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 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 MON-LB119 Euglycemic Diabetic Ketoacidosis in a Patient on Canagliflozin Presenting With Hypoglycemia

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Sindhura Inkollu ◽  
Sindhuja Korem ◽  
Sudha Ganne
Keyword(s):  
Blood Glucose ◽  
Diabetic Ketoacidosis ◽  
Mental Status ◽  
Altered Mental Status ◽  
Sglt2 Inhibitors ◽  
Anion Gap ◽  
Hypoglycemic Agents ◽  
Tract Infections ◽  
Euglycemic Diabetic Ketoacidosis

Abstract Background: Sodium glucose co-transporter 2 (SGLT-2) inhibitors are newer class of antihyperglycemics that cause reversible inhibition of the sodium-glucose cotransporters in the renal proximal tubules resulting in increased urinary glucose. Common side effects include yeast and urinary tract infections. The US Food and Drug Administration issued a safety warning pertaining to the development of diabetic ketoacidosis (DKA) with the use of SGLT2 inhibitors. The mechanisms by which SGLT2 inhibitors cause euglycemic DKA are unclear. SGLT2 inhibitors may lead to a decrease in either endogenous or exogenous insulin and an increase in glucagon production.1 This insulin deficiency or resistance may be mild in Type 2 diabetics, however, preventing the profound spike in blood glucose seen in traditional DKA. Here, we report a case of euglycemic DKA in a patient on Canagliflozin who presented initially with hypoglycemia. Clinical case: A 70 year old female presented with altered mental status for 1 day duration. Her past medical history is significant for type 2 Diabetes Mellitus, being managed on Canagliflozin, Glimepiride and Janumet. One week prior to admission she had lumbar spinal fusion surgery. Since then she has been feeling weak and tired with poor oral intake, but continued to use her medications. Initial laboratory findings showed blood glucose of 68 (70-100 mg/dl) without any acidosis. Her altered mental status was attributed to higher opioid doses which she received prior. Oral hypoglycemic agents have been held. On 2nd day of hospitalization, patient became more lethargic and complained of nausea. Laboratory testing revealed a serum glucose of 250mg/dL, serum bicarbonate of 13 (21–31mmol/L), and Anion gap of 25 (3.6–11.0mmol/L). With the suspicion of DKA, a beta-hydroxy butyrate level was obtained which was elevated at 90.10 (0 – 4.16 mg/dL). Venous blood gas analysis was significant for pH 7.23 (7.31-7.41) and pCO2 – 28 (41-51 mmHg). Urinalysis showed ketosis and glucosuria. Patient was diagnosed as euglycemic diabetic ketoacidosis from Canagliflozin in presence of precipitating factors - stress and poor intake. Patient was treated with insulin drip and intravenous fluids with reduction in anion gap and correction of acidosis within 24hrs. There was a gradual improvement in her mental status. She was discharged on subcutaneous insulin, and all other diabetic medications were stopped. Conclusion: Our case highlights the importance of being vigilant in a patient on Canagliflozin, euglycemic DKA can occur even if they present initially with hypoglycemia and no acidosis. Reference: 1. Ogawa W, Sakaguchi K. Euglycemic diabetic ketoacidosis induced by SGLT2 inhibitors: possible mechanism and contributing factors. J Diabetes Investig. 2016;7(2):135-138.

scholarly journals SAT-LB118 Euglycemic Diabetic Ketoacidosis in Type 2 Diabetes Mellitus

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Kevin A Arao ◽  
Harikrashna Bhatt ◽  
Christina M Capistrano ◽  
Hui Zhang ◽  
Christopher Cosgrove
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Diabetic Ketoacidosis ◽  
Caloric Intake ◽  
Anion Gap ◽  
Medical Emergency ◽  
Diagnostic Challenge ◽  
Arterial Blood

