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Critical Care Management of DiabeticKetoacidosis Caused by Sodium-Glucose Co-Transporter 2 Inhibitor: A Case Report

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Critical Care Management of Diabetic

Ketoacidosis Caused by Sodium-Glucose Co-Transporter 2 Inhibitor: A Case Report

Elif Bombacı, Banu Cevik, Hakan Haydarlar, Kemal Tolga Saracoglu, Recep Demirhan

DOI: 10.14744/scie.2020.54872

South. Clin. Ist. Euras. 2020;31(3):287-288

Letter to the Editor

The sodium-glucose co-transporter 2 (SGLT2) is selectively expressed in the kidney and responsible for the reabsorption of glucose from proximal renal tubules.[1] The inhibition of this mechanism leads to increased glycosuria and decreased plasma glucose levels while the patient remains relatively euglycemic.[2] SGLT2 inhibitors were approved in 2013 by the Food and Drug Administration for the treatment of Type 2 Diabetes Mellitus (T2DM). However, the drug safety warning has been published about the risk of euglycemic Diabetic Ketoacidosis related to this group of drugs in 2015.[3] We reported our first case of euglycemic diabetic ketoacidosis complicated by an acute abdomen in the setting of SGLT2 inhibitor use.

A 53-year-old male patient admitted to the Emergency Department with complaints of severe abdominal pain, nausea and vomiting. Medical history included T2DM managed with oral antidiabetics (Sitagliptin Metformin HCL and Glipizide) combined with sub- cutaneous insulin therapy. A SGLT2 inhibitor (Empagliflozin) was prescribed because of the refusal of the insulin injections about two weeks ago. There was rebound ten- derness with decreasing the bowel sounds so; he was scheduled for emergency ex- plorative laparotomy. Blood biochemistry showed the following: glucose, 200 mg/dL;

creatinine,1.33 mg/dL; leucocyte count, 23.000/mm3. Urinalysis showed the ketonuria and glucosuria. An arterial blood gas analysis showed the metabolic acidosis with ph:

7.01, pCO2: 24 mmHg, pO2: 57 mmHg, BE: -23.1 mmol/L, HCO3: 7.8 mmol/L, Lactate:

4.2 mmol/dL, SatO2: 77.9%. Sodium bicarbonate infusion was commenced throughout surgery but metabolic acidosis worsened. The patient was transferred to the intensive care unit (ICU) and mechanical ventilation was conducted. Diabetic ketoacidosis pro- tocol was initiated and crystalloid therapy was administered to treat dehydration. His blood glucose levels remained between 200–250 mg/dL and renal function remained normal. Continuous venovenous renal replacement therapy was initiated to manage the metabolic acidosis for up to 55 hours. By the improvement of acidosis and respiratory parameters, sedation was discontinued to wean the patient. However, a sudden supra- ventricular tachycardia (200 beats/min) developed and treated with diltiazem. He was extubated on the 76hrs of his ICU admission. Electrolyte imbalance was corrected and he was discharged to the General Surgery Department on the 7th day.

The widespread use of SGLT 2 inhibitors is a clinical concern due to the contribution of this group of drugs with concomitant medications particularly other antihyperglycemic drugs, statins, and diuretics. Many clinicians are unaware of the guidelines limiting the use of SGLT2 inhibitors so; the initiation of these drugs may potentiate the adverse effects.[4] The risks may accelerate especially in the elderly population.[5] If the multidrug treatment in diabetic patients is concerned, the prescription of these new medications necessitates the long-term follow up. In case of unexpected adverse reactions, interdis- ciplinary approach is essential for the management of these patients.

Peer-review

Internally peer-reviewed.

Department of Anesthesiology and Reanimation, University of Health Sciences, Kartal Dr. Lütfi Kırdar Training and Research Hospital, İstanbul, Turkey

Correspondence: Banu Cevik, Sağlık Bilimleri Üniversitesi, Kartal Dr. Lütfi Kırdar Eğitim ve Araştırma Hastanesi, Anesteziyoloji ve Reanimasyon Kliniği, İstanbul, Turkey Submitted: 17.03.2020 Accepted: 22.04.2020

E-mail: [email protected]

This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

(2)

Conflict of Interest None declared.

REFERENCES

1. Chacko B, Whitley M, Beckmann U, Murray K, Rowley M. Postop- erative euglycaemic diabetic ketoacidosis associated with sodium-glu- cose cotransporter-2 inhibitors (gliflozins): a report of two cases and review of the literature. Anaesth Intensive Care 2018;46:215−9.

2. Rieg T, Masuda T, Gerasimova M, Mayoux E, Platt K, Powell DR, et al. Increase in SGLT1-mediated transport explains renal glucose reabsorption during genetic and pharmacological SGLT2 inhibition

in euglycemia. Am J Physiol Renal Physiol 2014;306:F188−93.

3. FDA. FDA revises labels of SGLT2 inhibitors for diabetes to include warnings about too much acid in the blood and serious urinary tract infections. Available at: https://www.fda.gov/drugs/

drug-safety-and-availability/fda-drug-safety-communication-fda- revises-labels-sglt2-inhibitors-diabetes-include-warnings-about. Ac- cessed March, 2020.

4. D’Elia JA, Segal AR, Bayliss GP, Weinrauch LA. Sodium-glucose co- transporter-2 inhibition and acidosis in patients with type 2 diabetes:

a review of US FDA data and possible conclusions. Int J Nephrol Renovasc Dis 2017;10:153−8. [CrossRef ]

5. D’Elia JA, Segal AR, Weinrauch LA. Metformin-SGLT2, Dehydra- tion, and Acidosis Potential. J Am Geriatr Soc 2017;65:e101−e102.

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