Stay hydrated, give insulin and urinate as needed is the general guidance. If too high, medical intervention may be required.
And course change devices and insulin if you don’t feel like you are getting enough good insulin…if In doubt, change it out.
I find blood ketone tests invaluable when I suspect Omnipod malfunction. I’ve also used them on a near-keto diet and the experience was informative.
My ketone levels are usually in the 0.5-2.0 range and that is nowhere near DKA.
I’ve never found an authoritative opinion on the levels for ketones in the presence of significant BG. Do you have one?
I did find a whole load of levels from people on keto diets where they had no significant available BG (because they were on a keto diet).
Because I’m a T1 with no insulin production I regard those numbers are dangerous, for me; not for them.
Yet hospitals do order BG test strips by the thousand; Abbott’s supplies are based on lots of a thousand so far as I could see when I was trying to buy some. Hospitals must have a reason for ordering them. Perhaps it is as a part of general diagnostic tests in ERs but I suspect there is a rubric somewhere for determining whether DKA is happening in a “diabetic” and I suspect it involves BG ketone tests.
All I know about DKA is that it is highly associated with a high BG and a high ketone level. I don’t know an authoritative source.
I understand that the primary driver of DKA is the absence of insulin over several hours. I’ve observed that basal insulin failure is key.
The magic phrase to search for is, “Euglycemic diabetic ketoacidosis” (“EDKA”). Here’s a review/summary/educational paper which has lots of links to original research:
Lack of insulin in IDDs (Insulin Dependent Diabetics; diabetics who require insulin) is almost invariably associated with high BG. This is particularly true because of the impaired glucagon response; IDDs with an impaired glucagon response (mostly T1s but some T2s) continuously produce glucagon (the impairment) and this causes the liver to continuously release glucose, raising BG if there is no insulin to cover it.
Summarizing the paper: EDKA is uncommon but significant (2.6% to 3.2%) in patients suffering from DKA. The summary of known causes comes right at the start:
Euglycemic diabetic ketoacidosis (EDKA) is an uncommon diabetic complication associated with several risk factors such as fasting, surgery, pregnancy, and now the use of sodium-glucose cotransporter 2 (SGLT2) inhibitors.
I fast periodically and I often combine that with exercise. I’ve also tried keto; it works quite well but it does raise blood ketone levels to quite significant values. The keto diet does this through ketosis not, under normal circumstances, ketoacidosis.
One paragraph from that paper struck me as particularly apposite here:
Often, insulin-using patients do not recognize their symptoms as DKA because serum glucose is not elevated, and they may maintain or decrease their insulin dose.[1] If insulin dosing is adequate for glucose levels, it prevents gluconeogenesis, resulting in euglycemia. EDKA can be considered a “partially treated DKA” in this setting.[9]
That alone is a justification for combining blood ketone measurements with blood glucose measurements. HOWEVER education, of both doctors and patients is clearly required, a lot of education.
Maybe the effect of SGLT2s will cause more research and more education. It seems sad that so little work was done before SGLT2s started producing EDKA as a side effect. I guess there’s more money in curing drugs than people.