SAT439 Euglycemic Diabetic Ketoacidosis When Combining Empagliflozin With Cocaine

Disclosure: F.A. Squicimari-de Cardenas: None. J. Bosques-Lorenzo: None. L. Alejandro: None. C. Rodriguez: None. C. Carlos: None. J.M. Colon Castellano: None. Background: Euglycemic DKA (eu-DKA) is a life-threatening emergency that can occur in patients with either type 1 or type 2 DM, and manifests as a milder degree of hyperglycemia with glucose levels around 200mg/dL. Cocaine abuse alone has been associated with DKA and eu-DKA by inducing cortisol, epinephrine, and norepinephrine release from adrenal glands, and by its anorexigenic effects by suppressing the feeding centers in the central nervous system. Here we present a case of eu-DKA in a patient that combined SGLT2i with cocaine. Clinical Case: A 66 y/o male with past medical history significant for DM type 2 treated with empagliflozin 25mg daily, metformin 1000mg BID, glargine 45 units am and pm, and exenatide 2mg. Patient presented to the ER with general malaise, dyspnea, abdominal pain, and nauseas. On initial evaluation, vital signs were remarkable for temperature at 97.8 F, pulse at 101 bpm, blood pressure 172/113 mmHg, respiratory rate at 20 bpm. Physical examination significant for a tachypneic, restless, and acutely ill patient that was alert, oriented and able to provide medical history. He and his family members denied him using illicit drugs or alcohol. Laboratories were found with severe metabolic acidosis. Central CO2 at 3.8 mEq/L (24-32 mEq/L), central glucose 241 mg/dL (70-99 mg/dL), elevated anion gap at 29.2 mEq/L, B-hydroxybutyrate markedly elevated at >83.3 mg/dL (0.2 - 2.81 mg/dL), arterial blood gases with pH at 7.11 (7.38-7.46) and HCO3 at 3.0 mmol/L (21-29 mmol/L). Urinalysis was positive for ketones and glucosuria. Toxicology came back positive for cocaine, and negative for alcohol. Due to patients’ severe acidosis and concerns for cardiac arrest, he was intubated for airway protection and admitted to the ICU for further management. DKA protocol was initiated and treatment with IV insulin, IV 5% Dextrose, 0.45% normal saline, potassium replacement, and IV bicarbonate provided until anion gap closed and acidosis resolved. Eventually, patient was successfully extubated and transferred to ward for further management and diabetic treatment optimization. Conclusion: Cocaine use is an independent trigger for DKA and eu-DKA. Euglycemic DKA has been raising with the surge of SGLT2i. As in our patient, concomitant use of SGLT2i and cocaine can precipitate patients for development for DKA/eu-DKA. It is important to educate patients to avoid concomitant use of this two and to perform toxicology screening in patients presenting with DKA or eu-DKA. Presentation: Saturday, June 17, 2023