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Euglycemic Diabetic Ketoacidosis Treatment

Euglycemic Diabetic Ketoacidosis: The Clinical Concern Of Sglt2 Inhibitors

Euglycemic Diabetic Ketoacidosis: The Clinical Concern Of Sglt2 Inhibitors

Euglycemic diabetic ketoacidosis is a post market warning in patients with type 1 diabetes and type 2 diabetes treated with SGLT-2 inhibitors. We report a case of a 39-year-old obese female with presumed type 2 diabetes for seven years who presented to the emergency department with three days of nausea, vomiting, and abdominal pain. Due to previous total non-adherence with a prescribed insulin regimen, she was recently started on canagliflozin and liraglutide. The diagnosis of euDKA was missed in the initial evaluation as the blood glucose level was only 167 mg/dL. Further work up showed severe metabolic acidosis with an anion gap of 25 and positive ketones in the urine. She was treated successfully with dextrose water 5%/half normal saline and an insulin drip. As part of the work up, she tested positive for glutamic acid decarboxylase autoantibodies. Given the increasing utilization of SGLT-2 inhibitors and the fact that patients can present with near-normal glycemia, the diagnosis can be missed. Vigilance with the use of SGLT-2 inhibitors is necessary to decrease morbidity and potentially mortality particularly in patients with long-standing type 2 diabetes associated with marked β-cell insufficiency, type 1 diabetes mellitus, or latent autoimmune diabetes of adult onset. Continue reading >>

Euglycemic Diabetic Ketoacidosis: A Review

Euglycemic Diabetic Ketoacidosis: A Review

Euglycemic Diabetic Ketoacidosis: A Review Author(s): Anar Modi , Department of Endocrinology, Diabetes & Metabolism, Cooper University Hospital, Camden, New Jersey, United States Abhinav Agrawal* , Department of Medicine, Monmouth Medical Center, 300 Second Avenue, Long Branch, New Jersey, United States Farah Morgan . Department of Endocrinology, Diabetes & Metabolism, Cooper University Hospital, Camden, New Jersey, United States Introduction: Diabetic ketoacidosis (DKA) is one of the most serious complications of diabetes.It is characterised by the triad of hyperglycemia (blood sugar >250 mg/dl), metabolic acidosis(arterial pH <7.3 and serum bicarbonate <18 mEq/L) and ketosis. Rarely these patients can present withblood glucose (BG) levels of less than 200 mg/dl, which is defined as euglycemic DKA. The possibleetiology of euglycemic DKA includes the recent use of insulin, decreased caloric intake, heavy alcoholconsumption, chronic liver disease and glycogen storage disorders. DKA in pregnancy has also beenreported to present with euglycemia. The recent use of sodium glucose cotransporter 2 (SGLT2) inhibitorshas shed light on another possible mechanism of euglycemic DKA. Clinicians may also be misledby the presence of pseudonormoglycemia. Conclusion: Euglycemic DKA thus poses a challenge to physicians, as patients presenting with normalBG levels in ketoacidosis may be overlooked, leading to a delay in appropriate management strategies.In this article, we review all the possible etiologies and the associated pathophysiology of patients presentingwith euglycemic DKA. We also discuss the approach to diagnosis and management of suchpatients. Despite euglycemia, ketoacidosis in diabetic patients remains a medical emergency and mustbe treated in a quick and appropriate mann Continue reading >>

Dka That Wasn't: A Case Of Euglycemic Diabetic Ketoacidosis Due To Empagliflozin | Oxford Medical Case Reports | Oxford Academic

Dka That Wasn't: A Case Of Euglycemic Diabetic Ketoacidosis Due To Empagliflozin | Oxford Medical Case Reports | Oxford Academic

