What is it?
DKA without the elevated glucose that usually triggers us to think about DKA in the first place. Patients often have blood glucose levels less than 250 mg/dl.
Why do we care?
Because untreated DKA can lead to cerebral edema, ARDS, renal failure, shock and death.
Why does it happen?
Euglycemic DKA can occur in any diabetic, but there is a rising incidence in those taking SGLT2 inhibtors (-gliflozins) (listed below). The pathophysiology behind this isn't totally clear yet though there are some theories.
US approved: Dapagliflozin (Farxiga), Canagliflozin (Invokana), Empagliflozin (Jardiance)
It can also occur in those who have underlying disease that depletes the liver's ability to make glucose (putting those who are pregnant or have long bouts of nausea and vomiting under increased risk).
And of course, think of the usual triggers for DKA (ie infection, alcohol use, etc)
When to suspect it?
In any patient with a history of diabetes, including but not limited to those taking SGLT2 inhibitors, who come in for vomiting, generalized weakness, or SOB. Also consider euglycemic DKA in those who have a metabolic acidosis without other clear cause. Draw serum ketones or obtain urine ketones in these patients.
Sounds a lot like alcoholic ketoacidosis--how to tell the difference?
History: history of heavy alcohol use vs a diabetic on an SGLT2 inhibitor.
Signs: those with alcoholic ketoacidosis tend to have a very low glucose.
And maintain a high level of suspicion.
How do we treat it differently than hyperglycemic DKA?
Overall, we treat it pretty similarly. A key difference is that you will need to start fluids with dextrose initially or much earlier than you would with hyperglycemic DKA.
Sources
https://rebelem.com/euglycemic-dka-not-myth/
https://emcrit.org/ibcc/dka/#euglycemic_DKA
https://emergencymedicinecases.com/euglycemic-dka/
http://www.emdocs.net/diabetic-ketoacidosis-sneaky-triggers-clinical-pearls/