SAT-624 - SGLT-2 Inhibitor-Induced Euglycemic Diabetic Ketoacidosis Complicated by Takotsubo Cardiomyopathy

Background:  Euglycemic diabetic ketoacidosis (EDKA) is an uncommon but increasingly recognized complication associated with sodium–glucose cotransporter-2 inhibitors (SGLT-2i). Takotsubo cardiomyopathy has been described in the setting of classic diabetic ketoacidosis; however, its association with SGLT-2i–induced EDKA is not well reported. We report a case of EDKA complicated by Takotsubo cardiomyopathy.

Case Description:  A 44-year-old woman with poorly controlled type 2 diabetes mellitus, coronary artery disease status post stent placement, and gastroesophageal reflux disease presented with nausea, vomiting, and abdominal pain. Her medications included tirzepatide and empagliflozin, initiated eight weeks prior. On admission, she was hemodynamically stable with diffuse abdominal tenderness. Laboratory evaluation revealed an anion gap 19, bicarbonate 16 mmol/L, serum beta-hydroxybutyrate 50 mmol/L, venous pH < 7.18, fasting glucose 188 mg/dL, and HbA1c 7.6%, consistent with EDKA. Empagliflozin was suspected of being the precipitant of EDKA and was discontinued.
Several hours later, the patient developed acute chest pain. Electrocardiogram showed sinus tachycardia with new anterolateral T-wave inversions and an elevated troponin I of 1.5 ng/mL. Transthoracic echocardiography demonstrated a reduced left ventricular ejection fraction (25–30%) with severe global hypokinesis, consistent with Takotsubo cardiomyopathy, compared to a normal study one year prior. Coronary angiography revealed non-obstructive coronary artery disease (LAD 50% stenosis and left circumflex 40% stenosis). She was managed in the intensive care unit with insulin infusion and intravenous fluids, resulting in resolution of acidosis. Abdominal CT scan with contrast showed no contrast filing beyond D1/2 duodenal junction with mural thickening. Endoscopy revealed only mild pyloric spasm. Tirzepatide was discontinued due to concern for impaired oral intake and gastric dysmotility. The patient was initiated on guideline-directed medical therapy with carvedilol, spironolactone, lisinopril and atorvastatin. She was discharged with a LifeVest, which was discontinued 2 months later after a cardiac MRI revealed improved EF of 56%.

Conclusion:  This case highlights a rare but serious complication of SGLT-2i–associated EDKA complicated by Takotsubo cardiomyopathy, likely precipitated by catecholamine surge in the setting of metabolic stress. Clinicians should maintain a high index of suspicion for EDKA in patients taking SGLT-2 inhibitors, even in the absence of significant hyperglycemia, as early recognition may prevent rare but serious complications such as stress-induced cardiomyopathy.

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