POS-106 A NOT SO SWEET COMPLICATION OF DIABETES MELLITUS THERAPY(EUGLYCEMIC DKA)

Abstract

Diabetic ketoacidosis (DKA) is the most feared and well-known life-threatening complication of diabetes generally due to noncompliance or an active infectious process. But, what if DKA were to take place with adequate medication adherence? Euglycemic diabetic ketoacidosis is a clinical diagnosis that encompasses an increased anion gap metabolic acidosis, ketonemia or ketonuria in the setting of normal blood glucose levels (<200 mg/dL). This entity is a diagnostic challenge as euglycemia cover-ups the underlying diabetic ketoacidosis. Seeing as how sodium-glucose cotransporter 2 (SGLT2) inhibitor use has increased following studies that demonstrate its cardioprotective and renoprotective effects a high index of clinical suspicion is warranted now more than ever, and other diagnosis must be ruled out. This is the case of a 66 y/o male patient with past medical history of type 2 diabetes mellitus on empagliflozin, insulin and metformin, arterial hypertension, major depressive disorder, dyslipidemia who was initially admitted to a psychiatric hospital for management of depression and psychosis. Two days after admission he presented with diffuse abdominal discomfort associated with nausea, vomiting, poor appetite and difficulty voiding for which he was transferred to our institution for Internal Medicine evaluation. After evaluation at the Emergency Department he was admitted to IM ward with diagnostic impression of acute prostatitis and obstructive uropathy. Initial laboratories were remarkable for WBCs at 9.4x10-3uL, no bandemia and no neutrophilia, adequate hemoglobin and platelet count. Chemistry with Glucose at 136mEq/L, Potassium at 4.5mEq/L, HCO3 at19mEq/L, normal hepatic enzymes, normal lactic acid and normal pancreatic enzymes. Laboratories the next morning revealed glucose 127 mg/dL, bicarbonate 14 mEq/L with a pure high anion gap metabolic acidosis of 23mEq/L (delta-delta of 1.1), beta-hydroxybutyrate at 65mg/dL, normal lactate 0.8 mmol/L, negative toxicology and arterial blood gases revealing metabolic acidosis with adequate respiratory compensation (pH 7.314, pCO2 31.3 mmHg and bicarbonate 15.5 mmol/L). Diagnosis of euglycemic DKA secondary to empagliflozin precipitated by acute bacterial prostatitis and decreased oral intake was made. Patient subsequently transferred to t he medical intensive care unit where crystalloid volume expansion was provided, DKA protocol with intravenous insulin infusion initiated along with D10W intravenous fluid administration. After approximately 16 hours of treatment, metabolic acidosis and anion gap normalized. Patient was successfully discharged home after completion of antibiotherapy with follow up with his primary care physician. Euglycemic DKA secondary to SGLT2i is a diagnosis often missed by physicians accustomed to seeking for elevated blood sugars. Its presentation is often vague and insidious for which cases are underreported and incidence remains unknown. Nonetheless, ketoacidosis in diabetic patients remains a medical emergency despite euglycemia. High clinical suspicion is warranted in order to begin prompt treatment and reduce hospital stay as well as associated costs.