MON-127 Euglycemic Diabetic Ketoacidosis: A Rare Complication of a Common Disease

INTRODUCTION Euglycemic diabetic ketoacidosis (EDKA) is a clinical triad comprising of blood glucose (BG) levels<200mg/dL, increased anion gap (AG) metabolic acidosis and ketonemia or ketonuria. It remains one of the most serious complications of diabetes as in the absence of hyperglycemia, DKA may be overlooked leading to a delay in appropriate diagnosis and management. CLINICAL CASE A 43-year old male with history of uncontrolled type 1 DM of 20 years, complicated by peripheral neuropathy, diabetic retinopathy, ESRD on hemodialysis, CVA, and hypertension presented with abdominal pain and bloody stools for three days. On admission, he was hemodynamically stable. On examination, he had dry mucous membranes and diffuse abdominal tenderness. Lab work revealed leukocytosis, electrolyte derangements, normal AG and BG of 94mg/dL. Liver chemistry and lipase were normal. CT scan of the abdomen showed a wedge shaped infarct in the anterolateral spleen. Fluid resuscitation with normal saline was started. To maintain glycemic control in the hospital, low dose basal insulin was administered. However, patient developed significant symptomatic hypoglycemia overnight with BG as low as 26mg/dL. 5% dextrose in half normal saline and dextrose were administered which improved BG to 134mmol/L. Labs and blood gas drawn the next morning revealed an AG metabolic acidosis (pH:7.26, HCO3:18mmol/L) with gap of 25mmol/L. Betahydroxybutyrate was elevated (2.5mmol/L). He was diagnosed with EDKA and started on intravenous insulin drip per protocol. A basic metabolic panel was checked every 4 hours with glucose monitored every hour. Subsequently his anion gap closed and acidosis resolved. He was carefully transitioned to basal and bolus insulin regimen. DISCUSSION The mechanism of EDKA is not well known but is thought to be commonly due to decreased gluconeogenesis in liver during fasting state or enhanced urinary excretion of glucose induced by an excess of counter regulatory hormones. EDKA has been associated with low caloric intake, fasting, dehydration, pregnancy, pancreatitis, cocaine intoxication, prolonged vomiting, diarrhea, SGLT2 inhibitor and insulin pump use (1). In our patient, EDKA most likely occurred due to dehydration and low caloric intake in setting of his abdominal pain due to splenic infarct. The principle of treatment of EDKA is to restore fluid and electrolyte losses along with insulin administration to resolve the anion gap. CONCLUSION Euglycemic DKA poses a diagnostic challenge and remains a rare complication of a common disease. A high clinical suspicion is warranted to diagnose and treat it appropriately as a medical emergency. REFERENCES 1. Peters AL, Buschur EO, Buse JB, Cohan P, Diner JC, Hirsch IB. Euglycemic Diabetic Ketoacidosis: A Potential Complication of Treatment With Sodium-Glucose Cotransporter 2 Inhibition. Diabetes Care. 2015;38(9):1687-1693. doi:10.2337/dc15-0843