04/02/2026
I have mentioned euglycaemic DKA in past posts, fairly briefly. Let us dive a bit deeper, and with more background.
Originally this term was used mostly in hospital, where people on SGLT2 inhibitors (empagiflozin, dapagliflozin), who were fasting due to illness or surgery, would become acidotic with normal or barely elevated glucose levels (unlike normal DKA where glucose is almost always high because of lack of insulin). In hospital, it is treated with IV fluids, insulin and glucose.
Traditionally SGLT2 inhibitors were used mostly in T2 diabetes, but these days people with T1D may well be prescribed them as well, to aid in lowering insulin requirements.
T1s also use GLP1 receptor agonists these days, to reduce insulin needs, and for weight control in some cases.
GLP1 RAs include semeglutide (Wegovy, Ozempic) and tirzepatide (Mounjaro). For the remainder of this post they will be called GLP1s.
We all know that T1s (and T3cs) need insulin to stay alive and not develop DKA and eventually die. An interesting phenomenon has emerged in the past few years, since smart (sensor augmented) pumps have become more mainstream.
Sometimes, if a T1 using a smart pump is exercising very heavily or performing heavy incidental physical work (moving house, shifting or chopping firewood, building a wall etc etc), the pump may turn insulin off for a few hours in order to try and prevent a low glucose. If the T1 performing the heavy exertion is not eating much, then the pump can turn off long enough for ketones to develop. The way I understand this is that the muscles are very sensitised to insulin, and are gobbling up all the glucose they can, but the brain, heart, kidneys and other internal organs also need insulin to function, and if it is not available, then ketosis commences.
The result in an otherwise healthy T1 with good body awareness is a feeling of nausea, weakness, headache, and feeling like ketones might be occurring, but with a tidy or even low glucose. Ketones should be checked if feeling gross while undertaking heavy, unaccustomed exertion.
It is relatively quickly fixed in the early stages - carbs, fluids, and a decent bolus.
This phenomenon is highly unlikely in people using long acting insulin, or using a ādumb pumpā that gives a continuous dribble of insulin.
If a pump fails, then regular DKA with high glucose will happen.
Both SGLT2is and GLP1s make this low or normal glucose DKA more likely, because they reduce the amount of insulin needed generally, and may suppress appetite to the degree people forget to eat.
Why do people with T1 eating very low carb diets not experience this? Well, they absolutely can, if their basal insulin is turned off or down to low enough levels. But if basal insulin is happening normally, then a low carb diets is not a concern (but can be very tedious, in my opinion).
Some athletes with and without T1D do a thing where they eat very low carb habitually, and are able to fuel distance athletics by eating just fat and proteinš³. This cannot be done quickly by anyone (with or without a functioning set of Islet cells), it takes 12ish weeks of very low carb eating and athletic training to become āfat adaptedā and able to run a marathon on avocado salad and chicken fillets. I do not understand this process in the slightest.
Basic message here is: you can develop DKA with normal glucose if exerting yourself and your pump stops insulin for long enough. Treat it with insulin, carbs and hydration. If vomiting stops that happening, head to ED for IV glucose and fluids. Oh, influenza can cause sustained low glucose in some folks (yes, me, and others), so watch out for euglycaemic DKA on top of the flu. And get your vaccination!
