Endocrine Abstracts

JOINT54

Background: Euglycemic Diabetic Ketoacidosis is a rare but potentially life-threatening complication of diabetes characterized by ketoacidosis with blood glucose levels typically <200 mg/dL. The absence of hyperglycemia is a conundrum for physicians in the emergency department; it may delay diagnosis and treatment causing worse outcomes. Euglycemic DKA is an uncommon diagnosis but can occur in patients with type 1 or type 2 diabetes mellitus. Usually with the addition of sodium/glucose cotransporter-2 inhibitors in diabetes mellitus management, euglycemic DKA incidence has increased. We present a case of a 16-year-old male with a history of type 1 diabetes who developed euglycemic DKA following a prolonged poor appetite (fasting). Notably, the patient was not on any SGLT2 inhibitors. This case highlights the importance of recognizing euglycemic DKA in patients with diabetes, even in the absence of significant hyperglycemia or SGLT2 inhibitor use. Euglycemic DKA was first described in 1973 by Munro et al [1] among type 1 DM. Euglycemic DKA is an uncommon diagnosis with an incidence ranging between 2.6% to 3.2% of admissions with DKA [2,3].

Case Presentation: A 16-year-old male with a history of type 1 diabetes mellitus presented to the emergency department with a chief complaint of body malaise. The patient reported a 3-day history of body malaise, accompanied by poor appetite for the past week. He also described experiencing burning epigastric pain and nausea. He was compliant with his insulin. He denied any history of infection, fever, cough, or urinary symptoms. On PE, the patient was well-nourished, alert, and oriented with a Glasgow Coma Scale (GCS) of 15. He was not in respiratory distress. Vital signs were within normal limits: blood pressure 100/70 mmHg, pulse rate 98 bpm, respiratory rate 20 cpm, temperature 36.6 °C, oxygen saturation 97%, height 171 cm, and weight 58 kg. Laboratory investigations revealed a blood glucose level of 108 mg/dL, arterial blood gas showing metabolic acidosis with an increased anion gap, and ketonemia. Based on these findings, a diagnosis of euglycemic diabetic ketoacidosis secondary to fasting starvation was established. The patient was promptly started on intravenous fluids, insulin therapy, and electrolyte replacement.

Conclusion: This case report underscores the importance of recognizing euglycemic diabetic ketoacidosis as a potential complication in patients with diabetes, even in the absence of marked hyperglycemia or SGLT2 inhibitor use. Prompt recognition and management of euglycemic DKA are crucial for optimizing patient outcomes and preventing potentially life-threatening complications.