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scott@vtx-cpd.com

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  • scott@vtx-cpd.com
    Keymaster

    Hello.

    It was a school boy error!

    Yes. There has been a lot of work carried out looking at oral cobalamin supplementation in dog and cats. The 12-13 weeks is based on a number of studies looking at the time required to reach normal levels:

    https://pubmed.ncbi.nlm.nih.gov/30606444/
    https://pubmed.ncbi.nlm.nih.gov/29428088/
    https://pubmed.ncbi.nlm.nih.gov/26648590/

    I would always check a week after supplementation stops.

    Hope that helps.

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster

    This is a really good point and the number of cases with normal liver enzymes is quite concerning when you look at those percentages.

    First thing is always that bigger picture question. Does the rest of the puzzle fit… are there compatible clinical signs? Common clinical signs included lethargy, vomiting, weight loss and decreased appetite. Physical examination abnormalities are not common, but include fever (22%), icterus (34%) and hepatomegaly (21%).

    Abnormalities on complete blood counts are detected in less than half of cats with NC and, when present, include leukocytosis (39%), band neutrophils (33%), and anaemia (34%). Cats with moderate to severe cholangitis can have normal serum liver enzyme activities but increases in aspartate transaminase activity (AST) have been noted in 98% of cats. Variable increases in alanine transaminase (ALT) in 50-57%, alkaline phosphatase activities (ALP) in 14-48% and gamma-glutamyl transferase (GGT) have been noted. Many cats with cholangitis have liver enzyme values (ALT, ALP, GGT) within laboratory reference intervals, but about 2/3 are hyperbilirubinemic. Hepatic function parameters were infrequently abnormal (hypoglycaemia 7%, decreased blood urea nitrogen 0%, hypoalbuminemia 13%, and hypocholesterolaemia 6%). Fasting and post-prandial serum bile acid concentrations, using cut offs of 15 micromol/L and 20 micromol/L, respectively, had higher specificity than did enzymatic testing and should be considered if hepatic disease is suspected in cats with normal enzyme activities and bilirubin concentration.

    On balance, most cases will have an abnormality that is compatible somewhere along the way. If not, AST and bile acids may play a role in cases where you still have a strong suspicion of NC. I know I have discounted how useful bile acids and AST are before… but they would have a place in this situation.

    Hope that helps.

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster

    Thanks for sending.

    I would definitely not pin too much significance on this result, especially when everything else is very normal.

    Is the dog on any liver ‘support’?

    I hope you get away tomorrow. The session will be recorded and available like the other sessions.

    It is so typical of veterinary practice… whenever you have plans… you never get away on time!!!

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster

    E-Clinpath is an amazing resource!!!

    You can upload images on here using thus website and just paste the link:

    https://imgbb.com/

    If you are coming to the live session we could also discuss there?

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster

    Hello.

    Really sorry about the delay with this one. Thank you so much for the question. Basically, the evidence is varied regarding which exact dose to use:

    Prednisolone-Treatment-Table

    I would normally start with 2mg/kg/day as this would be appropriate for immune mediated disease. Having said that, I have chickened out and started with 1mg/kg/day.

    Depending on response (clinical and bloods), I would normally reduce the dose by 25% every 4 weeks.

    Hope that helps.

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster

    Hello.

    Thank you so much for your question and sorry for the delay in getting back to you! No idea how I missed this one! In cases of acute hepatitis, I would indeed focus mainly on supportive care. This would normally include IVFT, antiemetic medication (maropitant, metoclopramide), sliymarin, SAMe and vitamin E. In animals that are not eating, I will often give them injectable N-acetylcysteine for the first couple of days.

    I will check for leptospirosis in most cases of acute hepatitis. Really important to get samples for urine and serum PCR before any antibiotics are started. I would then often start antibiotics pending the leptospirosis results.

    I would still be considering imaging (ultrasound) in cases of suspected acute hepatitis, but would not be rushing to biopsy. Many of these cases are sick and will resolve with supportive care. Remember many will have drug, infective or toxic causes. Biopsies will not help in the management of any of these cases.

    Some of these cases of acute hepatitis will go on to develop chronic hepatitis, and there would be indication for biopsy in these cases.

    From a anaesthetic point of view, most drugs are metabolised by the liver. Important to only use necessary drugs and really pay attention to the dose used. Methadone would be fine as a pre-med combined with a low dose of ACP. I would use propofol as an induction agent.

    Hope that helps.

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster

    Really great question! It is not something we have on our liver profiles. Could you post a copy of the full results? How is the patient doing and is it mon any medication?

    It is definitely something that is used more in large animal medicine.