Sodium glucose co-transporter (SGLT-2) inhibitor is a relatively new medication used to treat diabetes. At present, the Food and Drug Administration (FDA) has only approved three medications (canagliflozin, dapagliflozin and empagliflozin) in this drug class for the management of Type 2 diabetes. In May 2015, the FDA issued a warning of ketoacidosis with use of this drug class. Risk factors for the development of ketoacidosis among patients who take SGLT-2 inhibitors include decrease carbohydrate intake/starvation, acute illness and decrease in insulin dose. When identified, immediate cessation of the medication and administration of glucose must be done, and in some instances, starting an insulin drip might be necessary. We present a case of a patient with diabetes mellitus being on empagliflozin (SGLT-2 antagonist) who was admitted for acute cholecystitis. The hospital course was complicated by euglycemic diabetic ketoacidosis after being kept nothing per orem before a contemplated cholecystectomy. The management of diabetes has evolved since its discovery in 1910. A gamut of medications has become available to address the glycemic control among diabetics especially for Type 2 diabetics. Empagliflozin is a sodium glucose co-transporter (SGLT-2) inhibitor that has been approved by the Food and Drug Administraiton (FDA) in August 2014. It has been the latest drug approved in the drug class since 2013. This case highlights a case of euglycemic ketoacidosis with the use of empagliflozin. A 61-year-old female presented to her primary care doctor with right upper quadrant abdominal pain for a day. Her onlymedical history is diabetes Type 2 maintained on empagliflozin and diet controlled hypertension. Patient used to be on the combination of metforminrepaglinide but has bee Continue reading >>

Euglycemic Diabetic Ketoacidosis Sometimes Seen With Sglt2 Inhibitors

Euglycemic Diabetic Ketoacidosis Sometimes Seen With Sglt2 Inhibitors

Craig Cocchio, PharmD, BCPS, is an Emergency Medicine Clinical Pharmacist at Trinity Mother Frances Hospital in Tyler, Texas. Follow on Twitter @iEMPharmD and on his blog at empharmd.blogspot.com Diabetic ketoacidosis (DKA) in patients with presenting serum blood glucose <200 mg/dL isn’t common. More often, it’s seen in patients with type 1 diabetes in conjunction with starvation and acute illness.1 It’s difficult to determine an incidence of euglycemic DKA (euDKA) among all DKA cases in the literature, given the migration of the serum glucose cutoff from ≤300 mg/dL to ≤200 mg/dL. The best estimation based on an analysis of case reports suggests an incidence anywhere between 0.8% and 7.5%.1 However, the sodium-glucose cotransporter-2 (SGLT2) inhibitors canagliflozin, dapagliflozin, and empagliflozin can apparently induce this once-rare form of DKA.2,3 SGLT2 inhibitors are a class of oral hypoglycemic drugs indicated only for type 2 diabetes. Their novel mechanism of action prevents glucose reabsorption from the proximal renal tubules, resulting in increased glucosuria and decreasing plasma glucose. SGLT2 inhibitors lower serum glucose and HBA1C levels, and even produce weight loss. However, the increased glucose concentration in the bladder is a terrific incubation environment for fungi and bacteria, so much so that the FDA stuck a post-marketing warning on the drug class for the increased risk of serious urinary tract infections and urosepsis, in addition to euglycemic DKA. The proposed mechanism suggests that while SGLT2 inhibitors lower serum glucose, they also reduce insulin secretion from pancreatic beta cells in a negative feedback fashion. The lower serum insulin coupled with lower serum glucose consequently shifts energy metabolism to antilipolytic act Continue reading >>

