Case Of Euglycemic Diabetic Ketoacidosis Research Articles

The significance of precise diabetes diagnosis: a case of euglycemic diabetic ketoacidosis induced by the introduction of empagliflozin with simultaneous reduction of insulin dosage

Euglycemic diabetic ketoacidosis (euDKA) is a rare but severe metabolic complication of diabetes mellitus characterised by elevated anion gap metabolic acidosis despite normal or mildly elevated blood glucose levels. Sodium-glucose cotransporter 2 inhibitors (SGLT2i) have emerged as effective antidiabetic medications, yet their use is associated with an increased risk of euDKA, especially when coupled with insulin dose reduction. We present the case of a 50-year-old male with a 20-year history of diabetes mellitus, initially managed with insulin and metformin, who developed euDKA following the introduction of empagliflozin and sitagliptin alongside a reduction in insulin therapy. Despite normoglycaemia the patient exhibited symptoms of ketoacidosis, including chronic fatigue, polydipsia, and polyuria. Diagnostic workup revealed metabolic acidosis, elevated inflammatory markers, acute kidney injury and ketonuria. Subsequent specialised laboratory tests confirmed type 1 diabetes mellitus (T1DM) with the presence of anti-glutamic acid decarboxylase (anti-GAD) antibodies and the absence of C-peptide secretion. Management involved fluid therapy, intravenous insulin and glucose administration. This case underscores the diagnostic challenges of euDKA and emphasises the importance of differentiating between T1DM and T2DM, as management strategies vary significantly. Patient education on insulin therapy and injection techniques is crucial to prevent complications such as improper insulin delivery and dose reduction, which can precipitate euDKA. In conclusion, clinicians should be vigilant for euDKA in patients on SGLT2 inhibitors, particularly when insulin dose reduction is involved. Comprehensive patient education and accurate differentiation between diabetes types are essential for timely diagnosis and optimal management, thereby reducing the risk of severe complications.

Euglycemic Diabetic Ketoacidosis Associated With SGLT2 Inhibitor Therapy: A Case Report.

Sodium-glucose cotransporter-2 inhibitors are now considered second-line treatment agents for type 2 diabetes and offer a unique treatment approach with added cardiorenal benefits. Drugs in this class increase the risk of euglycemic diabetic ketoacidosis, which may be difficult to diagnose if clinicians are not aware of the risk factors and subtle symptoms. This article describes a case of euglycemic diabetic ketoacidosis in a patient with coronary artery disease who was taking a sodium-glucose cotransporter-2 inhibitor and experienced acute mental status changes immediately after heart catheterization.

LBODP036 A Case of Euglycemic Diabetic Ketoacidosis After Distal Pancreatectomy

Abstract The patient is a 68-year-old female with a past medical history of type 2 diabetes mellitus, pancreatic mass, hypertension, hyperlipidemia, and coronary artery disease who presented to the hospital for elective surgical resection of her pancreatic mass. She underwent robotic-assisted laparoscopic distal pancreatectomy, splenectomy, and gastric wedge resection. Her hospital course was complicated by post-operative bleeding with hemoperitoneum the day after her initial surgery. She returned to the operative room for exploratory laparotomy during which the source of bleeding was identified and repaired. She was transferred to the intensive-care unit for post-operative monitoring. On the fourth day of admission, the patient became markedly acidotic. Her labs revealed a bicarbonate level of 12 mmol/L and a pH of 7.24. Her anion gap was elevated to 17. Endocrinology was consulted for suspected euglycemic diabetic ketoacidosis. Beta-hydroxybutyrate was elevated to 5.10 mmol/L (0 - 0.29 mmol/L). The patient's blood glucose was 159 mg/dL. Of note, the patient does take Empagliflozin at home. This medication has been associated with euglycemic diabetic ketoacidosis; however, she had not received this medication for five days prior to the onset of diabetic ketoacidosis. Glucosuria is expected to return to baseline after discontinuation of Empagliflozin within approximately three days. A urinalysis was checked at the time of consultation, and the patient did have a large amount of glucose in her urine which suggests that Empagliflozin was still acting to produce glucosuria. The patient was treated with intravenous insulin and fluids per the institution's protocol for the management of diabetic ketoacidosis. Her acidosis rapidly improved, and she was transitioned to subcutaneous insulin to manage her diabetes prior to discharge. This is an interesting case of euglycemic diabetic ketoacidosis due to the multifactorial precipitants: the dwindling effect of Empagliflozin five days after discontinuation, the loss pancreatic beta cell mass after distal pancreatectomy, and the stress of multiple surgeries complicated by life-threatening post-operative bleeding. Presentation: No date and time listed

Characterization, management, and risk factors of hyperglycemia during PI3K or AKT inhibitor treatment.

