scholarly journals DIABETIC KETOACIDOSIS WITH LOWER-THAN-ANTICIPATED GLUCOSE LEVELS WITH SGLT-2 INHIBITOR CANAGLIFLOZIN: A CASE REPORT AND REVIEW OF THE LITERATURE.

2020 ◽  
pp. 1-2
Author(s):  
Ajay Budhwar ◽  
Parul Malhotra
Keyword(s):  
Case Report ◽  
Blood Glucose ◽  
Diabetic Ketoacidosis ◽  
Sglt2 Inhibitor ◽  
Gas Analysis ◽  
Glucose Levels ◽  
Arterial Blood ◽  
History Of ◽  
Euglycemic Diabetic Ketoacidosis

We describe a case report of a patient who presented with euglycemic diabetic ketoacidosis (euDKA), six days after starting treatment with sodium-glucose cotransporter-2 (SGLT2) inhibitor, Canagliflozin. ‘Euglycemic diabetic ketoacidosis’ or ‘DKA with lower-than-anticipated glucose levels’ (as recommended by AACE/ACE) is a rare, challenging and easy to miss the diagnosis A 41-year-old male with a history of type 2 Diabetes Mellitus presented with uncontrolled hyperglycemia. Canagliflozin (SGLT2 inhibitor) was added to his anti-diabetic regimen of Metformin and Sitagliptin. Six days later, he presented with symptoms of diabetic ketoacidosis with normal blood glucose of 131mg/dl. The patient was further investigated with arterial blood gas analysis and serum ketone studies, keeping in view of the potential of euglycemic diabetic ketoacidosis (euDKA) with SGLT2 inhibitor use. The clinical picture and lab values of the patient were consistent with diabetic ketoacidosis(DKA), although it is rare in type 2 DM. Blood glucose was in the normal range which could have delayed the diagnosis if the physician was not vigilant. If one had only focused on the blood glucose, then this potentially fatal condition could have been missed. However, when other causes of anion gap metabolic acidosis were excluded and the lab values of urine ketones, elevated beta-hydroxybutyrate, reduced bicarbonate, and normal lactate interpreted, it leads to the diagnosis of SGLT2 inhibitor-associated euglycemic DKA. We performed a literature review of this topic and discuss the history of euglycemic diabetic ketoacidosis, risk factors, pathophysiology, diagnosis, management, and prevention of SGLT2 inhibitor-induced euDKA.

scholarly journals Euglycemic Diabetic Ketoacidosis Secondary to SGLT2-inhibitor Use in Combination With a Ketogenic Diet

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A380-A381
Author(s):  
Joi C Hester ◽  
Stacy Zimmerman ◽  
Teresa Allison Nimmo ◽  
Wesley Cunningham ◽  
Joshua Liu ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Blood Glucose ◽  
Diabetic Ketoacidosis ◽  
Ketogenic Diet ◽  
Sglt2 Inhibitor ◽  
Perioperative Period ◽  
Anion Gap ◽  
Arterial Blood ◽  
Euglycemic Diabetic Ketoacidosis

