Synopsis
Detect ketoacidosis despite modest glucose, identify SGLT2 and physiological drivers, and maintain insulin with glucose substrate until ketonaemia resolves.
- Euglycaemic DKA is ketoacidosis with glucose lower than expected for classic DKA, not benign nutritional ketosis with normal acid–base status.
- SGLT2 inhibitors increase urinary glucose loss, so serious ketogenesis can develop while capillary glucose appears only mildly raised or even within range.
- Test blood ketones and venous pH in an unwell exposed patient with nausea, vomiting, abdominal pain, dyspnoea, dehydration, drowsiness or unexplained high-anion-gap acidosis.
Key red flags
Current or recently interrupted dapagliflozin, empagliflozin, canagliflozin or ertugliflozin exposure should lower the threshold for blood ketone testing during acute symptoms.
Investigation priorities
Detect substantial ketonaemia promptly and follow response during insulin therapy.
Management branches
An acutely unwell person has SGLT2 exposure, fasting, surgery, pregnancy or insulin deficiency but no marked hyperglycaemia.
- Check capillary blood ketones and a venous gas immediately alongside bedside glucose, renal profile, lactate, observations, fluid state and a focused cause assessment.
- Stop any SGLT2 inhibitor and confirm the insulin regimen, last doses, food intake and operation or illness timeline without allowing medicines reconciliation to delay resuscitation.
Key medicines
Fixed-rate intravenous insulin in euglycaemic DKAFollow the adult DKA prescription at 0.1 units/kg/hour while providing sufficient intravenous glucose to maintain safe glycaemia; specialist protocols supersede this in pregnancy, children and unusual insulin sensitivity.
SGLT2 inhibitor after ketoacidosisStop the medicine when DKA is suspected; do not restart after an associated episode unless a different cause has been identified and resolved and an informed specialist decision supports re-exposure.