Euglycemic diabetic ketoacidosis following traumatic brain injury - 12/02/24

Doi : 10.1016/j.ajem.2024.01.006

Sung Woo Jang, MD ^a, Haekyung Lee, MD ^b,^c,^{^⁎}
^a Department of Surgery, National Trauma Center, National Medical Center, 245 Eulji-ro, Jung-gu, Seoul 04564, Republic of Korea
^b Division of Nephrology, Department of Internal Medicine, Soonchunhyang University Seoul Hospital, 59 Daesagwan-ro, Yongsan-gu, Seoul 04401, Republic of Korea
^c Hyonam Kidney Laboratory, Soonchunhyang University Seoul Hospital, Seoul, 59 Daesagwan-ro, Yongsan-gu, Seoul 04401, Republic of Korea

^⁎Corresponding author at: Division of Nephrology, Department of Internal Medicine, Soonchunhyang University Seoul Hospital, 59 Daesagwan-ro, Yongsan-gu, Seoul 04401, Republic of Korea.Division of Nephrology, Department of Internal MedicineSoonchunhyang University Seoul Hospital59 Daesagwan-ro, Yongsan-guSeoul04401Republic of Korea

Abstract

Sodium-glucose cotransporter 2 (SGLT2) inhibitors lower glucose levels by reducing glucose reabsorption in the kidneys, which can lead to ketogenesis. Euglycemic diabetic ketoacidosis (DKA) is a rare but potentially life-threatening complication of SGLT2 inhibitors that can be triggered by trauma. However, the absence of significant hyperglycemia can delay its diagnosis and treatment, which may lead to detrimental consequences. Herein, we report a case of euglycemic DKA following traumatic brain injury in a patient with type 2 diabetes who was taking an SGLT2 inhibitor. Delayed recognition of euglycemic DKA in this case led to progressive metabolic deterioration. This report emphasizes the importance of promptly suspecting, diagnosing, and treating euglycemic DKA in patients with traumatic injuries who exhibit high anion-gap metabolic acidosis, ketonuria, and glucosuria—even if they do not have significant hyperglycemia.

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Keywords : Euglycemic diabetic ketoacidosis, Sodium-glucose cotransporter 2 inhibitors, Traumatic brain injuries