Abstract Sodium-glucose cotransporter 2 (SGLT-2) inhibitors are cardiorenal protective agents increasingly used in patients with diabetes. Cases of euglycemic diabetic ketoacidosis (euDKA) have been reported particularly among patients with type 1 diabetes. Our case is an example that highlights the role SGLT-2 inhibitors play in the development of euDKA in a patient with type 2 diabetes with confounding factors of strict adherence to a ketogenic diet and ankle fracture. A 72-year-old female with a history of type 2 diabetes presented to the emergency department (ED) with right ankle pain and obvious deformity after a mechanical fall. Radiography of the right lower extremity confirmed distal fracture of the tibia and fibula. After reduction of her fracture in the ED, she was admitted in anticipation of an open reduction internal fixation. Her diabetes was controlled on empagliflozin monotherapy and adhering to a ketogenic diet. She monitored her blood ketones daily at home and reported values in the 3–4 mmol/L range. On admission, her basic metabolic panel (BMP) revealed a blood glucose of 148 mg/dL, bicarbonate of 20 mEq/L, anion gap of 18 mEq/L, Cr of 1.3 mg/dl, and eGFR of 40 mL/min. Her beta-hydroxybutyrate (BHB) was 5.09 mmol/L. The initial assessment was presumed starvation ketosis. On hospital day three, she complained of continued nausea, polydipsia, and abdominal pain. Chart review revealed nocturia with approximately 3–4 voids per night. Repeat BMP showed a blood glucose of 152 mg/dL, bicarbonate of 16 mEq/L, anion gap still at 18 mEq/L, Cr 1.4 mg/dl, and eGFR of 37 mL/min. Since admission, all of her blood glucose levels ranged between 118–178 mg/dL. She denied dyspnea but exhibited Kussmaul respirations on physical exam. Repeat labs revealed a BHB of 8.92 mmol/L, and arterial blood gas (ABG) showed pH 7.2, pCO2 23, pO2 100, bicarbonate 8.6 mEq/L, consistent with high-anion gap metabolic acidosis, confirming the diagnosis of euDKA. Her empagliflozin had been held since admission, but she had not received any insulin up to this point due to euglycemia. She was immediately started on a weight-based dose of 12 units of insulin glargine with subsequent improvement of her BHB and anion gap. This patient’s use of an SGLT2-inhibitor in combination with her being on a ketogenic diet, contributed to a nonregulated state of ketone production leading to euDKA in the perioperative period. As SGLT2-inhibitors become more readily available, it is important to educate physicians and patients about the risk of euDKA during fasting, ketogenic diets, and the perioperative period.

scholarly journals Euglycemic Diabetic Ketoacidosis With SGLT-2 Inhibitor

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A381-A382
Author(s):  
F N U Manas ◽  
Barbara L Mols-Kowalczewski ◽  
Shobha Mandal
Keyword(s):  
Blood Glucose ◽  
Diabetic Ketoacidosis ◽  
Side Effect ◽  
Blood Gas Analysis ◽  
Gas Analysis ◽  
Anion Gap ◽  
Blood Gas ◽  
Glucose Levels ◽  
Beta Hydroxybutyrate ◽  
Euglycemic Diabetic Ketoacidosis

Abstract Introduction: The SGLT-2 inhibitors (SGLT-2i) are a newer anti-diabetic drugs. Their use has tremendously increased due to their favorable profile but they are also the focus of attention because of their side effect of euglycemic diabetic ketoacidosis (euDKA), which is challenging to diagnose because of its rarity and normal or mildly elevated blood glucose levels. SGLT2i decrease blood glucose independently of insulin secretion, by reversibly inhibiting SGLT2 protein which is responsible for reabsorbing glucose from the proximal renal tubule. Beside glycemic control with reduced glycated hemoglobin, they also decrease all-cause mortality, cardiovascular mortality, and hospitalization for heart failure. The major side effect is genitourinary infections, euDKA and volume depletion. EuDKA is characterized by blood glucose <200mg/dl, anion gap metabolic acidosis and positive serum ketones. It can, therefore, present without hyperglycemia and the symptoms of dehydration, making it challenging to identify. DKA is rarely seen in DM-2 and the normal glucose levels can cause misinterpretation of the patient’s condition, causing a delay in treatment. The beta-hydroxybutyrate and arterial pH should be checked in suspected SGLT2i associated euDKA. The mainstay of treatment of euDKA is immediately stopping SGLT2i and traditional DKA treatment protocol. Patient should be educated regarding adequate hydration and adequate calorie intake while using SGLT2i and physician should avoid using SGLT2i in patients with poor oral intake, alcohol dependence or pregnancy. Case Presentation: A 52-year-old male with uncontrolled type 2 diabetes, on Metformin and Sitagliptin, presented to clinic. Canagliflozin (SGLT-2i) was added to his oral hypoglycemic regimen. Six days later he presented with blurred vision, lightheadedness, nausea, vomiting, and abdominal pain. On examination, he had tachycardia and tachypnea. Labs were significant for glucose levels of 131mg/dL, bicarbonate 12meq/l, anion gap 20, creatinine 0.7mg/dl, normal lactic acid. Serum ketones were positive with elevated beta-hydroxybutyrate of 5.9mmol/l. Blood gas analysis showed a pH of 7.14. The patient was admitted to ICU and managed according to the guidelines for DKA. The symptoms resolved within 24 hours, with a reduction of anion gap to 12. Canagliflozin was discontinued indefinitely and the patient was discharged with the diagnosis of SGLT2i-induced euDKA. Conclusion: SGLT2i-induced euDKA can present without the classical laboratory findings of DKA. The patients, with a history of SGLT2i use and, signs and symptoms of DKA, even in the absence of hyperglycemia, should be suspected of euDKA. The complete lab work with blood gas analysis, blood and urine ketones including beta-hydroxybutyrate level must be done to ensure that the diagnosis is not missed and timely interventions are made to manage this serious condition.

