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.

scholarly journals Euglycemic diabetic ketoacidosis: a diagnostic and therapeutic dilemma

2017 ◽  
Vol 2017 ◽  
Author(s):  
Prashanth Rawla ◽  
Anantha R Vellipuram ◽  
Sathyajit S Bandaru ◽  
Jeffrey Pradeep Raj
Keyword(s):  
Metabolic Acidosis ◽  
Blood Glucose ◽  
Diabetic Ketoacidosis ◽  
Clinical Suspicion ◽  
Anion Gap ◽  
Normal Blood ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
High Clinical Suspicion ◽  
Euglycemic Diabetic Ketoacidosis

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. Learning points: 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.

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 &lt;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.

scholarly journals Euglycemic Diabetic Ketoacidosis in Pregnancy

2019 ◽  
Vol 4 (1) ◽  
pp. 26-28
Author(s):  
Júlio Garcia de Alencar ◽  
Geovane Wieblling da Silva ◽  
Sabrina Correa da Costa Ribeiro ◽  
Júlio Marchini ◽  
Rodrigo Neto ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Blood Glucose ◽  
Blood Glucose Level ◽  
Diabetic Ketoacidosis ◽  
Clinical Presentation ◽  
Fasting Glucose ◽  
Glucose Levels ◽  
Euglycemic Diabetic Ketoacidosis ◽  
In Pregnancy

The clinical presentation of diabetic ketoacidosis in pregnancy (DKP) is similar to that observed in nonpregnant women, although reports suggest the presenting blood glucose level may not be as high. It is hypothesized that lower, maternal fasting glucose levels are a result of both the fetus and the placenta consuming glucose. We report the case of a 38-year-old woman gravida 2, para 0, abortion 1 with type 1 diabetes who had euglycemic diabetic ketoacidosis and review the literature on DKP, with a focus on diagnosis, treatment, and monitoring of the mother and fetus.

scholarly journals 345. Acute Onset Diabetic Ketoacidosis/Hyperosmolar Hyperglycemic State in Patients Taking Integrase Strand Transfer Inhibitors

2019 ◽  
Vol 6 (Supplement_2) ◽  
pp. S183-S184 ◽  
Author(s):  
Afua Duker Ntem-Mensah ◽  
Nina Millman ◽  
Niyati Jakharia ◽  
Amanda Theppote ◽  
Mona-Gekanju Toeque ◽  
...  
Keyword(s):  
Weight Gain ◽  
Blood Glucose ◽  
Blood Glucose Level ◽  
Diabetic Ketoacidosis ◽  
Glucose Level ◽  
Case Reports ◽  
Acute Onset ◽  
Anion Gap ◽  
Hyperosmolar Hyperglycemic State ◽  
Hba1c Levels

Abstract Background A few case reports have noted uncontrolled hyperglycemia in patients switched to dolutegravir. Several cohort studies have found increased weight gain among patients treated with integrase inhibitors (INSTI). We present clinical observations among 3 patients admitted to hospital for diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) while receiving INSTIs for the management of HIV. Methods Case 1: A 44-year-old man with HIV and dyslipidemia presented with altered mental status and lethargy. A fingerstick glucose was >600 mg/dL. Chemistries revealed glucose of 1,600 mg/dL and an elevated β-hydroxybutyrate. HbA1c was 12.4%. His antiretroviral regimen consisted of cEVG/TAF/FTC for the last 3 years. Previous HbA1c levels were 5.7% and 6.2% (Figure 1). Case 2: A 55-year-old woman with HIV, hypertension, dyslipidemia, and obesity presented with polyuria and polydipsia. The blood glucose level was >1,200 mg/dL with an anion gap >30 and HbA1c of 15%. Previous HbA1c levels ranged between 5.6 and 5.8% (Figure 2). She had been taking ABC/FTC/DTG for 2 years. Case 3: A 64 yo man with a history of HIV, hypertension, and obesity presented with polyuria and polydipsia. The blood glucose level was 1,152 mg/dL with no anion gap and HbA1c of 13.4%. Six months before, he had been switched from a c/DRV- based ART regimen to ABC/FTC/DTG. Previous HbA1c levels ranged between 5.8% and 6.2% (Figure 3). Results Discussion: In the first 2 patients, the presentation with acute onset DKA occurred more than a year after being on an INSTI-based regimen; however, the latter patient presented with HHS within 6 months of being switched to an INSTI-containing regimen. The mechanism of action of INSTIs causing weight gain or an association with hyperglycemia is still under investigation. Conclusion Although the temporal onset of DKA and HHS while receiving INSTIs was not precise, the possible association of INSTIs and their direct effects on insulin resistance and diabetes warrant additional attention from post-market data. Meanwhile, providers should monitor INSTI-treated patients closely, especially those with features of metabolic syndrome. Disclosures All authors: No reported disclosures.

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 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 Euglycemic Diabetic Ketoacidosis in the ICU: 3 Case Reports and Review of Literature

2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
Pablo Lucero ◽  
Sebastián Chapela
Keyword(s):  
Diabetes Mellitus ◽  
Diabetic Ketoacidosis ◽  
Ketone Bodies ◽  
Case Reports ◽  
Type I ◽  
Diagnostic Challenge ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Sodium Glucose Cotransporter ◽  
Euglycemic Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is an acute complication of diabetes mellitus, both type I and type II, as well as other types with diabetes such gestacional diabetes mellitus. It is characterized by blood glucose levels greater than 250 mg/dL and metabolic acidosis (pH < 7.3 and serum bicarbonate < 15 mEq/dL) with an increased anion gap and the presence of ketone bodies in the blood or urine. Within this pathology, there is a subgroup of pathologies which are characterized by being present with no signs of hyperglycemia, posing a diagnostic challenge due to the absence of the main sign of the pathology and the diversity of their pathophysiology. In this article, we will present 3 clinical cases with 3 different forms of clinical presentation: a case of DKA in pregnancy, a case of DKA associated with the use of sodium-glucose cotransporter 2 (SGLT-2) inhibitors, and a third case related to sepsis, together with a narrative review of the literature on the topic.

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.

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