Euglycemic Diabetic Ketoacidosis: A Diagnostic And Therapeutic Dilemma

Euglycemic Diabetic Ketoacidosis: A Diagnostic And Therapeutic Dilemma

Prashanth Rawla1, Anantha R Vellipuram2, Sathyajit S Bandaru3 and Jeffrey Pradeep Raj4[1] Department of Internal Medicine, Memorial Hospital of Martinsville and Henry County, Martinsville, Virginia, USA [2] Texas Tech University Health Sciences Center, El Paso, Texas, USA [3] Senior Research Associate, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA [4] Department of Pharmacology, St John’s Medical College, Bangalore, India Summary Euglycemic diabetic ketoacidosis (EDKA) is a clinical triad comprising increased anion gap metabolic acidosis, ketonemia or ketonuria and normal blood glucose levels <200 mg/dL. This condition is a diagnostic challenge as euglycemia masquerades the underlying diabetic ketoacidosis. Thus, a high clinical suspicion is warranted, and other diagnosis ruled out. Here, we present two patients on regular insulin treatment who were admitted with a diagnosis of EDKA. The first patient had insulin pump failure and the second patient had urinary tract infection and nausea, thereby resulting in starvation. Both of them were aggressively treated with intravenous fluids and insulin drip as per the protocol for the blood glucose levels till the anion gap normalized, and the metabolic acidosis reversed. This case series summarizes, in brief, the etiology, pathophysiology and treatment of EDKA. Euglycemic diabetic ketoacidosis is rare. Consider ketosis in patients with DKA even if their serum glucose levels are normal. High clinical suspicion is required to diagnose EDKA as normal blood sugar levels masquerade the underlying DKA and cause a diagnostic and therapeutic dilemma. Blood pH and blood or urine ketones should be checked in ill patients with diabetes regardless of blood glucose levels. Background Diabetic ket Continue reading >>

Best Case Ever 58 Euglycemic Dka

Best Case Ever 58 Euglycemic Dka

This is EM Cases Best Case Ever 58 – Euglycemic DKA with Walter Himmel, the walking encyclopedia of emergency medicine. It’s not only run of the mill DKA, starvation and alcoholic ketoacidosis that can cause a metabolic acidosis with elevated ketones. Euglycemic DKA can be caused by the newer diabetes medications sodium-glucose co-transporter 2 inhibitors like Canagliflozin; and it’s important to recognize this tricky diagnosis early and initiate treatment for DKA despite a normal serum glucose level, because DKA can lead to serious complications like renal failure, cerebral edema, ARDS, shock, and death. Podcast production, sound design and editing by Anton Helman; Written by Anton Helman, June 2017 Euglycemic DKA can occur in any diabetic and has been reported in the literature since the 1970’s, but there has recently been a rise in incidence of euglycemic DKA associated with sodium-glucose co-transporter 2 inhibitors (SGLT-2 inhibitors, or the “zins”) such as Canagliflozin, Dapagliflozin and Empagliflozin. When to suspect euglycemic DKA Any patient with Type 1 or 2 diabetes taking SGLT-2 inhibitors who presents with nausea, vomiting, SOB or malaise or is found to have a metabolic acidosis should have blood drawn for serum ketones. Triggers of euglycemic DKA are similar to the triggers for any DKA: Alcohol use, infection and reduced oral intake. Distinguishing euglycemic DKA from alcoholic DKA Alcoholic ketoacidosis may also present with nausea, vomiting, malaise, ketones and anion gap metabolic acidosis. The key differentiating factor besides the obvious history of heavy alcohol use vs a diabetic taking an SGLT-2 inhibitor, is that patients with alcoholic ketoacidosis tend to have frankly low glucose. How is treatment of euglycemic DKA different? In addit Continue reading >>

Euglycemic Dka Secondary To Sglt2 Inhibitors

Euglycemic Dka Secondary To Sglt2 Inhibitors

Authors: Priyanka Kailash (MS-4, Campbell University School of Osteopathic Medicine), Kevin Weaver, DO (Program Director, Lehigh Valley Health Network), and Krystle Shafer, MD (Attending Physician, York Hospital) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit) A 35-year-old male with a past medical history of type 2 diabetes arrives at the Emergency Department (ED) with altered mental status, nausea, vomiting, and diffuse abdominal pain that started 10 hours ago. The patient was recently started on an SGLT2 inhibitor. On examination, the patient is tachycardic (HR 126) and tachypneic (RR 25), with normal blood pressure (110/90). He is further noted to have dry mucous membranes and poor skin turgor. Blood glucose is noted to be 140 mg/dl, serum ketones 6.2 mmol/L, and arterial pH of 6.9. The patient is diagnosed with euglycemic DKA and quickly admitted to ICU for treatment. Pathogenesis of Typical DKA Two major complications from type 1 diabetes mellitus and type 2 diabetes mellitus are diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS). DKA is typically seen in younger individuals, while HHS is typically seen in older patients(1). In the pathogenesis of typical DKA, the body experiences a starved state. Insulin deficiency (either through decreased production or decrease sensitivity) leads to the inactivation of GLUT4 receptors on cells. GLUT4 receptors function to help transport glucose molecules into cells so that it can be converted into energy. Without GLUT4 receptor activation, the glucose entry into cells remains shut. Thus, the cells start to experience a starved state. To compensate, the body activates an alternative energy pathway Continue reading >>

