Related Experiment Video
Updated: Jul 2, 2025

Improving IV Insulin Administration in a Community Hospital
Published on: June 11, 2012
[Sodium glucose cotransporter-2 inhibitors (SGLT2i) and risk of ketoacidosis]
Lina-Maria Nordvall1, Bertil Ekstedt2, Jörn Schneede3
1MSc i organisk kemi och biomedicin, ST-läkare i klinisk farmakologi, Läkemedelscentrum.
Abstract:
SGLT2i can induce euglycemic diabetic ketoacidosis (eDKA) in conditions with relative insulin deficiency, such as infections, surgery, or fasting state. In comparison with classical DKA, eDKA typically presents with lower blood glucose levels and more diffuse symptoms like tiredness, tachypnea, nausea and abdominal pain. The diagnosis is commonly delayed, and signs are often attributed to other factors. Early diagnosis and prevention are critical due to the risk of lethal outcome or prolonged hospital stay. Generous screening for ketonemia in risk situations allows identification of eDKA. To minimize the risk, we propose that SGLT2i should be discontinued 3-4 days before surgery (1-2 weeks prior to bariatric surgery) and during infections, acute disease, or poor oral intake. Postoperative slow infusion of low-dose insulin may prevent eDKA if SGLT2i could not be stopped in time or in prolonged fasting state. In this overview, the pathogenesis behind eDKA is discussed.
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Glucose Transporters
Facilitated diffusion-glucose transporters (GLUTs) are encoded by the solute-linked carrier (SLC) family 2, subfamily A gene family, or SLC2A. The 14 GLUT protein members are distributed into three classes:

