scott@vtx-cpd.com
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Replying to Daphna S. 03/11/2021 - 14:24
No problem!
Let me know if you have any other questions.
Scott π
Replying to Emma Holt 02/11/2021 - 20:04
It is amazing indeed!
I must admit I do the same. We would take between 30-5 samples and assess them for cellularity. When I see hepatocytes I am happy. I can’t find any literature to support a specific number… so lets stick with 3-5!
Scott π
Replying to Emma F. 02/11/2021 - 20:37
Hey Emma.
Thank you so much for this. I will pass on to Jon. I am so pleased you are enjoying the course.
Scott π
Replying to Anna Deen 03/11/2021 - 08:32
Thank you Anna!
I will see if we have any other comments before I post the pathology report!
Scott π
Replying to Emma Holt 21/08/2021 - 10:04
Emma,
Thanks again for your amazing answer here.
I just wanted to shar the full report from the pathologist:
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.You basically were spot on!
Scott π
Replying to Jeanette Tungesvik 28/10/2021 - 15:02
Great question.
Yes, formalin would kill bacteria. I would take some fresh tissue and wrap it in a swab soaked in sterile saline. I would then pop it in a sterile pot.
Hope that helps.
Scott π
Replying to Jeanette Tungesvik 28/10/2021 - 14:59
Thanks.
Keep us updated with how the case gets on.
Scott π
Replying to Rosemary S. 01/11/2021 - 11:25
Hello.
I tend not to convert between one and another.
I would accept that 0.3mg/kg of dexamethasone is immunosuppressive and 2mg/kg of prednisolone would be immunosuppressive.
0.3mg/kg of dexamethasone is equivalent to 2mg/kg of prednisolone. This would be the factor of 7 that you were mentioning. To get the prednisolone dose from the dexamethasone dose, you would multiply by a factor of 6.7.
Hope that helps.
Scott π
Replying to Rachel Roper 12/10/2021 - 13:49
Again, a brilliant question.
Geographic data is lacking a little, and is being worked on as we speak.
Annual vaccination with 4-serovar vaccines is generally recommended for at-risk dogs, regardless of breed, with the understanding that the definition of βat-riskβ may vary geographically. In geographic locations in which infection occurs in urban, backyard dogs, all dogs may be at risk, and the vaccine may be considered part of a core vaccination protocol. In other locations, only dogs that contact wildlife, swim, hunt, or roam on farmland may be at risk.
Funnily enough, I recorded a podcast about this exact subject, including a chat with a PhD student who is working on this right now:
https://medivetpodcast.podbean.com/
Hope that helps.
Scott π
Replying to Rachel Roper 12/10/2021 - 13:49
Hello.
Great question. I am really sorry about the delay in reply. I will answer in a couple of posts if that is OK? Firstly I wanted to share a few really useful Leptospirosis papers (most of which are open access):
Taylor, C., Brodbelt, D.C., Dobson, B., Catchpole, B., OβNeill, D.G., Stevens, K.B., 2021. Spatio-temporal distribution and agroecological factors associated with canine leptospirosis in Great Britain. Prev. Vet. Med. 193, 105407. https://doi.org/10.1016/j.prevetmed.2021.105407
Taylor, Collette, OβNeill, D.G., Catchpole, B., Brodbelt, D.C., 2021. Incidence and demographic risk factors for leptospirosis in dogs in the UK. Vet. Rec. 1β9. https://doi.org/10.1002/vetr.512
Schuller, S., Francey, T., Hartmann, K., Hugonnard, M., Kohn, B., Nally, J.E., Sykes, J., 2015. European consensus statement on leptospirosis in dogs and cats. J. Small Anim. Pract. https://doi.org/10.1111/jsap.12328
Sykes, J.E., Hartmann, K., Lunn, K.F., Moore, G.E., Stoddard, R.A., Goldstein, R.E., 2011. 2010 ACVIM small animal consensus statement on leptospirosis: diagnosis, epidemiology, treatment, and prevention. J. Vet. Intern. Med. 25, 1β13. https://doi.org/10.1111/j.1939-1676.2010.0654.x
AzΓ³car-Aedo, L., Monti, G., 2016. Meta-Analyses of Factors Associated with Leptospirosis in Domestic Dogs. Zoonoses Public Health 63, 328β336. https://doi.org/10.1111/zph.12236
Lee, H.S., Guptill, L., Johnson, A.J., Moore, G.E., 2014. Signalment changes in canine leptospirosis between 1970 and 2009. J. Vet. Intern. Med. https://doi.org/10.1111/jvim.12273
Major, A., Schweighauser, A., Francey, T., 2014. Increasing incidence of canine leptospirosis in Switzerland. Int. J. Environ. Res. Public Health 11, 7242β7260. https://doi.org/10.3390/ijerph110707242
Smith, A.M., Arruda, A.G., Evason, M.D., Weese, J.S., Wittum, T.E., Szlosek, D., Stull, J.W., 2019. A cross-sectional study of environmental, dog, and human-related risk factors for positive canine leptospirosis PCR test results in the United States, 2009 to 2016. BMC Vet. Res. 15. https://doi.org/10.1186/s12917-019-2148-6
I know you will all be so busy, but this gives some brilliant bedtime reading if you have a second!
Scott π
Replying to Emma A. 25/10/2021 - 23:51
Hello.
