[QUOTE=prairiewind2;5650790]
No, we don’t know what he died of. No one does necropsies here, and vet just said, “old dog.” As I also mentioned, we were younger and stupider then, and had more faith in vets.
We did not take him in for pain or stronger meds. He was doing fine. We were in for a checkup. The vet said they had a newer, better painkiller, and so “let’s get him off aspirin.” Not our idea. So I took in a dog who was doing very well for his age, gave him a new med, and he died. Is there a chance that something unrelated to the Rimadyl caused his death. Sure, I suppose so. Most all things are possible. But am I suspicious because a pretty healthy old guy went in, was given a new med with no tests or aspirin layoff, and died with a couple of days after becoming anorexic? You bet.
I was under the impression that Rimadyl (carprofen) inhibited Cox 2.
As far as Addison’s and glucocorticoids - you are describing primary Addison’s. That is not what my dog had. Checked my records last night, and he had what my vet generally called secondary Addison’s, though that may not be the scientific name. (Remember, no specialists here.) I looked in the Merck Manual to see if I could find what she was talking about and found with this page.
http://www.merckmanuals.com/professional/sec12/ch153/ch153c.html
Prolonged steroid use can bring it about, whether or not the steroid is stopped abruptly. There are other possible causes, and the dog/person probably has underlying issues. But do I still doubt the vet that put my puppy on months of steroids? Yes, because the next vet we took him to did allergy tests, and had allergy shots made that took care of the dog’s allergies with no steroids. Obviously the steroids were the easy way out, and may have contributed to my beloved dog’s illness and death. Perhaps I would have been more understanding if that same vet clinic hadn’t given my old dog Rimadyl with no tests, and nearly declawed my kitten (and I absolutely DO NOT believe in declawing cats!).
As far as anesthesia goes - I am probably misspeaking. It is not the protocols that I have trouble with, it is anesthesia in general and surgery. I’ve had three sighthound breeds, one of them rare in this country. That one has a problem with malignant hyperthermia. I don’t know that the anesthesia protocol has anything to do with that, just anesthesia in general. I agree that protocols for sighthounds are much safer now than they used to be, in general anyway.
Factor VII can be tested for, and has proven to be of questionable predictive value in my rare breed. Some dogs with it don’t bleed, and some dogs without it do. No one knows why.
I can’t speak of DIC in all sighthounds, just in my three breeds (of which I have only one now, the rarest). And DIC is a problem in this rare breed. But because the breed is rare, there won’t be lots of testing and studies. Sighthound studies are usually done on greyhounds, because there are a reasonable number of those and lots of money in racing them. (At least there used to be.) DIC is a mystery and a terror to us owners, though less so to me because in my breed anyway, it most often happens in females and I only have males.
Liz[/QUOTE]
Yes, rimdadyl inhibits COX2. That is the reason we use it. However it, and ALL the NSIADS, inhibit COX1 too. To some degree or another. That is the effect we DON’T want and is responsible for the side effects.
Addisons: There is primary, which is the dog’s adrenal, all by itself for no identifiable reason, stops working. There is secondary, or iatrogenic, addisons, which is due to us putting to much of the steroids into the dog causing the normal negative feedback mechanism to cause the adrenal to “take it easy”. It is still working but has backed way down. So when the long term, high doses of steroids are suddenly removed, there is no adrenal function. This is (usually) temporary, but still needs to be treated until the adrenal resumes it normal function.
With primary, there are 2 “types”: typical and atypical. It seems, at least in my world, that most are atypical. Ie they don’t come in with dramatically elevated K and dramatically low Na, bradycardic, in shock, etc. Most present with vague, waxing and waning, non-specific signs. Perhaps your dog was an atypical addisonian?
With secondary addisons, as long as the dog is on steroids, he is fine. If anything, they become iatrogenically CUSHINGOID due to the excess steroids.
And speaking of Cushings, when treating a dog with “real” Cushings, one of the risks we are taking is perhaps making the dog addisonian.
MH: it is a genetic disease and not caused by anesthesia. It is TRIGGERED by some anesthetics, which are seldom if ever used any more in veterinary anesthesia. However there is a syndrome that looks alot like MH, but isn’t. And is brought on by drugs we often use for sedation. It is not a sighthound specific problem though. If the dog lived thru the “MH” episode, it wasn’t MH. And again, you can test for MH.
Factor 7: Bleeding, or not, is a funciton of the amount of factor present. Many von Wilibrands dogs wont’ bleed, until something upsets their apple cart. Some bleed if you look at them wrong. The former have low amoungs of the factor involved but “enough”. The later have virtually none of the factor involved. Not an all or nothing.
If you think (or know) your dog has a facto 7 problem, then advse the vet to either do an IN HOUSE PT clotting test to see if he has enough to clot at that time, or just go ahead and administer fresh frozen plasma to replace the factor if the dog needs surgery.
DIC is a mystery and terror to ALL of us. Once we know what is triggering that particular patient to develope it, we might be able to treat it and it will no longer stand for Death Is Coming or Dead In Cage.
If you have any PROOF you have or know of some breed that is predisposed to developing it, I want to see it. I am not being a smart as here. I really do want to see it. And you PM me the info.