scott@vtx-cpd.com
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Hello.
Hope you are well. Sorry for the delay in getting back to you. Overall, the pre insulin glucose and clinical signs might be a better way to go. The problem with the 6h post insulin, is that this one result can be very variable. Remember, the main issue normally in the initial stages of treatment is avoiding hypoglycaemia.
In the more stable patients, I would be happy to rely on the fructosamine and clinical signs. Again, there may be some use in the pre-insulin BG value if other monitoring is not possible. Ultimately, a BG curse will give you more information.
Overall, clinical signs really are the most important part of this. There is definitely not a one size fits all!
Hope that helps.
Scott 🙂
Kerida!
I am so excited that this all went well with the sensor!!!
I am really happy to help with the interpretation of the results too, let me know.
Scott 🙂
Hey Alice.
So sorry for the delay. I normally place BG sensors in cats behind the head at the back of the neck. Is that what you would normally do? I would then cover it with a bit of dressing around the neck like when we bandage in an oesophageal feeding tube. Does that make sense? I have popped a picture below:
Hope that helps.
Scott 🙂
Kerida…
There are many benefits of being a vintage vet! I too need to brush up on my cardiology knowledge.
Scott 🙂
It is a really good question.
In this situation, particularly of the renal parameters are normal and there is not an ‘obvious’ other problem from basic bloods then I probably would be treating the calcium, even without a definitive diagnosis. The reason for running the PTH and PTHrp is often as part of the exclusion process in the diagnosis of idiopathic hypercalcemia.
So, in this case, where cash is limited, it would not be ridiculous to start aledronate.
Hope that helps.
Scott 🙂
Really good question!
What was the ionised calcium value?
Were the renal parameters normal?Scott 🙂
Hello!
My name is Scott, I am one of the other directors of vtx. I am a specialist in internal medicine and had the great joy of doing my residency with Liz. I am often the one delivering the lectures, so it is going to be lovely to be the one listening! Cardiology is definitely a weak area for me! I am excited to learn.
Scott
Great question!
Persistent fasting hyperlipidemia is abnormal and can be either primary or secondary to other diseases or drug administration. Secondary hyperlipidemia is the most common form of hyperlipidemia in dogs. Most commonly, secondary canine hyperlipidemia is the result of an endocrine disorders. Primary lipid abnormalities are usually, but not always, associated with certain breeds. Depending on the breed, the prevalence of a primary lipid abnormality can vary widely. Primary hyperlipidemia is very common in Miniature Schnauzers. Primary hyperlipidemia in the Miniature Schnauzer is typically characterized by hypertriglyceridemia with or without hypercholesterolemia. Primary hyperlipidemias have also been reported in Shetland Sheepdogs (in Japan and possibly other countries), Beagles, Briards, a family of rough-coated Collies from the United Kingdom,18 and anecdotally in Doberman Pinschers and Rottweilers.
Hyperlipidemia itself does not seem to lead directly to the development of major clinical signs, it has been shown to be associated with the development of other diseases that are clinically important and potentially life-threatening. Hyperlipidemia, and more specifically hypertriglyceridemia, has long been suspected as a risk factor for canine pancreatitis. The results of two recent clinical studies provided stronger evidence that hypertriglyceridemia, especially when severe (>900 mg/dL), is a risk factor for pancreatitis in Miniature Schnauzers. Therefore, severe hypertriglyceridemia in Miniature Schnauzers should be treated even when clinical signs are not present, due to the risk of developing pancreatitis. In summary, I would treat (mostly with low-fat diet) in Miniature Schnauzers.
In other breeds, a more general and wide selection of tests might be necessary for patients that have vague or no clinical signs. It should be noted that dogs with hyperlipidemia are often clinically healthy. It is likely that at least some of these dogs have some form of primary hyperlipidemia. If it is mild or moderate, there may be no need for detailed diagnostic investigations. If hypercholesterolemia is the main abnormality (without or with only mild hypertriglyceridemia), then it is more likely that the dog has some form of secondary hyperlipidemia, warranting recommendations for further diagnostic investigation.
I hope that helps a little bit. Let me know if that makes sense.
Scott 🙂
Hello.