Euglycemic Diabetic Ketoacidosis: A Diagnostic And Therapeutic Dilemma

Euglycemic Diabetic Ketoacidosis: A Diagnostic And Therapeutic Dilemma

Euglycemic diabetic ketoacidosis: a diagnostic and therapeutic dilemma 1Department of Internal Medicine, Memorial Hospital of Martinsville and Henry County, Martinsville, Virginia, USA, 2Texas Tech University Health Sciences Center, El Paso, Texas, USA, 3Senior Research Associate, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA, 4Department of Pharmacology, St Johns Medical College, Bangalore, India, Received 2017 Jul 18; Accepted 2017 Aug 4. This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License . Euglycemic diabetic ketoacidosis (EDKA) is a clinical triad comprising increased anion gap metabolic acidosis, ketonemia or ketonuria and normal blood glucose levels <200 mg/dL. This condition is a diagnostic challenge as euglycemia masquerades the underlying diabetic ketoacidosis. Thus, a high clinical suspicion is warranted, and other diagnosis ruled out. Here, we present two patients on regular insulin treatment who were admitted with a diagnosis of EDKA. The first patient had insulin pump failure and the second patient had urinary tract infection and nausea, thereby resulting in starvation. Both of them were aggressively treated with intravenous fluids and insulin drip as per the protocol for the blood glucose levels till the anion gap normalized, and the metabolic acidosis reversed. This case series summarizes, in brief, the etiology, pathophysiology and treatment of EDKA. Euglycemic diabetic ketoacidosis is rare. Consider ketosis in patients with DKA even if their serum glucose levels are normal. High clinical suspicion is required to diagnose EDKA as normal blood sugar levels masquerade the underlying DKA and cause a diagnostic and therapeutic dilemma. Blood pH and blood or urine Continue reading >>

Prolonged Ketosis In A Patient With Euglycemic Diabetic Ketoacidosis Secondary To Dapagliflozin

Prolonged Ketosis In A Patient With Euglycemic Diabetic Ketoacidosis Secondary To Dapagliflozin

Sodium-glucose cotransporter 2 inhibitors (SGLT2) are the newest class of oral agents to receive US Food and Drug Administration (FDA) approval for the treatment of type 2 diabetes (T2DM). SGLT2 inhibitors currently approved by the FDA include canagliflozin, dapagliflozin, and empagliflozin as well as various combination drugs (Table 1). The enthusiasm this class of drugs has been greeted with stems from the benefits associated with SGLT2 inhibitors. They include decrease in A1c by 0.5% to 1%, reduction in insulin doses, modest weight loss, and improved systolic and diastolic blood pressure.1 In addition, the EMPA-REG OUTCOME trial showed a reduction in all-cause and cardiovascular mortality with empagliflozin.2 Also, a post hoc analysis of a study on dapagliflozin in type 2 diabetics with moderate renal impairment showed improved albuminuria and delayed progression to severe renal failure.3 The popularity of SGLT2 inhibitors is understandable considering the paucity of oral diabetic drugs that promote both weight loss and reduction of insulin needs. Endocrinologists and internists alike have increasingly prescribed this class of drugs as to avoid initiation of insulin or escalation of insulin doses. With more patients using SGLT2 inhibitors, reports of euglycemic diabetic ketoacidosis (euDKA) have emerged. While DKA can be expected with off-label use of SGLT2 inhibitors in patients with T1DM, it has also occurred in T2DM patients. Thus, the FDA posted a drug safety communication on DKA in 2015.4 Greater understanding of how to safely use this newest tool in our arsenal against diabetes is essential. A 50-year-old African American female with T2DM since the age of 35 presented with 10 days of constipation and fatigue, as well as reduced oral intake for 3 days prior to a Continue reading >>

