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.
- Recognised triggers include acute illness, surgery, reduced carbohydrate or prolonged fasting, dehydration, alcohol excess, insulin omission or reduction and low endogenous insulin reserve.
- Treat confirmed disease with the dedicated adult DKA fixed-rate insulin pathway; glucose-containing fluid is commonly needed from the outset or early to permit continued insulin safely.
- Use blood rather than urine ketones for acute monitoring because urine may lag and SGLT2-associated guidance specifically prioritises blood measurement.
- MHRA advises interruption of SGLT2 treatment for major surgery or acute serious medical illness and restarting only when ketones are normal and the person is stable.
- After an SGLT2-associated DKA episode, do not restart the drug unless another cause has been identified and resolved and the specialist risk–benefit decision is explicit.
Key red flags
Current or recently interrupted dapagliflozin, empagliflozin, canagliflozin or ertugliflozin exposure should lower the threshold for blood ketone testing during acute symptoms.
Vomiting, abdominal discomfort, tachypnoea, malaise or drowsiness that seems too severe for the measured glucose may be the key clue to hidden ketoacidosis.
Fasting, surgical stress, reduced insulin and dehydration can combine after an operation; medication reconciliation must establish the last SGLT2 dose and current ketones.
Pregnancy accelerates starvation ketosis and changes normal acid–base physiology, so unwell pregnant patients need immediate obstetric and diabetes specialist assessment under the dedicated pathway.
Lactate, renal failure, toxic alcohols, salicylate and sepsis may cause or coexist with high-anion-gap acidosis; ketones do not end the diagnostic assessment.
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.
- If ketonaemia and acidosis meet the clinical DKA syndrome, activate the adult fixed-rate pathway and senior diabetes input despite a glucose value that appears reassuring.