Successful renal replacement therapy of extreme ertugliflozin and alcohol induced euglycaemic ketoacidosis (ph 6.6)

Objective: Sodium-Glucose Cotransporter 2 (SGLT2) inhibitors have become a cornerstone in the treatment of type 2 diabetes. However, since 2015 shortly after their approval an increasing number of cases of euglycaemic diabetic ketoacidosis (EDKA) related to SGLT2 inhibitors have been described. We present the case of extreme, life-threatening ertugliflozin and alcohol excess induced euglycaemic ketoacidosis in a patient with pancreatogenic diabetes.

Case Report: A 39-year old man with a 7-year history of pancreatogenic diabetes due to chronic alcohol abuse with recurrent episodes of severe pancreatitis was admitted to the intensive care unit. Over the course of hours he developed severe abdominal pain with recurrent vomiting and nausea. His wife verified that he had consumed three bottles of vodka and an unknown quantity of beer and had poor dietary intake over the two days preceding his admission. In the months preceding his admission, the patient was treated with a combination of 15 mg ertugliflozin and 2x1000 mg metformin per day. The alert, well nourished (BMI 32kg/m2) but dehydrated patient showed motoric unrest and severe hyperventilation. His pulse was 106 beats/min, blood pressure was 95/50 mmHg and respiratory rate was 30 per minute. He reported epigastric pain necessitating morphine administration. The patient presented an extreme EDKA (arterial pH 6.6; HCO3 3.4 mmol/l; anion gap 23.6 mmol/l; blood glucose 190 mg/dl; serum ß-hydroxybutyrate 5679 µmol/l; serum aceton 654 µmol/l). Apart from a marked leukocytosis, further biomarkers of systemic inflammation were unremarkable as well as liver function tests and lipase. To compensate for the massive acidosis, four bolus infusions of 100 mg bicarbonate were administered, followed by immediate bicarbonate haemodialysis over three hours, resulting in a ph of 7.0. Further continuous veno-venous haemodialysis 12 hours after admission finally normalized the acidosis (pH 7.3). Guided by haemodynamic status, electrolyte levels and urinary output, the i.v. fluid replacement totaled 5000 ml crystalloid within the first seven hours. Additionally, 1000 ml 10% glucose i.v. was administered. Low dose i.v. regular insulin (0.3-0.5 I.U./h) was given to maintain blood glucose concentrations of 110-140 mg/dl. After seven days the patient was discharged in stable condition. An intensive insulin regimen was initiated and the patient was instructed to discontinue SGLT2 inhibitors.

Conclusions: In our patient, crucial precautions to the use of SGLT2 inhibitors were disregarded. The extreme acidosis (pH 6.6) was striking and has never been reported before in SGLT2 inhibitor related EDKA – nor in sole alcoholic ketoacidosis. The application of early renal replacement therapy to effectively manage the extreme acidosis was a life saving measure. A careful clinical indication for the use of SGLT2 inhibitors and patient education highlighting sick day rules is indispensable and may help to reduce the risk of EDKA.

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Artikel online veröffentlicht:
28. Mai 2025