Euglycemic DKA on an SGLT2 Inhibitor
72-year-old woman with type 2 diabetes on empagliflozin, metformin, and glipizide presents with 2 days of nausea, vomiting, and abdominal pain. She recently had a viral illness and reduced oral intake. Vitals: BP 102/64, HR 112, RR 28, temp 37.1°C, SpO2 98%. She is lethargic but arousable. Labs: glucose 212 mg/dL, pH 7.19, bicarbonate 11 mmol/L, anion gap 26, beta-hydroxybutyrate 5.8 mmol/L, creatinine 1.5 (baseline 0.9), potassium 5.4. She took her usual medications this morning, including empagliflozin. Her abdomen is soft but diffusely tender. The emergency clinician is considering a diagnosis of gastroenteritis.
1. Why is euglycemic DKA a plausible diagnosis despite a glucose of 212 mg/dL, and what immediate management is indicated?
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SGLT2 inhibitors promote glycosuria, so glucose can be only modestly elevated even when ketoacidosis is severe. Her illness and reduced intake increase counterregulatory hormones and ketogenesis, while the drug continues to lower glucose. The pH of 7.19, bicarbonate of 11, anion gap of 26, and beta-hydroxybutyrate of 5.8 confirm a high-anion-gap ketoacidosis. Immediate management includes holding empagliflozin, giving isotonic IV fluids, checking an ECG, and starting an insulin infusion. Her potassium is 5.4 mmol/L, so insulin can start now, but potassium must be checked hourly because insulin drives it intracellularly. Add dextrose when glucose falls below about 200 mg/dL so insulin can continue until the anion gap closes. Bicarbonate is not indicated unless pH is below 6.9. Treat the precipitating illness.
2. What are the key monitoring parameters and pitfalls in the first 12 hours?
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Monitor glucose hourly, potassium and electrolytes every 2 to 4 hours, venous pH and bicarbonate, anion gap, beta-hydroxybutyrate, phosphate, magnesium, creatinine, and urine output. The main pitfall is stopping insulin when glucose normalizes while ketones and acidosis persist; dextrose should be added so insulin continues. Another pitfall is missing hypokalemia as insulin shifts potassium into cells. Watch for fluid overload, especially if she has kidney disease or heart failure, and for hypoglycemia. Mental status should improve as acidosis resolves; if it worsens, consider cerebral edema or another cause. Do not rely on glucose alone to judge resolution; closure of the anion gap and clearance of ketones are the targets.
3. How would you address the diagnostic uncertainty with gastroenteritis and the patient's medication regimen at discharge?
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Abdominal pain, nausea, and vomiting are common in DKA and can mimic gastroenteritis, so the acidosis and ketones should drive the diagnosis. I would explain this to the team and avoid giving antiemetics as the only treatment. At discharge, I would review the SGLT2 inhibitor and provide sick-day rules: hold empagliflozin during acute illness, vomiting, or poor intake, and restart only when eating and drinking normally. I would check the eGFR because metformin may need dose adjustment or discontinuation with a creatinine of 1.5 mg/dL, and I would review glipizide for hypoglycemia risk. She needs diabetes education, follow-up within a week, and a written plan for when to call or return. If DKA recurs, consider an alternative agent.