Abstract Introduction Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes. It is characterized by the triad of hyperglycemia (>250mg/dL), high anion gap metabolic acidosis (HAGMA), and ketonemia. Rarely, it would present with normal or mildly increased glucose levels (<200mg/dL) making it a diagnostic challenge. We present a case of euglycemic DKA in type 2 diabetes mellitus (T2DM). Case Presentation A 77-year-old woman living in a nursing home with a history of T2DM treated with insulin glargine, but for the past three days refused medications with decreased caloric intake. There were no new medications or ingestion of alcohol or toxic substances. She then developed worsening altered mental status hence admission to the hospital. Her vital signs were within normal limits. Physical examination revealed no abdominal tenderness. Initial laboratory studies showed glucose 83 mg/dL, bicarbonate 10 mmol/L, and anion gap 23 meq/L. Urinalysis significant with trace ketones. The following day, further work-up was done remarkable with beta-hydroxybutyrate 8.3 mmol/L, lactic acid 0.8 mmol/L, and toxicology panel negative. Arterial blood gas showed pH 7.137, pCO2 14 mmHg, and bicarbonate 4.8 mmol/L. DKA protocol was initiated and she was treated with insulin drip, bicarbonate drip, and intravenous fluid administration with D5W. After two days, DKA resolved and was subsequently transitioned to subcutaneous insulin. Discussion Similar to the findings of Burge et al, our case showed that decreased caloric intake predisposes patients with diabetes mellitus to euglycemic DKA during periods of insulin deficiency. A proposed mechanism for the accelerated ketosis is due to the effects of elevated levels of glucagon or catecholamines on lipolysis. Other causes of euglycemic DKA include pregnancy, heavy alcohol use, SGLT2 inhibitors, cocaine abuse, pancreatitis, sepsis, and chronic liver disease. It is also important to rule out other causes of HAGMA. In our case, although she has decreased caloric intake, starvation ketoacidosis usually leads to serum bicarbonate levels >18mmol/L. Management is similar to DKA but important difference is the dextrose administration to prevent hypoglycemia. Conclusion Euglycemic DKA is a medical emergency that may be overlooked as patients present without marked hyperglycemia. Physicians should have a high suspicion as this may result in delayed management and potential adverse metabolic consequences.

scholarly journals Nephrology Consultation for Severe SGLT2 Inhibitor-Induced Ketoacidosis in Type 2 Diabetes: Case Report

Medicina ◽  
2019 ◽  
Vol 55 (8) ◽  
pp. 462 ◽  
Author(s):  
Felice Nappi ◽  
Antonietta La Verde ◽  
Giovanni Carfora ◽  
Carlo Garofalo ◽  
Michele Provenzano ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Diabetic Ketoacidosis ◽  
Sglt2 Inhibitor ◽  
Delayed Diagnosis ◽  
Kidney Injury ◽  
Dialysis Unit ◽  
New Class ◽  
Sodium Glucose Cotransporter ◽  
Euglycemic Diabetic Ketoacidosis

Euglycemic diabetic ketoacidosis (euDKA) related to sodium-glucose cotransporter 2 inhibitor (SGLT2-I), despite being reported as consistent, though infrequent, adverse effect in all trials on SGLT2-I in type 2 diabetes mellitus (T2D), still remains poorly known in the real world. On the other hand, the use of this new class of antihyperglycemic agents is expected to increase based on the recent solid evidence of remarkable cardiorenal protection. Therefore, improving awareness on risk factors, diagnosis, and treatment of euDKA is essential to allow correct implementation of SGLT2-I in clinical practice. We here report a T2D patient admitted to the emergency department and then transferred to the nephrology-dialysis unit because of severe euglycemic diabetic ketoacidosis (euDKA) related to sodium-glucose cotransporter 2 inhibitor (SGLT2-I). In our patient, a concurrent acute kidney injury at presentation, initially attributed to excessive use of nonsteroid anti-inflammatory agents, and the absence of severe hyperglycemia led to delayed diagnosis and proper therapy. The detailed description of decision-making process for diagnosis and therapy, and the analysis of precipitating factors as well, discloses the helpful contribution of nephrologist to optimize prevention and management of euDKA.