Euglycemic Dka: It’s Not A Myth

Euglycemic Dka: It’s Not A Myth

Background: Diabetic ketoacidosis (DKA) is traditionally defined as a triad of hyperglycemia (>250mg/dL), anion gap acidosis, and increased plasma ketones. There is another entity that providers must be aware of known as euglycemic DKA (euDKA), which is essentially DKA without the hyperglycemia (Serum glucose <200 mg/dL). Euglycemic DKA is a rare entity that mostly occurs in patients with type 1 diabetes, but can possibly occur in type 2 diabetes as well. The exact mechanism of euDKA is not entirely known, but has been associated with partial treatment of diabetes, carbohydrate food restriction, alcohol intake, and inhibition of gluconeogenesis. euDKA, can also be associated with sodium-glucose cotransporter 2 (SGLT-2) inhibitor medications. These medications first came onto the market in 2013 and are FDA approved for the treatment of type 2 diabetes, however many physicians use them off-label for type I diabetes due to their ability to improve average glucose levels, reduce glycemic variability without increasing hypoglycemia, and finally promote weight loss. Does euDKA Exist even in Patients not Using SGLT-2 Inhibitors? The short answer is YES. Munro JF et al [5] reviewed a case series of 37 episodes of euDKA in a publication from 1973. Although, dated and not robust evidence some take home messages can be derived: All but one episode was in insulin dependent diabetics Vomiting was the most frequent symptom of euDKA in 32% of patients Management in most cases consisted of: Intravenous fluids and electrolyte replacement. No deaths occurred in this case series What are the Names of the SGLT-2 Inhibitors? Ipragliflozin (Suglat) – Approved in Japan Dapagliflozin (Farxiga) – 1st SGLT2 Inhibitor Approved; Approved in US Luseogliflozin (Lusefi) – Approved in Japan Tofo Continue reading >>

Euglycemic Diabetic Ketoacidosis: An Easily Missed Diagnosis

Euglycemic Diabetic Ketoacidosis: An Easily Missed Diagnosis

SESSION TITLE: Critical Care Student/Resident Case Report Posters I SESSION TYPE: Student/Resident Case Report Poster INTRODUCTION: A 47 year-old woman with type 1 diabetes presented with euglycemic diabetic ketoacidosis (DKA) that initially went undiagnosed. Recognition and treatment with insulin resulted in rapid resolution of her clinical condition. CASE PRESENTATION: A 47 year-old woman presented to our hospital with four days of fever, abdominal pain, diarrhea, nausea, vomiting, lethargy and malaise. She had a history of type 1 diabetes mellitus managed with an insulin pump. Her blood pressure was 88/51. She was disoriented with a diffusely tender but soft abdomen. Laboratory studies revealed blood glucose of 109 mg/dL, bicarbonate of 15 mmol/L, anion gap of 27 mmol/L, lactic acid of 2.4 mmol/L, and a bandemia of 11%. Rapid flu test was positive. She was admitted to the intensive care unit, resuscitated with intravenous fluid, and started on oseltamivir, cefepime and vancomycin. Hemodialysis was initiated soon thereafter. The patient received no insulin due to her euglycemia. Influenza A was detected by PCR on the second hospital day and antibiotics were discontinued. Her gastrointestinal symptoms improved but her mental status remained poor. Furthermore, while her lactate normalized and blood glucose remained under 120 mg/d, her anion gap persisted at 23-36 mmol/L and her bicarbonate remained low at 15-17 mmol/L. Beta hydroxybutyrate was found to be 4.88 mmol/L. An insulin infusion was started, along with dextrose 5% in water, and her mental status rapidly improved as her acidemia and anion gap normalized. DISCUSSION: Euglycemic DKA is a rare condition that can easily go undiagnosed. It has been previously described in the context of critical illness.1 The pathoge Continue reading >>

