Euglycaemic diabetic ketoacidosis in a 43-year-old woman with type 2 diabetes mellitus on SGLT-2 inhibitor (empagliflozin)

2020 ◽  
Vol 13 (6) ◽  
pp. e235117
Author(s):  
Azka Latif ◽  
Aheli Arce Gastelum ◽  
Akshat Sood ◽  
Joseph Thilumala Reddy

We report a case of euglycaemic diabetic ketoacidosis (EDKA) in a 43-year-old woman with type 2 diabetes mellitus who presented to the emergency department with problems of vomiting, cough, shortness of breath and generalised weakness after following a ketogenic diet for 2 weeks. Therapy with sodium glucose transport protein-2 empagliflozin had been started 2 months prior. Initial evaluation revealed high anion gap metabolic acidosis with blood glucose level of 169 mg/dL. Treatment for EDKA with fluid resuscitation, intravenous insulin and dextrose resolved her acidosis and symptoms in less than 24 hours. Empaglifozin was discontinued on discharge. This entity represents a diagnostic challenge since the differential diagnosis is broad with a potentially misleading clinical presentation that can result in delayed diagnosis and adverse outcomes including acute kidney injury, multiple electrolyte abnormalities, cerebral oedema, acute respiratory distress syndrome, shock and death.

2021 ◽  
Vol 14 (8) ◽  
pp. e243696
Author(s):  
Timothy Xin Zhong Tan ◽  
Steven Hoon Chin Lim ◽  
Joan Khoo

A 54-year-old woman with insulin-requiring type 2 diabetes mellitus presented with acute shortness of breath and drowsiness on a background of polydipsia, weakness and significant weight loss. One year ago, she had decided to stop her insulin and other medications and adopt lifestyle modifications instead. Initial emergency department (ED) blood samples were highly lipaemic and appeared strawberry pink. She was eventually diagnosed with diabetic ketoacidosis (DKA) with severe hypertriglyceridaemia, intubated for airway protection, and managed with fluid resuscitation and intravenous insulin to good effect. We share an uncommon DKA presentation at the ED. History was limited as the patient was drowsy and minimally communicative. Physical examination was unremarkable. Blood investigations were also delayed in view of the need for additional centrifugation. These contributed to a paucity of information in the acute setting and resulted in a diagnostic challenge.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Kevin A Arao ◽  
Harikrashna Bhatt ◽  
Christina M Capistrano ◽  
Hui Zhang ◽  
Christopher Cosgrove

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.


2022 ◽  
Vol 16 (1) ◽  
Author(s):  
Edwin Sze Sian Yii ◽  
Athirah Wan Azli ◽  
Premela Naidu Sitaram

Abstract Background Sodium–glucose cotransporter 2 inhibitors are among the new-generation oral antihyperglycemic agents that have been used in the treatment of type 2 diabetes mellitus. With the recent coronavirus disease 2019 pandemic and rise of cases in the third wave, diagnosis of life-threatening euglycemic diabetic ketoacidosis may easily be overlooked or missed. Case presentation We present the case of a 37-year-old Malay gentleman with underlying type 2 diabetes mellitus on empagliflozin, who presented to our hospital with symptomatic coronavirus disease 2019 infection and diabetic ketoacidosis. He developed severe rebound euglycemic diabetic ketoacidosis due to the continuous usage of empagliflozin for glycemic control alongside intravenous insulin. Conclusions Physicians should have a high index of suspicion in diagnosing and managing euglycemic diabetic ketoacidosis, including withholding treatment of sodium–glucose cotransporter 2 inhibitors during the acute management of diabetic ketoacidosis.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Sarah Chhabra ◽  
Alex Manzano ◽  
Neha Garg

Abstract Background Sodium glucose cotransporter-2 inhibitors (SGLT-2i) are a promising class of oral anti-hyperglycemic agents with mounting evidence of reduced cardiovascular risk and renal failure, in patients with type 2 diabetes mellitus. Recent increase in their use has led to identification of hitherto unknown side effects of these drugs. Euglycemic Diabetic Ketoacidosis (eDKA), found to be associated with SGLT-2i use, is a life-threatening condition and commonly goes unrecognized due to absence of the cardinal sign of hyperglycemia. Clinical Case We describe a 47 year old male with history of coronary artery disease and recently diagnosed type 2 diabetes mellitus who presented to our hospital with one week history of nausea, lethargy, progressive fatigue, and shortness of breath. He was diagnosed with type 2 diabetes three weeks prior, with HBA1c of 12%. His regimen included basal insulin and recent transition to empagliflozin due to severe GI intolerance with metformin use. On arrival he was noted to be tachycardic with a heart rate of 113/min, afebrile and normotensive. Physical exam was mostly unremarkable except for dry oral mucous membranes. Serum chemistry was consistent with high anion gap metabolic acidosis with bicarbonate of 6.9 mmol/L (21-32 mmol/L), anion gap of 29 mmol/L (10-20 mmol/L), mildly elevated blood glucose of 132 mg/dl (74-106 mg/dl), acute kidney injury with creatinine of 1.47 mg/dl (0.7- 1.3 mg/dl), and a beta hydroxybutyrate level of 82.7 mg/dl (0.20- 5.63 mg/dl). Urine analysis showed ketonuria. This was consistent with a clinical and biochemical diagnosis of eDKA. He was treated with IV D5%NS-20mEq/L KCL and an insulin drip. Upon resolution of his acidosis and normalization of the anion gap he was switched to subcutaneous Insulin Glargine and Lispro. Empagliflozin was held as it was thought to be contributing to the diagnosis of eDKA. Conclusion Our case yet again illustrates the importance of recognition of EDKA to aid prompt management, especially with the rising popularity of SGLT-2 inhibitors. It is also important to educate patients about this condition, mostly notable in the first two months of starting the medication, to recognize the concerning symptoms and precipitating factors like dehydration, improper insulin dosing, low calorie diet, alcohol, infection, surgery. An acceptable alternative to SGLT-2i can be glucagon like peptide receptor (GLP- 1) agonists, also associated with good cardiovascular outcomes.


