scott@vtx-cpd.com
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Really interesting!!!
Is this generally, or in cases of urethral obstruction. I have not heard this but have just fired off an email to an anaesthesia specialist to find out more! I will let you know.
Scott 🙂
Keppra is a good shout!
I often escalate like Zoe says. Diazepam/midazolam first choice with phenobarbitone next and then Keppra, then propofol?! It often feels like we are giving all at once!
Scott 🙂
Hey.
It does seem like it was a last resort in these cases. What would you use in really refractory cases in practice?
Scott 🙂
Thanks.
Is the diazepam and methadone alone enough to unblock some?
Scott 🙂
You may need the whole bottle by the end!
Let me know how you get on.
Scott 🙂
HAHA!
Agreed!
Scott 🙂
Hello Charlotte.
I hope you are well. Thank you so much for joining the course. I hope you are enjoying it so far.
It is a really good question regarding the notes. We had decided that we would not provide formal notes from previous feedback we have had. We are happy to provide PDF copies of all of the lectures if that would help.
Just drop me an email and we can sort that out info@vtx-cpd.com
Scott 🙂
Indeed… spread the word!
It is a nice paper.
Scott 🙂
It seems cost is the biggest issue.
That is such a shame because it is so much easier! I still have nightmares about having to give them that powdered form!
I wonder why is costs so much?! I would heave thought the active ingredient was quite cheap!
Scott 🙂
It is indeed.
It is that back and forward motion.
This is also the first time someone has posted a video in the forum… it works really well. Thank you for that.
I do like to have my patients a bit more sedated than this for liver FNA’s. I think especially if you are going it for the first time, it helps if they are still and not reactive!
Scott 🙂
Great question Sara and great points Simon.
There are a couple of studies in dogs where both drugs are used. Problem is that most involve maropitant being given and then around an hour later the apomorphine is given:
https://pubmed.ncbi.nlm.nih.gov/28042152/
https://pubmed.ncbi.nlm.nih.gov/19000276/I think the main point is due to the timing of the drug administration and how long to peak effect. If we are giving the maropitant SC after the apomorphine, it is probably starting to work after the emetic effect of the apomorphine has passed. I think it probably has little effect.
Makes us feel better for sure.
Scott 🙂
I think that is a really good point.
I definitely use them in a cumulative way. If maropitant id not effective enough. I will add in metoclopramide and then ondansetron. I really do think some cases need all three.
Scott 🙂
Interesting!
Have you often given it IV?
Scott 🙂
Hello.
Thank you so much for your question. I am so glad you are enjoying the course.
Electrolyte abnormalities also commonly occur as a complication of diuretic treatment. The normal physiologic response to increased sodium and water loss is the stimulation of homeostatic mechanisms that attempt to more vigorously retain sodium and water. Predominant among these mechanisms is the RAAS. Less commonly—although significantly—vasopressin release is sometimes also stimulated by a marked fall in blood pressure secondary to heart disease or diuretic treatment. One of the effects of the stimulation of these homeostatic mechanisms is altered handling of electrolytes. Increased activity of aldosterone will tend to favour sodium retention and potassium loss in the distal nephron. This leads to one of the more commonly observed consequences of loop diuretic administration: hypokalaemia. Hypokalaemia is less likely to be observed in patients if they are concurrently receiving treatments that tend to counteract the RAAS. More widespread use of angiotensin-converting enzyme inhibitors and spironolactone, in addition to loop diuretics, mean that hypokalaemia now is seen less frequently. The situation in which it is now probably most likely to be encountered is during the emergency stabilization of patients where they are likely to receive large doses of furosemide and might not yet have been started on other agents.
Hypokalaemia can contribute to the development, or worsen the symptoms, of hepatic encephalopathy. Hypokalaemia increases proximal tubule ammoniagenesis. Approximately 50% of proximal tubule ammonia production is returned to the systemic circulation via the renal veins.
Hope that helps.
Scott 🙂
Hello.
Thank you so much for you great questions. I wanted to start by discussing gallbladder sludge. “Sludge” in the gallbladder is defined as nonshadowing echogenic material in the gallbladder which is dependent on gravity and a commonly seen ultrasonographically during the investigation for hepatobiliary diseases. The clinical significance of this finding in small animal patients is not well established. The reported prevalence of the gallbladder “sludge” is 53- 57% in clinically healthy animals. Bromel et al. (1998) showed prevalence in clinically healthy animals is not significantly different from that in patients with hepatobiliary disease or other diseases “Sludge” seems to most commonly affect Labrador retrievers, Yorkshire terriers, Miniature Schnauzers, Beagles, Cocker spaniels, Poodles, and crossbreeds. Fewer studies have been performed to investigate prevalence and significance of gallbladder “sludge” in cats, but a lower prevalence of 14% is reported. In both dogs and cats, increased age is positively correlated with the prevalence of “sludge” but sex seems to have no effect. DeMonaco et al. (2016) identified healthy dogs with gall bladder sludge remained asymptomatic for 12 months. Biliary sludge was mild in 50%, moderate in 36%, moderate to severe in 9% and severe in 5% of this population and persistent in 88% and recurrent in 10%. Furthermore, there is no correlation between increases in liver enzymes or total bilirubin and the prevalence of “sludge” in dogs. Recently, a small study reported that the detection of immobile “sludge” had a 70% sensitivity and 100% specificity for diagnosis of bactibilia. Overall, the presence of “sludge” is not necessarily clinically significant. This finding needs to be considered in combination with clinical signs and other laboratory findings.
So, I would use ursodeoxycholic acid in cases of “sludge” if there were clinical signs/biochemical changes consistent with hepatobiliary disease. It may not be necessary to use in every case where “sludge” is detected if the animal is having ultrasound for a completely unrelated reason.
SAMe is a very safe product generally and can be used long term if necessary. I will use in cases of acute hepatitis for as long as the animal is being treated for. In these cases I will use until the point of resolution. This is normally the point where all biochemical abnormalities go back to normal. I will definitely use longer term in chronic cases. This could be lifelong if required.
I would always try and confirm inflammation with biopsy and exclude infection as you have mentioned. The evidence about what drugs to use in inflammatory/immune medicate hepatitis cases is variable. Some specialists combine corticosteroids with another immunosuppressive drug (either azathioprine or cyclosporine) to enable more rapid tapering of the corticosteroid administration to every other day anti-inflammatory doses. For most, maintenance on the second drug alone was the goal. For other specialists, single agent cyclosporine twice a day was used as first-line treatment to avoid the adverse effects of corticosteroids. Cyclosporoine is tapered to once a day as soon as remission is established.
Sorry for the long answer! I hope that helps.
Scott 🙂
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