Prolonged euglycemic diabetic ketoacidosis triggered by a single dose of sodium–glucose cotransporter 2 inhibitor

2020 ◽  
Vol 13 (10) ◽  
pp. e235969
Author(s):  
Maki Miwa ◽  
Mikio Nakajima ◽  
Richard H Kaszynski ◽  
Hideaki Goto
Keyword(s):  
Single Dose ◽  
Metabolic Acidosis ◽  
Blood Glucose ◽  
Diabetic Ketoacidosis ◽  
Sglt2 Inhibitor ◽  
Glucose Levels ◽  
Intravenous Insulin ◽  
Blood Glucose Levels ◽  
Sodium Glucose Cotransporter ◽  
Euglycemic Diabetic Ketoacidosis

A 45-year-old woman was admitted for diabetic ketoacidosis (DKA). Aggressive rehydration and continuous intravenous insulin resulted in improved blood glucose levels; however, metabolic acidosis persisted. One day prior to admission, the patient took a single dose of a sodium–glucose cotransporter 2 (SGLT2) inhibitor and this likely contributed to the prolonged euglycemic DKA. A single dose of this drug remained effective for over 100 hours as evidenced by massive excretion of urine glucose continuing long after blood glucose normalisation. SGLT2 inhibitor use should be refrained in cases in which DKA has already occurred as they may result in increasing severity or prolonged DKA.

scholarly journals SUCCESSFUL REIMPLEMENTATION OF A VERY LOW CARBOHYDRATE KETOGENIC DIET AFTER SGLT2 INHIBITOR ASSOCIATED EUGLYCEMIC DIABETIC KETOACIDOSIS

2020 ◽  
Vol 6 (6) ◽  
pp. e330-e333
Author(s):  
Ethan I. Fieger ◽  
Kristen M. Fadel ◽  
Amir H. Modarres ◽  
Edmond P. Wickham ◽  
Susan E. Wolver
Keyword(s):  
Diabetic Ketoacidosis ◽  
Ketogenic Diet ◽  
Sglt2 Inhibitor ◽  
Patient Portal ◽  
Rapid Weight Gain ◽  
Low Carbohydrate ◽  
History Of ◽  
Medical Weight Loss ◽  
Euglycemic Diabetic Ketoacidosis

Objective: We report a case of a successful reimplementation of a very low carbohydrate ketogenic diet (VLCKD) after a case of euglycemic diabetic ketoacidosis (euDKA). Methods: A 42-year-old female with a history of type 2 diabetes mellitus on a self-administered VLCKD was prescribed a sodium-glucose co-transporter 2 (SGLT2) inhibitor. Two weeks after initiation, she presented with nausea and vomiting and was found to be in euDKA which was treated with fluid resuscitation, insulin infusion, and cessation of the SGLT2 inhibitor. She was discharged on insulin and instructed not to resume a VLCKD. Results: After discharge, the patient experienced rapid weight gain and deteriorating glycemic control and desired to resume a VLCKD. She was referred to a university-based medical weight loss clinic that specializes in a VLCKD. The patient was monitored with daily contact via the electronic health record’s patient portal and serial laboratory testing while her carbohydrate intake was slowly reduced and her insulin titrated off. She has safely remained in ketosis for 2 years without a further episode of euDKA. Conclusion: As the clinical use of SGLT2 inhibitors and the VLCKD both become increasingly common, it is vital for practitioners to be aware that the combination can lead to euDKA. We present a case of successfully resuming a VLCKD after recovering from euDKA and cessation of SGLT2 inhibitor therapy.

