SAT-729 Epinephrine Induce Diabetic Ketoacidosis

Abstract E.J. Morales Quinones: None. M. Almonte: None. P. Lugo: None. Epinephrine induce diabetic ketoacidosis (DKA) is a diagnosis of exclusion that only two cases have been reported in the United States. Patient with any type of allergy can be at increased risk for anaphylaxis and shock that requires the use of epinephrine. The proposed mechanism for epinephrine induced DKA is via induction of glycolysis and lipolysis. Activation of these processes leads to free fatty acid release, which serves as precursor for ketone body formation and suppression of insulin, resulting in DKA. This is the case of a 77-year-old male patient with medical history of arterial hypertension, major depressive disorder and benzodiazepine abuser who was recently incarcerated 3 days ago, presented to the emergency department because he was found on his cell on hypoactive state and with involuntary movement. Vital sign were unremarkable. Dextro was taken upon arrival and it was 96mg/dL. Upon physical examination glasgow coma scale (GCS) was 6/15 and patient was immediately intubated for airway protection and admitted to the Intensive Care Unit. Complete blood count was unremarkable. Basic metabolic panel noted for euglycemia (115mg/dL), high anion gap metabolic acidosis (lactic acid 13mg/dL), mild hypokalemia (3.1mmol/L), stable renal function (1.17mg/dL) and creatinine phosphokinase (279 u/L). Electrocardiogram was remarkable for bradycardia of 40bpm. Chest X Rays was consistent with aspiration pneumonia. Patient was started on Zosyn 3.375 g Intravenous (IV) every 6 hours with IV normal saline at 80ml/hr. On day 2, patient was hypothermic (32.1°C) with bradycardia of 38 bpm. Atropine was administered without improvement for which benzopine ingestion was suspected as the etiology for the patient’s presentation. Labwork noted for hemoglobin A1c of 5.8%. An epinephrine infusion was started due to patient’s sustained bradycardia. On day 3, dextro was 442mg/dL. Labwork was noted for hyperglycemia (491mg/dL) with high anion gap metabolic acidosis (anion gap 20, pH 7.18 and CO2 15.5), osmolality 309, and lactate increased to 58mg/dL. Patient was diagnosed with diabetic ketoacidosis (DKA). The epinephrine infusion was discontinued, thereafter hyperglycemia state resolved without insulin administration. Patient had resolution of DKA, making the diagnosis of epinephrine induced DKA more likely. Subsequently patient was extubated, completed treatment for aspiration pneumonia and diagnosis of benzopine ingestion was confirmed. Only two cases of epinephrine induced DKA had been reported in the past, both on patients with known history of diabetes mellitus. This is the only case of epinephrine-induced ketoacidosis in a non-diabetic patient. Awareness of epinephrine induced DKA in patients with and without diabetic mellitus conditions is imperative as it can be lethal if it’s not promptly recognized. Saturday, June 1, 2024