erythrocytosis, claimed to have polycythemia vera (PV), was treated with dietary onion powder, as an oxidative hemolytic agent, for 15 months. The authors’ reasoning was that it was a difficult patient to phlebotomize, and chemotherapy was not an option. We would like to comment regarding this case and the presumed effectiveness and safety of onion powder, and to express our sincere concern and caution toward recommending an oxidative hemolytic agent as treatment of any erythrocytosis.
Polycythemia vera is a now well-defined myeloproliferative disease in humans,5 but has never conclusively been diagnosed in cats; no acquired JAK2 mutations have been reported in cats.3, 4 It should be noted that cytologic and histologic examination of bone marrow is not helpful to differentiate polycythemias; all exhibit erythroid hyperplasia. One of us has had several cats with chronic persistent (up to 10 years) or transient (un-)explained erythrocytosis, and found some to have secondary causes.1-3 However, we have never definitely diagnosed PV in cats, and have never seen any domestic animal with erythrocytosis develop thrombocytosis, myelofibrosis, or leukemic blast crisis as typically seen in human patients with PV.
Regarding this case report,6 no prior CBC results were available, leaving the actual onset of erythrocytosis unknown, and clinicopathological information provided was sparse. Renal changes were noted on initial presentation, which were dismissed, but may be responsible for excessive erythropoietin production and secondary erythrocytosis (no renal follow-up was reported). It also appears the massive erythrocytosis in the cat6 resolved within 5 to 15 months, suggesting a secondary cause rather than the presumed PV, which is generally persistent and progressive. Moreover, the reticulocyte count of the cat was never increased,6 indicating normal rather than increased erythroid production. While no obvious dehydration was observed, total protein concentrations and urinalyses were not reported, and thus a relative erythrocytosis may not have been excluded.
Hematocrits >48% are abnormal in any cat and not just >65% as stated in the report’s introduction.4, 5 This is one of the reasons erythrocytosis is frequently overlooked in cats until late in the course of disease.1-3 One phlebotomy followed by immediate hospital discharge and a scheduled reexamination only after 2 weeks for a seizuring cat with a hematocrit (HCT) of 73% on presentation, as reported in this case,6 may be considered clinically insufficient. Frequent daily phlebotomies and supportive care are typically required early on to reduce very high HCTs to near-normal ranges and alleviate the neurologic complications.1-4
For any cat with symptomatic or severe erythrocytosis, regular phlebotomies with sedation and skilled assistance every 2 weeks to 2 months are well tolerated similar to any blood collection from healthy feline blood donors.1-4 Repeated phlebotomies frequently control erythrocytosis, work immediately, are generally safe, and require only PCV and total protein concentration for monitoring (no adverse drug-induced cytopenias or, as in this case,6 feared excessive intravascular hemolysis and oxidative tissue damage). Phlebotomy is desirable to reduce the HCT and resolve clinical signs before considering and initiating any other treatment. Periodic phlebotomies eventually induce iron deficiency (potentially associated with microcytosis and reactive thrombocytosis), slow the regenerative erythroid response, and thereby prolong the necessary phlebotomy interval to control the HCT. We have not had much luck with medicinal leeches in cats, but blaming leeches for causing seizures, as stated in their case report,6 is far-fetched.
Onions (Allium cepa), the second most frequently consumed vegetable by humans worldwide, have been recognized since ancient times for medicinal properties, for example, against cancer and thrombosis, but have never before been proposed as a treatment for PV or for that matter any other diseases. In fact, onions, besides causing teary eyes when chopped, also contain toxic compounds such as allyl and propyl sulfides, which cause hemolysis and oxidative tissue damage in susceptible animals.7, 8 Cats are particularly prone to toxicity characterized by Heinz body anemia, because of their unique hemoglobin structure and limited drug metabolism, but cats fortunately do not fancy eating onions.
