ODP244 SGLT2 Inhibitor-Induced Euglycemic DKA and its Challenges
Authors: Penna Laurianne El Musa , Rivera Mónica Ortiz , Rosado Burgos Alexandra , Marin Luis Madera , Rivera Nieves Yadiel , Hernandez Cordero Nicole , Burgos Ortega Nydia , Alvarado Milliete , Ramirez-Vick Margarita , Gonzalez Rodríguez Loida 
Published: November 2022

Introduction

Sodium-glucose cotransporter type 2 inhibitors (SGLT2-i) have proven to be a gamechanger for patients with diabetes, cardiovascular, and renal disease. However, this class of medications confers an increased risk for adverse side effects such as genitourinary infections and, rarely, euglycemic diabetic ketoacidosis (EDKA). Studies have shown that the risk of euglycemic DKA from SGLT2 inhibitors increase sevenfold in patients with type 2 diabetes mellitus (T2DM) with an overall incidence of approximately 0.1%. These side effects need to be taken into consideration when prescribing this type of therapy.

Case Description

Case of a 61-year-old male, with hypertension, type 2 diabetes mellitus on glargine, insulin lispro and empagliflozin, adherent to his regimen. Also, patient had a history of CAD s/p PCI (2015), and urethral stricture with self-catheterization who presented to the ED complaining of genital pain of 4 days evolution. Patient had been treated at home with clindamycin without improvement of symptoms. Upon evaluation at ED, laboratories were remarkable for WBC: 25.90, glucose: 144mg/dL, sodium: 134mmol/L, potassium: 5.3mmol/L, CO2: 10mmol/L, ketones: large. Arterial blood gases with metabolic acidosis and anion gap: 26.3. [LAG1] Glycated hemoglobin was 6.8%. Urinalysis was significant for glucosuria 1000 mg/dL, SG 1. 036, 30 mg/dL of protein, negative for nitrites and leukocyte esterase, and few bacteria. Blood glucose levels remained between 145-194 the first 24 hours after admission. Urology service performed a penile exploration with the finding of bilateral corpus cavernosum abscesses that were drained and cultured. Patient was diagnosed with EDKA and started therapy with IV insulin infusion as per DKA protocol, however 10% dextrose infusion was required to continue insulin IV infusion until ketoacidosis resolution. Broad spectrum IV antibiotics were initiated. However, his clinical condition deteriorated and developed respiratory failure requiring mechanical ventilation. After 36 hours of insulin infusion, IV antibiotics and fluids, his anion gap normalized. Abscess and blood cultures reported Candida Glabrata. Antifungal therapy was started and after seven days, the patient's clinical condition improved with resolution of his sepsis and DKA, and was successfully extubated. Patient was discharged to a rehabilitation facility.

Conclusion

EDKA presents a diagnostic and treatment challenge. It should be suspected in patients with metabolic acidosis, ketonemia and under treatment with a SGLT2-i, even in the absence of hyperglycemia. Prompt treatment initiation with IV insulin infusion along with IV dextrose is important for resolution of DKA. Five-percent dextrose solution should be started and titrated as needed, but if ketoacidosis does not resolve, 10% dextrose can be considered to maintain the insulin infusion. Prescribing this class of hypoglycemic medication should be avoided in those who are clearly at high risk of this well-known complications. Patient education regarding early recognition and to seek early medical evaluation are essential. [LAG1]Anadir unidades

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