2013 ◽  
Author(s):  
Rene Rodriguez-Gutierrez ◽  
Emanuel I Gonzalez-Moreno ◽  
Carlos R Camara-Lemarroy ◽  
Dania L Quintanilla-Flores ◽  
Juan M Gonzalez-Chavez ◽  
...  

Children ◽  
2021 ◽  
Vol 8 (8) ◽  
pp. 627
Author(s):  
Pierluigi Marzuillo ◽  
Anna Di Sessa ◽  
Pier Luigi Palma ◽  
Giuseppina Rosaria Umano ◽  
Cesare Polito ◽  
...  

Type 2 Diabetes Mellitus (T2DM) is a main cause of chronic kidney disease (CKD) in adulthood. No studies have examined the occurrence of acute kidney injury (AKI)—that enhances the risk of later CKD—and renal tubular damage (RTD)—that can evolve to AKI—in children with onset of T2DM. We aimed to evaluate the prevalence and possible features of AKI and RTD in a prospectively enrolled population of children with onset of T2DM. We consecutively enrolled 10 children aged 12.9 ± 2.3 years with newly diagnosed T2DM. AKI was defined according to the KDIGO criteria. RTD was defined by abnormal urinary beta-2-microglobulin and/or tubular reabsorption of phosphate (TRP) < 85% and/or fractional excretion of Na > 2%. None of the patients developed AKI, whereas 3/10 developed RTD with high beta-2-microglobulin levels (range: 0.6–1.06 mg/L). One of these three patients also presented with reduced TRP levels (TRP = 70%). Proteinuria was observed in two out of three patients with RTD, while none of patients without RTD had proteinuria. Patients with RTD presented higher beta-2-microglobulin, acute creatinine/estimated basal creatinine ratio, and serum ketones levels compared with patients without RTD. In conclusion, in our pilot observation, we found that none of the 10 children with T2DM onset developed AKI, whereas three of them developed RTD.


2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
S Lee ◽  
J Zhou ◽  
CL Guo ◽  
WKK Wu ◽  
WT Wong ◽  
...  

Abstract Funding Acknowledgements Type of funding sources: None. Introduction Acute myocardial infarction (AMI) and sudden cardiac death (SCD) are major cardiovascular adverse outcomes in patients with type 2 diabetic mellitus. Although there are many risk scores on composite outcomes of major cardiovascular adverse outcomes or cardiovascular mortality for diabetic patients, these existing scores did not account for the difference in pathogenesis and prognosis between acute coronary syndrome and lethal ventricular arrhythmias. Furthermore, recent studies reported that HbA1c and lipid levels, which were often accounted for in these risk scores, have J/U-shaped relationships with adverse outcomes. Purpose The present study aims to evaluate the application of incorporating non-linear J/U-shaped relationships between mean HbA1c and cholesterol levels into risk scores for predicting for AMI and non-AMI related SCD respectively, amongst type 2 diabetes mellitus patients. Methods This was a territory-wide cohort study of patients with type 2 diabetes mellitus above the age 40 and free from prior AMI and SCD, with or without prescriptions of anti-diabetic agents between January 1st, 2009 to December 31st, 2009 at government-funded hospitals and clinics in Hong Kong. Risk scores were developed for predicting incident AMI and non-AMI related SCD. The performance of conditional inference survival forest (CISF) model compared to that of random survival forests (RSF) model and multivariate Cox model. Results This study included 261308 patients (age = 66.0 ± 11.8 years old, male = 47.6%, follow-up duration = 3552 ± 1201 days, diabetes duration = 4.77 ± 2.29 years). Mean HbA1c and high-density lipoprotein-cholesterol (HDL-C) were significant predictors of AMI under multivariate Cox regression and were linearly associated with AMI. Mean HbA1c and total cholesterol were significant multivariate predictors with a J-shaped relationship with non-AMI related SCD. The AMI and SCD risk scores had an area-under-the-curve (AUC) of 0.666 (95% confidence interval (CI)= [0.662, 0.669]) and 0.677 (95% CI= [0.673, 0.682]), respectively. CISF significantly improves prediction performance of both outcomes compared to RSF and multivariate Cox models. Conclusions A holistic combination of demographic, clinical, and laboratory indices can be used for the risk stratification of type 2 diabetic patients against AMI and SCD.


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