Absolutely no increase in Heinz bodies while supplemented with onion powder was documented in the cat of their report,6 and only rare (<1%) Heinz bodies were observed throughout the entire 15-month period. This is inconsistent with the claim that oxidative hemolysis was induced by onion powder. The authors of the case report6 were dosing onion power at the lowest dose the owner could dispense with food (which sounds archaic compared to the practice of compounding) and estimated that 1.2% dietary onion powder was administered, although the actual amount may have been lower. Experimentally, as little as 0.3% onion powder caused 5% Heinz bodies, and 1.5% to 2.5% onion powder caused 25% to 35% Heinz bodies.8 Because onion powder causes a strong linear, dose-dependent Heinz body response, 1.2% onion powder would have been expected to cause approximately 15% Heinz bodies within 2 weeks. Without an increase in Heinz bodies, there is no evidence to support any effect of the onion powder on erythrocytes. Furthermore, no reticulocytosis, hyperbilirubinemia, and other evidence of hemolysis was observed at any time point, despite a nearly 20% decrease in HCT within 10 days of treatment. The authors of the case report6 suggest there was intravascular hemolysis, but dietary onion-containing supplements produce a slower oxidative process causing Heinz body anemia primarily by erythrophagocytosis rather than intravascular hemolysis, which, if sufficient to reduce the HCT, would be expected to cause visibly hemolyzed plasma, increased mean cell hemoglobin and mean cell hemoglobin concentration, hemoglobinuria, and reticulocytosis. Thus, the dose of onion administered was (luckily) likely too small to cause hemolysis. Since the HCT normalized, it is likely the onion supplementation could have been stopped. Additional follow-up evaluation after ceasing onion powder supplementation might have been revealing.
It should be noted that high doses of onions, whether given experimentally or inadvertently, can cause acute intravascular hemolysis in susceptible animals, but fortunately, cats appear resistant to hemoglobin-induced nephropathies. Oxidative cell damage beyond the well-defined hemolytic effects of onions is more difficult to assess, but could be harmful due to cats' limited metabolism and when exposed long term, as proposed in this case report.6
“Dark pink” mucous membranes are hard to visualize but may indicate methemoglobinemia, which was not measured in this case as a cause. While ingestion of onion powder by cats has been associated with only a slight increase in methemoglobin concentration (<1%),8 hereditary (congenital) methemoglobinemia, typically caused by methemoglobin cytochrome b5 reductase deficiency, has been frequently overlooked in companion animals. In contrast, cherry red mucous membranes may indicate carbon monoxide intoxication and occasionally can be chronic.
In conclusion, besides PV, other primary or secondary causes may have led to erythrocytosis in the cat of their report.6 While onions can cause hemolysis with Heinz bodies, they were not observed in this case.6 Thus, the onion dose administered was likely too low, and the cat recovered on its own. While onions are an integral part of the diets of humans, they can be toxic to companion animals and livestock and are not a treatment. We hope we provided some food for thought to not recommend and not to use onion supplementation as treatment for PV, for erythrocytosis of any cause, or frankly, for any illness in any species.
REFERENCES
Chen Gilor, Demitria Vasilatis, Jennifer McGill
Journal of Veterinary Internal Medicine
A novel bone marrow‐sparing treatment for primary erythrocytosis in a cat: Onion powderDemitria M. Vasilatis, Jennifer E. McGill, Chen Gilor
Journal of Veterinary Internal Medicine
Primary erythrocytosis in the cat: Treatment with hydroxyureaA. D. J. Watson, A. S. Moore, S. C. Helfand
Journal of Small Animal Practice
PRIMARY BONE TUMORS IN THE CAT:Jane M. Turrel DVM, MS, Roy R. Pool DVM, PhD
Veterinary Radiology
Advances in the diagnosis of acute pancreatitis in dogsHarry Cridge, David C. Twedt, Angela J. Marolf, Leslie C. Sharkey, Jörg M. Steiner
Replying to Sybil Dryburgh 24/01/2022 - 23:13
I suppose the question is how to make more of a definitive link?
And more important… could it help us therapeutically?
Scott 🙂
Replying to Sybil Dryburgh 24/01/2022 - 23:13
Thank you so much for this Sybil.