scholarly journals A Case of Diabetic Ketoacidosis in a Patient on an SGLT2 Inhibitor and a Ketogenic Diet: A Critical Trio Not to Be Missed

2020 ◽  
Vol 2020 ◽  
pp. 1-3 ◽  
Author(s):  
Samantha Steinmetz-Wood ◽  
Matthew Gilbert ◽  
Katherine Menson
Keyword(s):  
Diabetic Ketoacidosis ◽  
Ketogenic Diet ◽  
Sglt2 Inhibitor ◽  
Sglt2 Inhibitors ◽  
Anion Gap ◽  
Low Carbohydrate ◽  
History Of ◽  
Ph Level ◽  
Beta Hydroxybutyrate ◽  
Euglycemic Diabetic Ketoacidosis

Results from major clinical trials have shown significant cardiorenal-protective benefits of SGLT2 inhibitors in patients with type 2 diabetes (T2DM), leading to increased popularity. A rare but serious side effect of SGLT2 inhibitors is euglycemic diabetic ketoacidosis (EDKA), which presents more covertly but has been described. Identification and report of modifiable risk factors would be an important step in helping clinicians appropriately counsel patients. In this case report, we present DKA in a patient on an SGLT2 inhibitor and ketogenic diet (KD). A 47-year-old male with a history of poorly controlled T2DM on metformin and empagliflozin presented to the emergency department (ED) with several days of pharyngitis, dyspnea, emesis, abdominal pain, and anorexia. Of note, one month prior to this event, he presented to the ED with malaise and was found to have an anion gap of 21, a bicarbonate level of 13 mmol/L, a pH level of 7.22, 3+ ketonuria, and a glucose level of 7 mmol/L (127 mg/dl). Additional workup was negative, and findings were attributed to his KD. His use of empagliflozin was not identified on his medication list. At second presentation, the patient was tachypneic and tachycardic and had mild abdominal tenderness. Labs revealed anion gap 28, bicarbonate 5 mmol/l, pH 6.94, 3+ ketonuria, glucose 14.9 mmol/L (269 mg/dl), and beta-hydroxybutyrate 8.9 mmol/L. The patient was diagnosed with DKA and was treated accordingly. With closure of anion gap, the patient was transitioned to insulin and metformin, and his empagliflozin was discontinued indefinitely. Before prescribing this medication class, physicians should inquire about low-carbohydrate diets given the higher risk for DKA, though knowledge of this risk is still not widespread.

scholarly journals Euglycemic Diabetic Ketoacidosis Secondary to Dapagliflozin in a Patient with Colon Malignancy

2019 ◽  
Vol 2019 ◽  
pp. 1-4 ◽  
Author(s):  
Eleni Papadokostaki ◽  
Evangelos Liberopoulos
Keyword(s):  
Type 2 Diabetes ◽  
Adverse Effect ◽  
Colon Cancer ◽  
Diabetic Ketoacidosis ◽  
Sglt2 Inhibitor ◽  
Sglt2 Inhibitors ◽  
Sodium Glucose Cotransporter ◽  
Euglycemic Diabetic Ketoacidosis ◽  
Type 2 Diabetic

The use of sodium-glucose cotransporter 2 (SGLT2) inhibitors for the treatment of type 2 diabetes is steadily increasing. SGLT2 inhibitors are associated with weight loss, lowering of blood pressure, and low hypoglycemia risk along with beneficial cardiovascular and renoprotective effects. In view of the increasing use of SGLT2i, physicians must be aware of their adverse effects. Euglycemic diabetic ketoacidosis (euDKA) is a well-recognized adverse effect of SGLT2i. We present here a case of euglycemic diabetic ketoacidosis secondary to dapagliflozin use in a type 2 diabetic patient with colon cancer. To the best of our knowledge, this is first report of SGLT2 inhibitor-associated euDKA in a patient with underlying colon cancer.

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.

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