@David49, I understand that these are just anecdata, and as such, not much to hang your hat on. I'm connecting a lot of docs in a pretty speculative manner. So you can bin this in the category of "medical hypothesis" rather than "well-substantiated, evidence-based assertion."
Stll, allow me to defend my speculation for a second
I do think that these intriguing, if isolated case reports, combined with all the data on SGLT-inhibotors, suggest that euglycemic DKA maybe underrreported, as stated in this article
In which case, I think it's worth it for people with diabetes to consider which circumstances may make that more or less likely.
I'm proposing that euglycemic DKA is probably more likely in people who are on a ketogenic diet compared to those who are not on a ketogenic diet. Also possibly more likely in people who are exercising or have increased oxygen needs, or take very little insulin beyond what is needed to supply their basal needs. That's not to say the overall rate of DKA will be higher in those on a keto diet; just that keto dieters are likelier to have good blood sugar at the time they're spiraling into DKA.
Obviously that paper is focused on the SGLT2s, but I thought this section was noteworthy:
There are multiple proposed theories exploring the link between SGLT2 inhibitors and ketoacidosis. One possible mechanism describes a decreased secretion of insulin from pancreatic cells in a response to the lowering of blood glucose via urinary excretion.2 This results in a decrease of circulating insulin and its antilipolytic activity, leading to increased free fatty acid production.2 Other evidence suggests that SGLT2 inhibitors stimulate the secretion of the counterregulatory hormone glucagon, which in turn contributes to the overproduction of ketone bodies.13,14 Another animal study suggests that SGLT2 inhibitors might decrease the renal clearance of ketone bodies.2 The net result is a stimulation of the ketogenesis pathway and an increase in serum ketones, which predispose the body to ketoacidosis. This effect is compounded in the event of physiologic stressors including, for example, starvation or dehydration.6,8,10 Although research on the pathophysiology is currently ongoing and no definitive causation has been established, the association between SGLT2 inhibitors and DKA cannot be ignored.
To me, that paragraph in the study questions the notion DKA is a condition that can easily be seen coming a mile in advance. Only half of these cases of DKA had any known trigger!
It also makes me skeptical of the idea that the ketones are just somehow passive bystanders and that dehydration is the real culprit in DKA. The fact is, no one knows exactly which elements of DKA are most critical to the cascade, but the SGLT2 data suggests ketones are a critical player. Sure dehydration may result and exacerbate the problem, but it's not the primary cause.
Obviously, people who are not on SGLT-2 inhibitors have different physiological tipping points. But it just seems like all these cases of euglycemic DKA are unmasking some of the necessary ingredients to generating the condition: lack of insulin and ketones, but not necessarily dehydration. And when you're ketogenic, you're adding a bit more of one of those ingredients (possibly two) to the pot. Whether you think the risk is worth doing regular blood ketone checks is different question: That's a risk assessment analysis, based on preliminary or speculative information, and of course will be different for everyone.
But I suspect that in a year or two we'll see more and more data showing that this is surprisingly common and that ketosis is not merely a "bystander" in DKA as seems to be argued on this forum quite a lot.
This is not to knock a low-carb diet, by the way; every type of intervention is going to have some pros and cons. For LCHF, I'd put: Pros: for many, better blood sugar control, less insulin, reduced weight, etc. Cons: No apple pie! No ice cream! No focaccia bread! And potentially: less warning for DKA, even if the overall risk is small and not elevated.