I think this has come from a letter to the editor in JAVMA. I have popped the letter below with the references:
Unique sensitivity of dogs to tartaric acid and implications for toxicity of grapes
The ASPCA Animal Poison Control Center has received several reports of dogs exposed to potassium bitartrate (cream of tartar). In one report, exposure to 2 teaspoons of cream of tartar resulted in acute vomiting and severe azotemia with serum creatinine concentration of 5.9 mg/dL (reference range, 0.5 to 1.8 mg/dL) and isosthenuria within 30 hours. In another report, a dog that ingested homemade play dough made with cream of tartar developed severe vomiting and azotemia (creatinine, 8.5 mg/dL) within 24 hours. The dog was euthanized, and renal histopathologic changes were similar to those described with grape and raisin toxicosis in dogs, including cortical tubular degeneration, necrosis, and mineralization, with some evidence of regeneration.
Potassium bitartrate is the salt of tartaric acid, and both potassium bitartrate and tartaric acid are uniquely present in high concentrations in grapes and tamarinds. Older studies have demonstrated species differences in absorption, elimination, and toxicity of tartaric acid and its sodium salt, potassium sodium tartrate (Rochelle salt), with dogs identified as having substantial absorption and rapid, high renal elimination.1 Information regarding the toxicity of potassium bitartrate in animals is lacking, although one study2 found obstructive nephropathy in rats. Tartrates are considered to have a wide margin of safety in humans, but there is a report3 of hyperkalemia following ingestion of cream of tartar in a human. In humans, tartaric acid is fermented by colonic bacteria to produce short-chain fatty acids, and absorption following ingestion is low.8,11
The amount of tartaric acid and potassium bitartrate in grapes varies with type, growing conditions, and ripening. At the beginning of ripening, tartaric acid concentrations may reach 20 g/L (2%) and, in general, range between 3.5 and 11 g/L (0.35% and 1.1%).5 The amount of acid in grapes at harvest is commonly studied for wine-making purposes, but it is unclear whether the amounts described include the potassium bitartrate salt, which increases at the expense of free tartaric acid concentrations during ripening. In dogs, ingestion of grapes at doses of 20 to 150 g/kg (0.32 to 2.4 oz/lb) has been reported to result in nephrotoxicosis.6 Assuming a tartaric acid content of 1%, this would represent tartaric acid doses of 196 to 1,484 mg/kg (89 to 675 mg/lb), consistent with the nephrotoxic range found in tartaric acid studies involving dogs.1 Another source4 reported that 5 g of cream of tartar is approximately equivalent to the amount of tartaric acid in 120 g (4.2 oz) of raisins. For a 10-kg dog, this would be a dose of 0.5 g of tartaric acid/kg (0.23 g/lb) or 12 g of raisins/kg (0.19 oz/lb), which is consistent with reported toxic doses of raisins (2.8 to 37 g of raisins/kg [0.045 to 0.59 oz/lb]).6 Interestingly, the ASPCA Animal Poison Control Center has had reports of severe vomiting and acute renal failure in dogs following large exposures to tamarinds, which are also uniquely high in tartaric acid.
Owing to the similar clinical courses (vomiting and acute renal failure) and histologic findings following ingestion of potassium bitartrate and grapes in dogs as well as the demonstrated dog susceptibility to tartaric acid, we propose that tartaric acid and its salt, potassium bitartrate, are the toxic principles in grapes leading to acute renal failure in dogs. Variable concentrations may explain the inconsistency in clinical signs in dogs following grape and raisin ingestion. Furthermore, excess tartrates are removed (detartrated) from commercial wine and juice products to protect flavor and appearance.
This removal of potassium bitartrate from processed products could account for the lack of toxicosis following ingestion of products such as juice, jam, and wine.