Sorry for the delay. I have posted some thoughts under your questions below:
1)He is on hypoallergenic diet as well due to IBD, do I continue with this diet instead of swap him to one for diabetes control and just feed the same amount daily?
“This is a really good question. There is always such a battle with these cases when there is more than one problem that will respond to very different diets. What hypoallergenic diet are you using? If it is not hydrolysed, I would definitely switch to a hydrolysed diet. I think in this case, I would prioritize the IBD. If the IBD is controlled by other measures then you will be able to get the steroid dose as low as possible”.
2)Also dog has very elevated ALP(2000), could this be purely due to DM or should i consider cushings? Or could be due to long term steroids? gGT is 2x upper refference as well, ALT and albumins normal. I was thinking to do a urine cortisol to crea ratio, do you think doing it now or should i stabilise diabetes first?
“I honestly think that this will be down to the DM and steroid use. I have seen the AP value go this high with DM alone. I think it would be almost impossible to test for Cushings’s in this case with the steroids on board. I think the priority is to get the steroid dose as low as possible”.
3)upc was 1.4, could it be high due to very concentrated urine and glucose in urine or should i consider treat the proteinuria?
“The UPC is really interesting in this case. I think there a few reasons for the UPC to be increased, particularly the oral steroids. I would definitely culture the urien/sediment exam. I would only treat the proteinuria if the was a persistent and consistent finding once the DM was better controlled. I would want to be demonstrating this increased UPC on three occasions 2 weeks apart”.
4)and last question ? how do you diagnose DKA if you can’t check blood gas? He had ketones on urine multistix and i did the urine strip with blood serum as well and positive for ketones. Is this enough though to diagnose ketoacidosis? His electrolytes were normal and hydrated so I sent him home on caninsulin. But is there a way to diagnose DKA other than confirm acidotic state with blood gas?
“The presence of ketones alone does not really help as many ‘normal’ DM dogs can have ketones. t is really hard to confirm a diagnosis of DKA without the blood gasses. The index of suspicion would be much higher if the patient was sick on presentation, rather than being a well DM dog”.
Hope that helps. Let me know if you have any questions.
Scott 🙂
Hello!
Can you send me the bloods? How high was the blood glucose?
I would still attempt to reduce the steroids. It might be good too do an even more gradual reduction in steroids on this occasion and see if you can get to a dose that does not cause DM but does control the signs.
The main this would be to consider alternative management while reducing the steroids. I would consider cyclosporine, azathioprine, chlorambucil, budesonide.
The other option would be to introduce an antibiotic like metronidazole, as some of these IBD cases will be antibiotic responsive.
If the dog requires the steroids to control the disease, there are some circumstances when you will have to continue the lowest dose of steroids possible and start insulin as you would a normal diabetic.
Hope that helps.
Scott 🙂
I think you are right though Rosie.
It did make me think twice how much I use them!
Scott
Hey.
In these cases, I think it is fine just to taper the steroid. With long-term use, I would normally taper relatively slowly. I would possibly consider a 25% dose reduction on a weekly basis. If the dog had very severe clinical signs, you could do this quicker.
If there is a need to reduce quicker, I would reduce to physiological doses over a period of 7 days.
An inhaler would be an option, but it is important to remember that this steroid will still be absorbed, so you will not be able to completely avoid side effects. Overall, the side effects will normally be fewer.
Hope that helps.
Scott 🙂
Hello.
I hope you are safe and well and enjoying the course!
You can consider once-daily dosing with the total daily dose, it will not offer such good control normally.
I think that the Vidalta may be a good option. You can indeed stop one drug one day and start the other the next.
Let me know how you get on.
Scott 🙂
Totally agree Areti,
I used to use a combination of steroids and would also use chlorphenamine in combination. Diphenhydramine and chlorphenamine both work on the H1 receptor, my question is, would chlorphenamine alone be enough?
Scott 🙂
Hello.
You are absolutely right. Most steroids will cross-react with the actual assay (apart from dexamethasone). The point with doing the ACTH with the iatrogenic Cushings is the flat line response. There will be no stimulation. So, the cortisol may be raised due to the patient being on a steroid, but no stimulation will be seen.
Hope that makes sense.
Scott 🙂
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