Euglycemic Ketoacidosis in Type 1 Diabetes on an SGLT2 Inhibitor
A 29-year-old woman with type 1 diabetes for 12 years, managed with a hybrid closed-loop insulin pump, presents with 14 hours of vomiting, abdominal pain and deep breathing. For 3 months she has also taken empagliflozin 10 mg daily off-label to slow decline in eGFR (baseline 78 mL/min/1.73 m²). She had a gastroenteritis-like illness 2 days ago and reduced her pump basal rate because she was not eating, but continued empagliflozin. Glucose is 13.9 mmol/L, pH 7.19, PaCO2 3.4 kPa, bicarbonate 9 mmol/L, sodium 132 mmol/L, chloride 98 mmol/L, potassium 5.4 mmol/L, creatinine 1.1 mg/dL and beta-hydroxybutyrate 5.8 mmol/L. Urine ketones are strongly positive. She is drowsy but protects her airway; BP 102/60 mmHg, pulse 118/min.
1. What is the diagnosis, and why is the glucose only modestly elevated?
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This is diabetic ketoacidosis with a relatively low glucose - so-called euglycemic DKA. The pH of 7.19, bicarbonate of 9 mmol/L, anion gap of 25 mmol/L and beta-hydroxybutyrate of 5.8 mmol/L establish a high-anion-gap ketoacidosis. The glucose of 13.9 mmol/L is below the traditional DKA threshold of 13.9–14 mmol/L (250 mg/dL), which can mislead clinicians into dismissing the diagnosis.
SGLT2 inhibition produces glycosuria and lowers plasma glucose while simultaneously promoting ketogenesis through insulin deficiency and glucagon excess. Reduced pump basal insulin during illness compounded the problem. The lesson is that glucose underestimates ketone production in this setting, and a normal or near-normal glucose never excludes DKA in a patient taking an SGLT2 inhibitor.
2. Outline your fluid, insulin and potassium management, including the endpoints you would use.
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Start isotonic crystalloid for volume resuscitation, then begin a fixed-rate IV insulin infusion of 0.1 units/kg/hour; do not stop her basal insulin entirely. Potassium is 5.4 mmol/L but total-body potassium is depleted: if potassium is <5.2 mmol/L, add 20–40 mmol/L potassium chloride to the fluids; if <3.3 mmol/L, hold insulin and replace potassium first.
When glucose falls below about 14 mmol/L, add 10% dextrose so the insulin infusion can continue. The endpoint is not a normal glucose - it is closure of the anion gap and clearance of ketones (beta-hydroxybutyrate <0.6 mmol/L). Check glucose and potassium hourly and venous blood gases every 2–4 hours. Bicarbonate is not indicated at pH 7.19; reserve it for pH <6.9. Treat the precipitant, monitor for hypokalemia as insulin drives potassium into cells, and watch for cerebral edema if consciousness deteriorates.
3. What are the common management pitfalls, and what should happen to the empagliflozin?
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The main pitfall is treating the glucose rather than the ketones: stopping insulin when the glucose normalizes allows ketogenesis to continue and causes rebound ketoacidosis. Another is failing to add dextrose, which forces a choice between hypoglycemia and inadequate insulin. Hypokalemia during treatment is common and must be anticipated. Bicarbonate is overused and can worsen hypokalemia and shift the oxyhemoglobin curve.
Empagliflozin should be stopped now and not restarted during the acute illness. If it is continued for renal protection, she needs explicit sick-day rules: hold the drug during vomiting, poor intake or acute illness, and stop it 3–4 days before elective surgery. The risks and off-label status should be discussed, and the diabetes team should review whether the modest renal benefit justifies the ketosis risk in type 1 diabetes.