Our cutoff is 250 BS at the time of procedure. We don't have a formal policy about A1c and steroids but should probably think of that. I would have to have a pretty convincing story to not consider a 27g needle for TPIs if I felt clinically indicated. If they are getting labs, insulin, (needle pokes). without issues I would find it hard to say no.
VA Ortho limits surgeries to less than 8.6 and we have adopted this for any steroid injection unless severe pain and recent glucose has been 120 or less
Random glucose is less useful but I generally use 250 as a cutoff but if it's a little elevated above that and A1c is otw below 8.5 I'll make exceptions (and usually won't use a steroid).
Random glucose is less useful but I generally use 250 as a cutoff but if it's a little elevated above that and A1c is otw below 8.5 I'll make exceptions (and usually won't use a steroid).
It would tell me I'm dealing with bad protoplasm and would tread cautiously if at all.
TPI, MBB, RFA - i dont consider A1C for these. not that i do a lot of TPI.
if there is evidence of poor healing clinically, that means a lot more to me than the current A1C. if a person has severe lower extremity ulcerations, then they shouldnt have a tpi or other procedure.
after all, these people get IVs and blood draws all the time without deleterious side effects. and i guarantee the phlebotomists are not as fastidious about sterile prep than i am.
if sugars are routinely out of control and they are working with end or have obvious ulcerations, etc, ill wait until they are under better control. that happens about 2x/decade
Nope. I’ve done 0 cases with IV sedation in the last year and almost never offer it.
I don’t order A1Cs or go hunting but the majority of patients I see have labs done in the same health system connected to my EMR so I see the results. IMHO choosing to ignore that part of the patients chart would be wrong.
I don't measure A1C, but will review if in chart. I don't have an A1C cutoff for injections, but will cancel steroid injections if glucose is greater than 250. I'm okay doing MBB/RF since I don't use steroids for those.
For implants, I was the A1C to be under control, but I don't do many implants. Ortho literature is for insertion of hardware and the associated post-op infection as well as wound healing. A low A1C makes sense for anytime you want to insert a foreign device.
I feel like people are all over the map with labs. I only get for SCS (including trial), kypho, Intracept. CBC, UA, coags looking for occult infection and bleeding risk. Plenty don't do this and I don't know if I'm opening a can of worms sometimes.
I stopped offering steroids to pts with an A1c>8.5 after I had a few brittle diabetics end up in the ED with DKA and hyperosmolar hyperglycemia. I'll give half my normal dose (40 mg Kenalog equivalent is my normal, so 20 mg) to diabetics in the 7-8.5 range the first time around to see how they respond.
i didn't check his labs but saw he had wounds and multiple wound care appts in the emr
when i spoke with him he said he checks his BS daily and they run 150s... so i thought, ok, sure let's schedule for tpi
then i checked his chart and a1c from within 2 weeks prior was 12. you don't get an a1c of 12 with fasting BS of 150.
my cutoff for steroids is a1c of 8. i have had a few brittle IDDM2 get their sugars up to 400-500s after CSI even with low a1c and strict monitoring at home with sliding scale. i was just curious how people handle non steroid injections, non implants etc.
so once i saw the a1c of a dozen i cancelled the procedure. not worth the risk...
Steroids are not mandatory for any of those procedures, so A1C and glucose are of no concern. Just do them without steroids. I do all my mob's and RFAs without steroids anyways. TPIs only with steroids sometimes (usually not).
Osteoarthritis (OA) is a degenerative joint disease affecting millions of people worldwide. In OA, chondrocytes, synovial cells and other joint cells become activated when exposed to an abnormal environment, including mechanical stress, inflammatory ...
Osteoarthritis (OA) is a degenerative joint disease affecting millions of people worldwide. In OA, chondrocytes, synovial cells and other joint cells become activated when exposed to an abnormal environment, including mechanical stress, inflammatory cytokines or disorganization of matrix proteins. Several analogues of the hormones called incretins have been developed and are used notably for treating type 2 diabetes mellitus. Data has accumulated to suggest that incretinomimetics, which bind to the glucagon-like peptide-1 receptor (GLP-1R), have beneficial pleiotropic effects such as immunomodulation, anti-inflammation and neuronal protection. Thus, because of their anti-inflammatory properties, GLP-1-based therapies could benefit OA patients. This review focuses on the GLP-1R pathway, molecular mechanisms and phenotypes related to OA pathogenesis. The translational potential of this article: The search for new therapeutic targets to treat people suffering from OA remains urgent as there is currently no disease-modifyingtherapy available for this disease. This review discusses how GLP-1 analogues could be potential DMOADs for treating OA thanks to their anti-inflammatory, immunoregulatory and differentiation properties. Keywords: Cartilage; Glucagon-like peptide-1 (GLP-1); Glucagon-like peptide-1 receptor (GLP-1R); Liraglutide; Osteoarthritis; Synovial tissue.
Osteoarthritis (OA) is a degenerative joint disease affecting millions of people worldwide. In OA, chondrocytes, synovial cells and other joint cells become activated when exposed to an abnormal environment, including mechanical stress, inflammatory ...
Osteoarthritis (OA) is a degenerative joint disease affecting millions of people worldwide. In OA, chondrocytes, synovial cells and other joint cells become activated when exposed to an abnormal environment, including mechanical stress, inflammatory cytokines or disorganization of matrix proteins. Several analogues of the hormones called incretins have been developed and are used notably for treating type 2 diabetes mellitus. Data has accumulated to suggest that incretinomimetics, which bind to the glucagon-like peptide-1 receptor (GLP-1R), have beneficial pleiotropic effects such as immunomodulation, anti-inflammation and neuronal protection. Thus, because of their anti-inflammatory properties, GLP-1-based therapies could benefit OA patients. This review focuses on the GLP-1R pathway, molecular mechanisms and phenotypes related to OA pathogenesis. The translational potential of this article: The search for new therapeutic targets to treat people suffering from OA remains urgent as there is currently no disease-modifyingtherapy available for this disease. This review discusses how GLP-1 analogues could be potential DMOADs for treating OA thanks to their anti-inflammatory, immunoregulatory and differentiation properties. Keywords: Cartilage; Glucagon-like peptide-1 (GLP-1); Glucagon-like peptide-1 receptor (GLP-1R); Liraglutide; Osteoarthritis; Synovial tissue.