Euglycemic Diabetic Ketoacidosis: A Potential Complication Of Treatment With Sodiumglucose Cotransporter 2 Inhibition

Euglycemic Diabetic Ketoacidosis: A Potential Complication Of Treatment With Sodiumglucose Cotransporter 2 Inhibition

Euglycemic Diabetic Ketoacidosis: A Potential Complication of Treatment With SodiumGlucose Cotransporter 2 Inhibition We are experimenting with display styles that make it easier to read articles in PMC. The ePub format uses eBook readers, which have several "ease of reading" features already built in. The ePub format is best viewed in the iBooks reader. You may notice problems with the display of certain parts of an article in other eReaders. Generating an ePub file may take a long time, please be patient. Euglycemic Diabetic Ketoacidosis: A Potential Complication of Treatment With SodiumGlucose Cotransporter 2 Inhibition Anne L. Peters, Elizabeth O. Buschur, [...], and Irl B. Hirsch Sodiumglucose cotransporter 2 (SGLT-2) inhibitors are the most recently approved antihyperglycemic medications. We sought to describe their association with euglycemic diabetic ketoacidosis (euDKA) in hopes that it will enhance recognition of this potentially life-threatening complication. Cases identified incidentally are described. We identified 13 episodes of SGLT-2 inhibitorassociated euDKA or ketosis in nine individuals, seven with type 1 diabetes and two with type 2 diabetes, from various practices across the U.S. The absence of significant hyperglycemia in these patients delayed recognition of the emergent nature of the problem by patients and providers. SGLT-2 inhibitors seem to be associated with euglycemic DKA and ketosis, perhaps as a consequence of their noninsulin-dependent glucose clearance, hyperglucagonemia, and volume depletion. Patients with type 1 or type 2 diabetes who experience nausea, vomiting, or malaise or develop a metabolic acidosis in the setting of SGLT-2 inhibitor therapy should be promptly evaluated for the presence of urine and/or serum ketones. SGLT-2 inhi Continue reading >>

Euglycemic Diabetic Ketoacidosis: A Potential Complication Of Treatment With Sodiumglucose Cotransporter 2 Inhibition

Euglycemic Diabetic Ketoacidosis: A Potential Complication Of Treatment With Sodiumglucose Cotransporter 2 Inhibition

Objective Sodiumglucose cotransporter 2 (SGLT-2) inhibitors are the most recently approved antihyperglycemic medications. We sought to describe their association with euglycemic diabetic ketoacidosis (euDKA) in hopes that it will enhance recognition of this potentially life-threatening complication. Research Design and Methods Cases identified incidentally are described. Results We identified 13 episodes of SGLT-2 inhibitorassociated euDKA or ketosis in nine individuals, seven with type 1 diabetes and two with type 2 diabetes, from various practices across the U.S. The absence of significant hyperglycemia in these patients delayed recognition of the emergent nature of the problem by patients and providers. Conclusions SGLT-2 inhibitors seem to be associated with euglycemic DKA and ketosis, perhaps as a consequence of their noninsulin-dependent glucose clearance, hyperglucagonemia, and volume depletion. Patients with type 1 or type 2 diabetes who experience nausea, vomiting, or malaise or develop a metabolic acidosis in the setting of SGLT-2 inhibitor therapy should be promptly evaluated for the presence of urine and/or serum ketones. SGLT-2 inhibitors should only be used with great caution, extensive counseling, and close monitoring in the setting of type 1 diabetes. Sodiumglucose cotransporter 2 (SGLT-2) inhibitors are the newest class of antihyperglycemic medications, first marketed in 2013 for the treatment of type 2 diabetes.[ 1 ] Limited studies suggest that SGLT-2 inhibitors may be effective in addressing many of the unmet needs of people with type 1 diabetes, including improving average glycemia, while reducing glycemic variability and postprandial hyperglycemia, without increasing hypoglycemia, as well as promoting weight loss while reducing insulin doses.[ 28 Continue reading >>

Euglycemic Diabetic Ketoacidosis With Persistent Diuresis Treated With Canagliflozin

