see also:

• diabetic ketoacidosis (DKA)
• oral hypoglycaemic agents
• gliflozins / SGLT2 inhibitors

• 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

• cease glilozones if:
  • surgery
  • severe infections
  • extreme exertion
• avoid starting gliflozones if:
  • high stress
  • inadequate CHO intake
  • unwell

• unwell diabetic patient on a gliflozin, and, raised blood ketone levels on fingerprick testing
• blood gases show:
  • high anion gap metabolic acidosis with low bicarb and low base excess

• IV line
• FBE, U&E, glucose, LFTs, lipase, troponin, CRP,
• blood gas and lactate
• ECG
• cease gliflozin
• rehydrate
• insulin and dextrose infusion
  • may need higher than usual dextrose compared to standard diabetic ketoacidosis (DKA) protocols
• potassium replacement as per standard diabetic ketoacidosis (DKA) protocols
• Rx underlying precipitant such as:
  • sepsis / septicaemia - may warrant septic workup
  • acute myocardial infarction (AMI/STEMI/NSTEMI)
  • trauma
  • surgery
  • excess alcohol
  • low CHO diet
  • missed insulin doses