    Increases in GLDH activity are used primarily to reflect leakage from damaged or necrotic hepatocytes. Since it is quite a large mitochondrial enzyme, injury needs to be sufficiently severe to damage mitochondria. GLDH is a useful enzyme for hepatocellular injury in large animals and exotic species (birds, amphibians, reptiles). GLDH is found in many tissues in the body, including hepatocytes, kidney, intestine, muscle, and salivary gland. However, most of serum GLDH originates from hepatocytes (in health and disease states). GLDH is located more in the centrilobular areas of the liver, whereas AST is more homogenously distributed and ALT is more periportal in rats. Due to its preferential location in centrilobular areas, liver injury involving these areas (e.g. hypoxia) may result in higher activity of GLDH than ALT. GLDH is a sensitive and specific marker of liver disease in all animals, including non-mammalian species. In rats, increases in GLDH were greater in magnitude, persisted longer or occurred without concurrent increases in ALT in drug-induced hepatic injury. In calves, horses and sheep, changes in GLDH paralleled changes in SDH after acute injury induced by chloroform. GLDH activity is not increased in horses or exotic animals with severe muscle injury (extremely high CK activity), supporting its specificity for liver injury. Like SDH, GLDH is not specific as to the cause of liver injury.

    Overall, I would question the significance here. Would be great to see the other results and a bit more about the case.

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster

    This is a really interesting question.

    I have had a look again through the literature. I can’t find any papers reporting using hepoprotectant supplements in dogs receiving phenobarbital.

    If the patient was to develop a hepatopathy that involved having to stop the phenobarbital, I would definitely use hepatoprotectant supplements in these cases.

    The question is… would we ever start hepatoprotectant medications as a preventative measure? I think we need to do this study!!!! The only one that would be similar would be the one looking at steroid use:

    https://pubmed.ncbi.nlm.nih.gov/15757136/

    I will reach out to some neurology specialist pals and see what they say.

    Hope that help.

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster

    Hello.

    This is an excellent question about the gastroprotectants. It is one of my favourite topics. We definitely massively overuse these drugs. If there is no obvious signs of gastroduodenal ulceration, there is really very little indication. I might pick this up in the liver Q&A tomorrow is that is OK, I can expand a bit more there. We also have a full webinar on the topic (shameless plug):

    Gastroprotectants: Taking the acid out of the suppression

    There is also a brilliant consensus from ACVIM, which is open access:

    https://onlinelibrary.wiley.com/doi/full/10.1111/jvim.15337

    The antibiotic question is also a great one! I am definitely more likely to start antibiotics in cats, as there seems to be more of a role of bacteria in their liver disease. I probably am ore inclined to start antibiotics in sicker patients. So yes, I would consider antibiotics if there was a neutrophilia and pyrexia. The degree of neutrophilia is not that helpful in decision making. If ultrasound was performed and there was evidence of gallbladder inflammation, I would also be more inclined to start antibiotics.

    I hope that helps.

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster

    Such great discussion!

    Has this really all come down to a question of basic maths?!

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster

    Hey Mike.

    Hope you are safe and well. These are really great questions. As with everything in medicine, there is never a black and white, but I will do my best.

    Regarding the ‘everything else’… I think the following table summarises well the other main causes of increases in liver enzymes:

    Non-Hepatic-Causes

    These would be the main things that I would want to rule out if you were at the stage of just having initial blood work.

    If things had progressed to a stage where you had taken biopsies… the following is the most useful regarding decision making:

    Liver-Biopsy-Decision

    Based on this I would do the following:

    1. If there was significant inflammatory change, copper came back as a non significant quantification and culture was negative then I would treat as immune mediated.

    2. If copped was in a significant range… I would treat copper first.

    3. If there was a positive culture… I would treat that first.

    4. If the inflammation was not that significant… I would be looking again for the possible causes in the table above.

    Hope that helps. Thanks again. This is a really great question.

    Really appreciated your interaction and support.

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster

    Thank you!

    So glad you enjoyed it!

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster

    Olga,

    Thank you for your question and a massive hello to you in Estonia. We are really excited for you to be joining us from there.

    What sort of information are you getting back from the laboratory? I suppose we always have to remember the limitations of FNA’s generally. In cats the FNA would be most useful for lymphoma, hepatic lipidosis and vacuolar change.

    There is not a specialist lab for liver aspirates. The first thing I would do is call the pathologist and talk through the cytology results. It may be that the results are not helpful as the FNAs do not represent the disease process.

    I would start my calling the lab and quizzing them about the results!

    Hope that helps.

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster

    No problem.

    I really would consider in this case. Particularly with it being a Greyhound.

    I would start 24 hours before the surgery and continue 24 hours after. It can make them feel quite sick so I would make sure to give maropitant too.

    I think vitamin K would be a good shout too. Lets do all we can to help! Vitamin K (0.5-1.5mg/kg SC q12h for 3 doses). I would start this the day before.

    Hope that helps.

    Scott 🙂

    scott@vtx-cpd.com
    Keymaster

    Thanks so much for this.

    Really interesting. I a really interested regarding the boswellia extract (boswellic acids) and bark extract (proanthocyanidins). Does it say why these are included or what the benefits are.

    I love looking at the labels and deconstructing the ingredients!

    Is that sad?! I think I need to get out more!

    Scott 🙂

Viewing 15 posts - 1,681 through 1,695 (of 1,804 total)