Colette Wegenast, dvm
Irina Meadows, dvm
ASPCA Animal Poison Control Center Urbana, Ill
Rachele Anderson, dvm
South Shore Veterinary Hospital Cicero, NY
Teresa Southard, dvm, phd
College of Veterinary Medicine Cornell University Ithaca, NY
1. ↑ Younes M, Aquilina G, Castle L, et al. Re-evaluation of l(+)-tartaric acid (E 334), sodium tartrates (E 335), potassium tartrates (E 336), potassium sodium tartrate (E 337) and calcium tartrate (E 354) as food additives. EFSA J 2020;18:e06030.
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2. ↑ Inoue K, Morikawa T, Takahashi M, et al. Obstructive nephropathy induced with dl-potassium hydrogen tartrate in F344 rats. J Toxicol Pathol 2015;28:89–97.
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3. ↑ Rusyniak DE, Durant PJ, Mowry JB, et al. Life-threatening hyperkalemia from cream of tartar ingestion. J Med Toxicol 2013;9:79–81.
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4. ↑ Spiller GA, Story JA, Furumoto EJ, et al. Effect of tartaric acid and dietary fibre from sun-dried raisins on colonic function and on bile acid and volatile fatty acid excretion in healthy adults. Br J Nutr 2003;90:803–807.
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5. ↑ Moreno J, Peinado R. Grape acids. In: Moreno J, Peinado R, eds. Enological chemistry. London: Academic Press, 2012;121–134.
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6. ↑ Eubig PA, Brady MS, Gwaltney-Brant SM, et al. Acute renal failure in dogs after the ingestion of grapes or raisins: a retrospective evaluation of 43 dogs (1992–2002). J Vet Intern Med 2005;19:663–674.
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Replying to Jessica W. 28/12/2021 - 15:02
Hello Jessica.
I am so sorry about my delay in reply… I have no idea how I missed your question!
I am glad you are enjoying the course.
This is a brilliant question. I was maybe not as clear as I should have been. Two weeks may indeed be enough. I may extend this if there has been a partial response.
Dogs with food-responsive disease typically show improvement to a strict dietetic therapy within 14 days (Allenspach et al. 2016). However, response may be individualised and relies heavily on the composition of the diet selected with respect to whether the dog has a nutrient (e.g. fat intolerance) or ingredient (e.g. chicken allergy) specific disease. Moreover, commercially available diets in each of these categories can still vary dramatically in their fibre composition and content, protein ingredient type and amount, and fat content. Thus, multiple diet trials should be considered before deeming the disease non-food responsive. Diets that are often considered for dogs with CE include highly digestible (i.e. low residue), fibre-enriched, low fat, novel, hydrolysed, limited ingredient protein or home-made.
Hope that helps.
Scott 🙂
Hello.
Thank you so much for this. I am so glad it was helpful.
I was not able to see the photo. Can you email it to me and I will try and attach it?
Scott xx
Replying to Daphna S. 10/01/2022 - 09:52
Hello Daphna.
Happy new year! I am so glad that the lesson was helpful!
Let me know if you have any quetions.
Scott 🙂
Hello everyone!
I hope you are all safe and well and have had a wonderful Christmas and New Year!
My name is Scott and I am one of the founders of vtx. I am a European and RCVS Veterinary Specialist in Small Animal Internal Medicine. I look forward to speaking to you later in the course!
Please let me know if you have any questions at anytime. I will do my best to answer. If you are not comfortable posting questions here, please drop me an email:
Scott 🙂
Replying to Gabriela Gonzalez-Ormerod 07/12/2021 - 18:49
Hello Gaby.
I am really sorry about the delay in getting back to you. It is a really great question. I have summarised some of the antithrombotic treatment information from the consensus statement below:
The terms “thromboprophylaxis” and “antithrombotics” encompass both antiplatelet drugs, designed to inhibit platelet function (primary haemostasis), and anticoagulant drugs, designed to inhibit the activity of clotting factors (secondary haemostasis). Clopidogrel is an antiplatelet and rivaroxaban is an anticoagulant drug.
