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.

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 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 in a Patient with Cocaine Intoxication

2016 ◽  
Vol 2016 ◽  
pp. 1-4 ◽  
Author(s):  
Asma Abu-Abed Abdin ◽  
Muhammad Hamza ◽  
Muhammad S. Khan ◽  
Awab Ahmed
Keyword(s):  
Metabolic Acidosis ◽  
Blood Glucose ◽  
Diabetic Ketoacidosis ◽  
Cocaine Abuse ◽  
Interesting Case ◽  
Anion Gap ◽  
Normal Blood ◽  
Diabetic Patients ◽  
Normal Blood Glucose ◽  
Insulin Dependent Diabetic

Diabetic ketoacidosis (DKA) is characterized by elevated anion gap metabolic acidosis, hyperglycemia, and elevated ketones in urine and blood. Hyperglycemia is a key component of DKA; however, a subset of DKA patients can present with near-normal blood glucose, an entity described as “euglycemic DKA.” This rare phenomenon is thought to be due to starvation and food restriction in insulin dependent diabetic patients. Cocaine abuse is considered a trigger for development of DKA. Cocaine also has anorexic effects. We describe an interesting case of euglycemic DKA in a middle-aged diabetic female presenting with elevated anion gap metabolic acidosis, with near-normal blood glucose, in the settings of noncompliance to insulin and cocaine abuse. We have postulated that cocaine abuse was implicated in the pathophysiology of euglycemic DKA in this case. This case highlights complex physiological interplay between type-1 diabetes, noncompliance to insulin, and cocaine abuse leading to DKA, with starvation physiology causing development of euglycemic DKA.

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 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 Incidence of metabolic diseases of dairy cows in Puerto Rico and its relationship with production and reproduction behavior

1969 ◽  
Vol 92 (1-2) ◽  
pp. 39-52
Author(s):  
Julio C. Meléndez ◽  
José Pantoja ◽  
Angel A. Custodio ◽  
John Fernández Van Cleve ◽  
Raúl Macchiavelli ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Body Condition ◽  
Metabolic Disorders ◽  
Metabolic Diseases ◽  
Body Condition Score ◽  
Normal Blood ◽  
Blood Calcium ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Condition Score

Data were obtained from 89 Holstein cows, distributed among seven commercial herds, to evaluate the incidence of metabolic disorders during the periparturient transition period. The herds were enrolled in the Dairy Herd Improvement Program (DHIP) and were routinely visited by veterinarians, who diagnosed any metabolic disorders. The cows were observed every two weeks to evaluate body condition score (1 to 5 scale), to discern clinical disorders and to obtain blood samples for chemical analyses. Clinical metabolic diseases were not diagnosed, but 34% of the cows showed sub-clinical hypocalcaemia (blood calcium less than 7.9 mg/dl) and 14% had blood glucose levels less than 39.9 mg/dl. Although not significant (P greater than 0.05), milk production was higher at the second and third milk weighings in the normal cows than in those with sub-clinical hypocalcaemia (27.5 and 25.6 vs. 25.1 and 23.6 kg, respectively). The interval between parturition and first service was shorter in cows with normal blood calcium levels than in those that suffered sub-clinical hypocalcaemia (74 vs. 91 days, P less than 0.05). Mean body condition score of the cows without sub-clinical hypocalcaemia or sub-normal blood glucose levels was higher than that of cows with these conditions (2.5 vs. 2.3 in both criteria, P less than 0.05). It is concluded that postpartum blood calcium concentrations affect the interval from parturition to first service and that the probability of occurrence of hypocalcaemia after parturition can be estimated from prepartum blood calcium concentrations.

Treatment of pregnant insulin-dependent diabetic women

1986 ◽  
Vol 113 (3_Suppl) ◽  
pp. S74-S76 ◽  
Author(s):  
K. Fuhrmann
Keyword(s):  
Blood Glucose ◽  
Congenital Malformations ◽  
Blood Glucose Concentration ◽  
Normal Blood ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Insulin Dependent ◽  
Normal Blood Glucose ◽  
Insulin Dependent Diabetic ◽  
In Pregnancy

Abstract. The treatment of 620 insulin-dependent diabetic pregnant women is reported. The goal of treatment was to achieve a normal blood glucose concentration as soon as possibly during early, or even before pregnancy. When intensified conventional insulin therapy was started before conception, about 88% of the patients achieved normal blood glucose levels during the first weeks of pregnancy. In only about 20% of the pregnant diabetics without intensified preconceptional treatment a normal blood glucose level was obtained during their first hospitalization in pregnancy. The rate of congenital malformations was 1.1% in the former and 7.1% in the latter group.

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