Euglycemic Diabetic Ketoacidosis With Persistent Diuresis Treated With Canagliflozin

Euglycemic Diabetic Ketoacidosis with Persistent Diuresis Treated with Canagliflozin 1Department of Internal Medicine, Ohkubo Hospital, Japan Correspondence to Dr. Junichiro Adachi, [email protected]_uorihcinuj The Internal Medicine is an Open Access article distributed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. To view the details of this license, please visit ( ). This article has been cited by other articles in PMC. Diabetic ketoacidosis is characterized by hyperglycemia, anion-gap acidosis, and increased plasma ketones. After the resolution of hyperglycemia, persistent diuresis is rare. We herein report the case of a 27-year-old Asian woman with type 2 diabetes who was treated with a sodium-glucose cotransporter 2 (SGLT2) inhibitor (canagliflozin) who developed euglycemic diabetic ketoacidosis and persistent diuresis in the absence of hyperglycemia. Physicians should consider euglycemic diabetic ketoacidosis in the differential diagnosis of patients treated with SGLT2 inhibitors. Keywords: sodium-glucose cotransporter 2 inhibitors, euglycemic diabetic ketoacidosis Sodium-glucose cotransporter 2 (SGLT2) inhibitors are oral hypoglycemic agents that augment the urinary excretion of glucose, thereby regulating glycemic control and promoting weight loss ( 1 ). SGLT2 inhibitors have an insulin-independent mechanism of action, which is being explored in patients with type 1 diabetes ( 2 ). Diabetic ketoacidosis is the most serious acute metabolic complication of diabetes ( 3 ). The incidence of diabetic ketoacidosis in patients treated with SGLT2 inhibitors is rare ( 4 , 5 ). Recently, the US Food and Drug Administration issued a Drug Safety Communication that SGLT2 inhibitors may lead to ketoacidosis with mild to moder Continue reading >>

Euglycemic Diabetic Ketoacidosis In Type 2 Diabetes Treated With A Sodium-glucose Cotransporter-2 Inhibitor

Euglycemic Diabetic Ketoacidosis In Type 2 Diabetes Treated With A Sodium-glucose Cotransporter-2 Inhibitor

Go to: Case A 51-year-old man with a known history of T2DM and hypertension presented to the emergency department with a 1-week history of malaise, cough, and intermittent shortness of breath. Over the preceding 2 days, he admitted to a history of decreased oral intake and fever, and he had abstained from taking his antihyperglycemic medications (canagliflozin and linagliptin-metformin). He reported 3 episodes of clear emesis the day of his presentation in the emergency department. He denied any other symptoms, sick contacts, or travel history. He reported no substance use, alcohol consumption, or other ingestions. He was not vaccinated against the flu. He was not taking insulin. Vital signs at triage were within normal limits except for a heart rate of 122 beats/min. The patient looked well and was in no acute distress. The only relevant physical examination findings were mild inspiratory crackles at the left lower lobe on auscultation of the lungs. A 12-lead electrocardiogram showed sinus tachycardia at 101 beats/min. Initial bloodwork revealed a hemoglobin level of 159 g/L (normal range 130 to 170 g/L); a white blood cell count of 12.1 × 109/L (normal range 4.8 × 109/L to 10.8 × 109/L); a neutrophil count of 11.0 × 109/L (normal range 2.0 × 109/L to 7.0 × 109/L); a platelet count of 405 × 109/L (normal range 130 × 109/L to 400 × 109/L); a random blood glucose level of 11.9 mmol/L (normal range 3.9 to 11.2 mmol/L); a sodium concentration of 139 mmol/L (normal range 136 to 144 mmol/L); a potassium level of 5.0 mmol/L (normal range 3.5 to 5.5 mmol/L); a chloride level of 93 mmol/L (normal range 98 to 109 mmol/L); a total CO2 level of 8 mmol/L (normal range 22 to 29 mmol/L); an anion gap of 38 mmol/L (normal range 4 to 12 mmol/L); a urea level of 9.3 mmol/L (nor Continue reading >>

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