Vomiting, acidosis and a normal glucose on an SGLT2 inhibitor

The glucose is misleading. This is diabetic ketoacidosis with a near-normal glucose because empagliflozin has been causing ongoing glycosuria, keeping serum glucose down while volume depletion and reduced carbohydrate intake drive lipolysis and ketogenesis. SGLT2 inhibitors also increase glucagon and reduce insulin secretion, favouring ketone production. Euglycaemic DKA is conventionally defined as glucose below 13.9 mmol/L with ketonaemia and acidosis.

Supporting features: vomiting and poor intake, anion gap 26, bicarbonate 8 mmol/L, pH 7.16, beta-hydroxybutyrate 6.2 mmol/L, and acute kidney injury (creatinine 132 versus 80 micromol/L). She stopped all medication when vomiting began, but the drug effect persists for days.

Co-existing issues to exclude: sepsis (urine, chest, blood cultures), pancreatitis (lipase), starvation ketosis alone (which would not usually give a pH of 7.16), metformin-associated lactic acidosis (check lactate; it can coexist), and pregnancy. Alcohol and cocaine are other causes of a high-anion-gap acidosis.

The pitfall is to dismiss DKA because the glucose is 11.4 and to treat this as gastroenteritis. The second pitfall is to attribute the acidosis entirely to metformin and miss the ketones.

First 12 hours

• Hold empagliflozin and metformin. Admit to a monitored bed with catheter and hourly urine output.
• Fluids: 0.9% saline 1 L over the first hour, adjusted for cardiac and renal status, then a slower rate. Avoid over-rapid fluid in a patient with normal cardiac function, but she is tachycardic and likely several litres down.
• Insulin: start a fixed-rate intravenous infusion of 0.1 units/kg/h. Do not give a bolus unless potassium is known and safe. Continue the infusion until the anion gap closes and beta-hydroxybutyrate is below 0.5 mmol/L, not until the glucose normalises.
• When glucose falls below 14 mmol/L, add 10% dextrose at 100 mL/h and continue insulin. This is the key step that prevents rebound ketosis.
• Potassium: she is 5.4 mmol/L, so do not replace until potassium is below 5.5 mmol/L and urine output is adequate; then add 20–40 mmol/L to fluids with 2–4 hourly checks.
• Bicarbonate: reserve for pH below 6.9; it worsens hypokalaemia and shifts ketone metabolism.
• Monitor: glucose hourly, potassium and venous gas 2-hourly, fluid balance, renal function and neurological status. Watch for hypoglycaemia, hypokalaemia, cerebral oedema (rare in adults) and worsening kidney injury.

Avoid: stopping insulin when glucose reaches 12–14 mmol/L; giving too much saline; missing a precipitant; restarting metformin while creatinine is rising.

Restart only when she is eating and drinking, the anion gap and ketones have normalised, pH is above 7.3, and renal function is stable or improving. Metformin can be restarted when eGFR is above 30 mL/min/1.73 m² and there is no ongoing acidosis, hypoxia, sepsis or contrast exposure; recheck renal function at 24–48 hours.

Empagliflozin should not be restarted during the acute illness. Reintroduce at the pre-admission dose once she is eating and euvolemic, usually 24–48 hours after resolution, with explicit sick-day rules: stop the drug during vomiting, diarrhoea, reduced intake, or before surgery. Consider a lower dose if she has recurrent episodes.

Document the episode as euglycaemic DKA. Counsel her to seek advice early during illness and not to assume that a normal glucose reading excludes serious illness. If she has type 1 diabetes, SGLT2 inhibitors are generally avoided; her C-peptide and antibody status should be checked because the presentation is atypical. Review whether metformin can be continued at the current dose given the admission creatinine, and arrange follow-up renal function.