What we definitely do know is that thromboprophylaxis be provided for all dogs with IMHA, except those with severe thrombocytopenia (platelet count <30 000/μL). A substantial body of evidence indicates that IMHA in dogs is associated with an increased risk of thrombosis, and that thrombotic disease is a leading cause of morbidity and mortality in dogs with IMHA. The pathophysiology of thrombosis in IMHA is complex, involving endothelial activation, intravascular tissue factor expression, procoagulant microparticle generation, platelet activation, and an imbalance of pro- and anticoagulant factors.
The following is a recommendation from the consensus with relatively weak evidence:
''Based on the pathophysiology of venous thromboembolism commonly encountered in dogs with IMHA, we suggest that a regimen incorporating anticoagulants may be preferred for thromboprophylaxis, particularly during the first 2 weeks after diagnosis. The available anticoagulants may be used alone or combined with antiplatelet drugs. If treatment with an anticoagulant, and its associated monitoring, is not available or feasible, we suggest administration of antiplatelet drugs in preference to no antithrombotic drug''.
Many of the anticoagulant drugs can be challenging to monitor/not as widely available, so often antiplatelet drugs are given alone.
Thrombosis in IMHA predominantly affects the venous system, where thrombi form under low-shear conditions. Such thrombi typically are rich in fibrin, and their formation is less dependent upon platelet number or function, providing a rationale for administration of anticoagulant drugs. Although platelet activation can be detected in dogs with IMHA, this phenomenon probably occurs secondary to pathologic tissue factor-mediated thrombin generation, rather than as a primary event. Nevertheless, the cell-based model of haemostasis posits that platelets are integral to haemostasis in vivo. There is thus a rationale for the use of antiplatelet drugs in venous thrombosis. Experimental data support this proposition to some degree, and evidence in humans suggests that antiplatelet drugs do decrease the risk of venous thrombosis. However, this should be viewed in the context of the substantial body of evidence in humans supporting administration of anticoagulants as first line prophylactic drugs for venous thrombosis.
The consensus actually recommends the following:
''We suggest the administration of unfractionated heparin (UFH) with individual dose adjustment (using an anti-Xa assay) in preference to other drugs. This drug should not be used without individual dose adjustment. If this is not available or feasible, we suggest administering injectable low-molecular-weight heparins or direct PO Xa inhibitors. When using injectable low-molecular-weight heparins, we suggest individual dose adjustment (using an anti-Xa assay) may be useful to achieve a therapeutic dose.
Suggested starting dosages for these drugs are:
Unfractionated heparin (IV): 100 U/kg bolus, then 900 U/kg/24 h
Unfractionated heparin (SC): 150-300 U/kg q6h
Dalteparin (SC): 150-175 U/kg q8h
Enoxaparin (SC): 0.8-1.0 mg/kg q6-8h
Rivaroxaban (PO): 1-2 mg/kg q24hInsufficient evidence is available to make strong recommendations on the choice of anticoagulant in IMHA. The strongest evidence supports the use of individually dose-adjusted UFH. Other anticoagulants including enoxaparin and rivaroxaban appear to be safe and may be efficacious, but RCTs are lacking.
Anti-Xa monitoring is not widely available to veterinarians. If an anti-Xa assay is not available, then it is reasonable to consider the activated clotting time, activated partial thromboplastin time (aPTT), thrombin generation, or viscoelastic tests to monitor anticoagulant treatment. Nomograms for adjustment of UFH treatment using aPTT and thromboelastographic assays have been proposed, but are currently only available in abstract form. The original derivation of UFH aPTT prolongation targets was performed using thrombotic models in dogs.
If antiplatelet drugs are administered, we suggest that clopidogrel be used in preference to aspirin. We suggest that clopidogrel be administered at a dosage of 1.1-4.0 mg/kg PO q24h. A single PO loading dose (eg, double the maintenance dosage or up to 10 mg/kg) may be useful for obtaining therapeutic plasma concentrations rapidly. If aspirin is selected as an antiplatelet drug, it should be administered at a dosage of 1-2 mg/kg q24h and could be combined with clopidogrel.''
In summary using anticoagulant therapy is recommended, but there are inherent challenges with the use of these drugs. Rivaroxaban is probably the most practical. I would probably use in combination with clopidogrel, especially in the first couple of weeks. Something is better than nothing and clopidogrel alone if nothing else!
