until the introduction of SGLT2 inhibitors (gliflozins), diabetic ketoacidosis (DKA) only occurred in type I insulin-dependent diabetic patients
these agents have been shown to cause a potentially life threatening euglycaemic form of diabetic ketoacidosis
this is thought to occur through the gliflozins reducing circulating glucose load and thereby reducing stimulation of endogenous insulin secretion to a level insufficient to prevent lipolysis
an additional mechanism may be increased renal tubular reabsorption of ketone bodies which also means reduced ketonuria, and increased glucagon secretion
Prevention
cease glilozones if:
surgery
severe infections
extreme exertion
avoid starting gliflozones if:
high stress
inadequate CHO intake
unwell
Diagnosis
unwell diabetic patient on a gliflozin, and, raised blood ketone levels on fingerprick testing