Some thought from Jon. Hope this helps:
“I always ligate tissue pedicles in the crush of a clamp – it compresses or breaks the surrounding connective tissue meaning that you can get a tighter knot on a ligature. If the new grads are horrified that you’re tying in to a crush, I’m equally horrified that they’re not!! If there is more tissue in the ligature, it will constrict the pedicle less. I would always suggest using a ‘3 clamp technique’, tying in to the crush of the most proximal clamp and then tearing / cutting between the remaining more distal 2 x clamps. Sometimes, for space reasons, I’ll place two clamps, then more the 1st one around to the opposite side of clamp number two, then tie in to the original crush – let me know if this doesn’t make sense. I also ‘flash’ the clamps for pedicles – so set the ligature into the crush, then release the above clamp as you tighten the knot, then replace the clamp in the same place.
There is lots of evidence now to say that catgut is really not a safe material to use. I would try and move away from this if possible.
Miller’s knots are fine. I wouldn’t know how to use one! I can tell you that Leitch published a paper a few years ago showing that there are better ones (constrictor, strangler and something else). I love a Weston knot myself. Standard square knots are spot on though – I’d probably get a bleed if I started trying to tie Millers.
Yep – I always close the abdomen with continuous PDS. I can think of 2x occasions when I used interrupted, but they were dogs that had blown their guts across the floor about 8 weeks post coeliotomy and had a collagen maturation disorder.”
Hope that helps.
Scott π
Replying to Rosemary S. 01/11/2021 - 11:25
Hello.
Thank you for your brilliant question.
Bone marrow suppression, especially anaemia, is the most common clinical syndrome associated with FeLV infection, resulting from infection of both hematopoietic stem cells and bone marrow stromal cells. Most commonly anaemia will be non-regenerative. Progressive infection with active viral replication is usually required for bone marrow suppression. Regressive infection is only rarely associated with myelosuppression. Thus, in a FeLV antigen-negative cat with bone marrow suppression, testing bone marrow for FeLV by PCR is only sometimes helpful. The most common form of FeLV-induced anaemia is pure red cell aplasia, a severe nonregenerative anaemia with marked depletion and maturation arrest of erythroid precursors in the bone marrow (with the characteristic finding of a lack of reticulocytes but a high mean corpuscular volume [MCV]). Regenerative anaemia in FeLV-infected cats, indicated by increased reticulocytes and, in some cases, nucleated red blood cells (RBCs), is less common than nonregenerative anaemia and is often associated with coinfection with Mycoplasma haemofelis or other haemotropic Mycoplasma spp..
Some cats with immune-mediated haemolytic anaemia are progressively FeLV-infected, and in some, haemolysis precedes the emergence of myeloproliferative disease or lymphoma. This would be a specific reason to test in these cases.
Even if myeloproliferative disease was not to develop in these cases, the would be possible management benefits of knowing the FeLV/FIV status:
1. Progressively FeLV-infected cats should be kept indoors to avoid spread to other cats and exposure of the cat to other infectious agents carried by other animals.
2. βRoutine vaccination programsβ should be maintained in cats with progressive FeLV infection. They might not be able to mount an adequate immune response to vaccines and protection might not be comparable to that in a healthy cat. Therefore, testing for the immune response (e.g., antibody measurement after feline panleukopenia virus vaccine) and protecting against exposure should be considered.
Hope that helps a little.
Scott π
- This reply was modified 3 years ago by scott@vtx-cpd.com.
Replying to Ilse v. 31/10/2021 - 06:09
Hello.
This is a brilliant question that I am not sure I am going to be able to give a definitive answer to. The consensus statement states:
“We suggest that thromboprophylaxis be initiated at the time of diagnosis and continued until the patient is in remission and no longer receiving prednisone or prednisolone”.
I must admit that I often do not continue this long. The maximum risk period for mortality associated with IMHA appears to be the first 2 weeks after initiation of treatment. This period represents the phase when pathophysiologic risk factors for thrombosis are maximal, likelihood of transfusion is highest, and any prothrombotic effect of immunosuppressive medications is greatest, if related to dosage. The risk of haemorrhage from recommended antithrombotic dosages is likely to be small. As the disease process responds to immunosuppression, the likelihood of thrombosis may diminish, but the continued use of immunosuppressive medications may generate ongoing thrombotic risk. Some dogs may require lifelong low doses of glucocorticoids to maintain remission. We suggest that thromboprophylaxis be discontinued if such dogs have been in remission for 6 months and no other risk factors exist.
I would usually use a combination of rivaroxaban and clopidogrel. I would normally discontinue the rivaroxaban after the first couple of weeks and discontinue the clopidogrel once the weaning of the steroid dose starts.
Hope that helps.
Scott π
Replying to Rosemary S. 01/11/2021 - 11:30
Hey.
Really good question. I hope you are safe and well. The reasoning behind prophylactic use of omeprazole will be different between the Palladia and the NSAIDs. I presume the reasoning behind the use of omeprazole prophylactically with the Palladia will be to prevent gastrointestinal side effects. Although the NSAIDs will also cause gastrointestinal side effects, the mechanism of this is different with both drugs.
I must admit… I had to phone a friend with the actual answer to this question! I spoke to two oncology specialist colleagues, neither of them use omeprazole prophylactically with Palladia. If there is gastrointestinal upset with this drug, it is unlikely that the modification of gastric pH will help the situation. An antiemetic possibly, but often the drug has to be withdrawn.
Hope that helps a bit.
Scott π
Replying to Alison Docherty 01/11/2021 - 12:34
Hey Alison.
I hop you are well and enjoying the course.
I would also love to hear what everyone’s thoughts are. I tend to use the MILA systems for this. I really do love their products. They can be on the wee bit more expensive side, but I think works really well:
Hope that helps.
Scott π
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