I will let Liz answer the bit about HCM!
Scott x
Replying to Rosemary S. 01/11/2021 - 11:31
Hello Rosemary.
I hope you have had a wonderful Christmas!
I have no idea how I have missed this question… I am so sorry! Probiotics is a great question. I find the following article is a good review:
https://drive.google.com/file/d/1GitsWnXb92Fs3Gk_Km3i4agw19Ff3qJj/view?usp=sharing
I think the summary points for this article are really useful and helpful from a clinical point of view:
1. When considering treatment for acute uncomplicated diarrhoea, probiotics are likely a better choice (unlikely to cause harm, possible shortening of recovery time) than antibiotics (can cause significant and long standing gut dysbiosis).
2. When considering probiotics as adjunctive treatment to infectious disease, there is so far only some evidence for the benefit of Enterococcus faecium for Tritrichomonas foetus infection in cats.
3. Saccharomyces boulardii is an interesting potential probiotic, that has shown promising results in reducing antibiotic-induced diarrhoea in dogs as well as improve clinical scores in dogs with chronic enteropathy and PLE.
4. Specific probiotic blends can be as efficient in treating canine chronic enteropathy than antibiotic and glucocorticoid treatment combined.
5. When treating feline chronic constipation, a specific probiotic blend can be considered as adjunctive treatment.
Overall, there is still a huge amount for us to learn about probiotic. The main benefit of their use is that they do no harm. So, I would pretty much use them whenever there may be any benefit. I tend to use the following products:
With the VSL, I would base it on the study that demonstrated a benefit. The VSL#3 group (D-VSL#3; n = 10) received between 112 and 225 billion (112 to 225×109) lyophilized bacteria per 10 kg daily for 60 consecutive days. The amount will depend on the exact product (they vary in bacteria concentration). There is a mixture of capsules or powder.
With the other would be Sivomixx:
https://www.sivomixx.net/en/author/sivoy/
Obviously there are lots of other veterinary probiotics in practice. For these, I would follow the individual manufacturer guidelines.
I hope that helps.
Scott 🙂
Replying to Josie B. 22/12/2021 - 12:40
Hello.
Thank you for your amazing comments. Let me share the pathologists report:
Site Liver
Microscopic Description
Liver: Preservation is moderate and nucleated cellularity is low to moderate. Slide no4 contains
predominantly dense blood. The remaining scans contain variable amounts of fresh blood and small lipid
spaces. There are low to moderate numbers of well-differentiated hepatocytes arranged in sheets and clusters. Low numbers of erythrocytes and focal clusters contain low numbers of small clear punctate
vacuoles. There is rare focal moderate intracanalicullar bile stasis (bile casts). There are rare isolated
slender fusiform mesenchymal cells (presumed to be fibroblasts). Streaked nuclear material is frequently
associated with a parasite clusters and, in these areas, neutrophils and small lymphocytes occasionally
appear overrepresented. Infectious agents and atypical cells are not identified.Microscopic Interpretation
Moderate focal cholestasis. Mild focal discrete vacuolar change.
Comments
Aspirates have harvested predominantly fresh blood however, within the hepatocytes there is evidence to
support cholestasis and although this is focal, it is moderate. The mild indiscrete vacuolar change is
non-specific and may be associated with elevated metabolic stress associated with inflammation of
varying aetiologies (hepatic and nonhepatic), as well as metabolic disease (e.g. pancreatitis).
Overt inflammation and infectious agents are not identified however this is a relatively small sample. The
fibroblast presence may be compatible with fibrosis however, this requires histopathology for definitive
diagnosis. Given the slightly increased numbers of leukocytes associated with hepatocytes, although overall
leukocyte numbers do not appear elevated mild inflammation cannot be excluded. Biopsy with
histopathology for evaluation of tissue architecture and tissue culture may be of value should changes
persist.I was interested with your pancreatitis comments, what made you suggest that?
Thanks again for your brilliant comments.
Scott 🙂
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