scholarly journals Euglycemic Diabetic Ketoacidosis after a Single Dose of Empagliflozin in a Patient with Pancreatitis

2021 ◽  
Vol 11 (2) ◽  
pp. 216-218
Author(s):  
Marta Brandão Calçada ◽  
Luís Fernandes ◽  
Rita Soares Costa ◽  
Sara Montezinho ◽  
Filipa Martins Duarte ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Diabetic Ketoacidosis ◽  
Drug Class ◽  
Clinical Suspicion ◽  
Laboratory Findings ◽  
Sodium Glucose Cotransporter ◽  
History Of ◽  
High Degree ◽  
Euglycemic Diabetic Ketoacidosis

Sodium-glucose cotransporter 2 inhibitors (SGLT2i) are the most recently approved drug class for the treatment of type 2 diabetes mellitus (T2D). Although they are largely well-tolerated, their intake has been associated with euglycemic diabetic ketoacidosis (DKA) in some rare cases. We report the case of a 70-year-old male with type 2 diabetes and no history of DKA, who started therapy with empagliflozin one day before presenting with acute pancreatitis and laboratory findings consistent with euglycemic DKA. SGLT2i can induce euglycemic DKA from the first dose. Given the atypical presentation, a high degree of clinical suspicion is required to recognize this complication.

scholarly journals Severe euglycemic diabetic ketoacidosis of multifactorial etiology in a type 2 diabetic patient treated with empagliflozin: case report and literature review

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Erasmia Sampani ◽  
Pantelis Sarafidis ◽  
Chrysostomos Dimitriadis ◽  
Efstratios Kasimatis ◽  
Dimitra Daikidou ◽  
...  
Keyword(s):  
Case Report ◽  
Literature Review ◽  
Diabetic Patient ◽  
Diabetic Ketoacidosis ◽  
Euglycemic Diabetic Ketoacidosis ◽  
Type 2 Diabetic

scholarly journals Euglycemic Diabetic Ketoacidosis in Pregnancy: A Case Report and Review of Current Literature

2019 ◽  
Vol 2019 ◽  
pp. 1-5 ◽  
Author(s):  
Johnny F. Jaber ◽  
Matthew Standley ◽  
Raju Reddy
Keyword(s):  
Blood Glucose ◽  
Diabetic Ketoacidosis ◽  
Case Reports ◽  
Anion Gap ◽  
Fetal Mortality ◽  
Glucose Levels ◽  
Elevated Glucose ◽  
High Doses ◽  
Euglycemic Diabetic Ketoacidosis ◽  
In Pregnancy

Diabetic ketoacidosis (DKA) in pregnancy is associated with high fetal mortality rates. A small percentage of DKA occurs in the absence of high glucose levels seen in traditional DKA. Prompt recognition and management is crucial. We report a case of a 30-year-old pregnant woman with type 1 diabetes mellitus admitted with euglycemic DKA (blood glucose <200 mg/dL). Initial laboratory testing revealed a severe anion gap acidosis with pH 7.11, anion gap 23, elevated β-hydroxybutyric acid of 9.60 mmol/L, and a blood glucose of 183 mg/dL—surprisingly low given her severe acidosis. The ketoacidosis persisted despite high doses of glucose and insulin infusions. Due to nonresolving acidosis, her hospital course was complicated by spontaneous intrauterine fetal demise. Euglycemia and severe acidosis continued to persist until delivery of fetus and placenta occurred. It was observed that the insulin sensitivity dramatically increased after delivery of fetus and placenta leading to rapid correction of ketoacidosis. This case highlights that severe ketonemia can occur despite the absence of severely elevated glucose levels. We discuss the mechanism that leads to this pathophysiologic state and summarize previously published case reports about euglycemic DKA in pregnancy.

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