PurposeThe phosphoinositide 3‐kinase (PI3K)/protein kinase B (AKT) pathway controls insulin sensitivity and glucose metabolism. Hyperglycemia is one of the most common on‐target adverse effects (AEs) of PI3K/AKT inhibitors. As several PI3K and AKT inhibitors are approved by the United States Food and Drug Administration or are being studied in clinical trials, characterizing this AE and developing a management strategy is essential.MethodsPatients with hematologic or solid malignancies treated at Memorial Sloan Kettering Cancer Center with a PI3K or AKT inhibitor were included in this retrospective analysis. A search for patients experiencing hyperglycemia was performed. The frequency, management interventions and outcomes were characterized.ResultsFour hundred and ninety‐one patients with 10 unique cancer types who received a PI3K or AKT inhibitor were included. Twelve percent of patients required a dose interruption, 6% of patients required a dose reduction and 2% of patients were hospitalized to manage hyperglycemia. No events occurred among patients receiving β‐, γ‐, or δ‐ specific PI3K inhibitor. There was one case where the PI3K or AKT inhibitor was permanently discontinued due to hyperglycemia. Metformin was the most commonly used antidiabetic medication, followed by insulin, sodium‐glucose transport protein 2 (SGLT2) inhibitors, and sulfonylurea. SGLT2 inhibitors were associated with the greatest reductions in blood sugar, followed by metformin. At least one case of euglycemic diabetic ketoacidosis (DKA) occurred in a patient on PI3K inhibitor and SGLT2 inhibitor. Body mass index ≥ 25 and HbA1c ≥ 5.7 are were independently significant predictors of developing hyperglycemia.ConclusionHyperglycemia is one of the major on‐target side effects of PI3K and AKT inhibitors. It is manageable with antidiabetic medications, treatment interruption and/or dose modification. We summarize pharmacological interventions that may be considered for PI3K/AKT inhibitor induced hyperglycemia. SGLT2‐inhibitor may be a particularly effective second‐line option after metformin but there is a low risk of euglycemic DKA, which can be deadly. To our knowledge, our report is the largest study of hyperglycemia in patients receiving PI3K/AKT inhibitors.

Euglycemic Diabetic Ketoacidosis in Type 1 Diabetes on Insulin Pump, with Acute Appendicitis: A Case Report.

IntroductionRecently, euglycemic diabetic ketoacidosis has been an increasing topic of discussion within emergency medicine literature. Euglycemic diabetic ketoacidosis can easily be missed, as a normal point-of-care glucose often mistakenly precludes the work-up of diabetic ketoacidosis.Case ReportA 16-year-old female with a past medical history of type 1 diabetes presented to the emergency department with altered mental status, vomiting, and abdominal pain. She was diagnosed with euglycemic diabetic ketoacidosis.ConclusionReported cases of euglycemic diabetic ketoacidosis are most frequently attributed to sodium glucose cotransporter-2 inhibitors, but other potential causes have been discussed in the literature. In this patient, a starvation state with continued insulin use in the setting of acute appendicitis led to her condition.

Euglycemic diabetic ketoacidosis - a rare side effect of sodium-glucose co-transporter-2 inhibitor in a patient of type 2 diabetes mellitus with left ventricular dysfunction: a case report

A 42 year old female with type 2 diabetes mellitus (T2DM), presented with angina on exertion and left ventricular (LV) dysfunction (global LV ejection fraction (EF)=26%). Patient was subjected to coronary angiography which revealed triple vessel disease. Patient was started on usual standard of care heart failure (HF) medications, including sodium-glucose co-transporter-2 (SGLT-2) inhibitor dapagliflozin which is promising new class of drug for treating T2DM and HF. Patient was advised myocardial revascularization in form of percutaneous transluminal coronary angioplasty (PTCA). Post angioplasty patient developed metabolic acidosis (high anion gap with normal lactate and increased ketone levels). Patient was diagnosed as case of euglycemic diabetic ketoacidosis (DKA) and patient was treated by volume resuscitation and insulin infusion.

Abstract #975885: Euglycemic Diabetic Ketoacidosis Secondary to SGLT2-inhibitor Use in Combination with a Ketogenic Diet: A Case Report

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 Case Report of Euglycemic Diabetic Ketoacidosis in the Setting of Keto Diet and SGLT-2 Inhibitors

Background: Euglycemic diabetic ketoacidosis is relatively uncommon. Studies of SGLT inhibitors, when added to either insulin pumps or multiple daily injections have shown glycemic benefit in type 1 diabetes mellitus (DM), with reductions of Hba1c, body weight, glucose variability, without increased hypoglycemia, but with increase of DKA. We report a case of euglycemic diabetic ketoacidosis in a patient with type 1 DM, precipitated by keto diet and SGLT-2 inhibitor use. Clinical Case: A 24 year-old female with 17 years of type 1DM, using insulin pump therapy and empagliflozin, started a keto diet, then stopped meal time boluses, and eventually turned off her pump. Urine ketones were high. After 12 hours, she developed fatigue, nausea, abdominal pain, and shortness of breath, and presented to the emergency room. She was afebrile with BP 112/68, HR 123 beats/minute, respiratory rate 18, and oxygen saturation on room air 99%. Physical exam: anxious in mild distress, abdomen was diffusely tender without guarding. Laboratory results: sodium 141 mmol/L, potassium 5.3 mmol/L, chloride 103 mmol/L, CO2 8 mmol/L, Anion gap 30 mmol/L, with blood glucose of 201 mg/dL,and BUN 22 mg/dL, creatinine 1.55 mg/dL, GFR 41 ml/min/1.73m, Hba1c 7.2%, Normal thyroid tests, WBC 23.1 10x3/ul, Hgb 16.6 g/dl, HCT 53.3%, normal differential, Urine: ketones >=80 mg/dl, Protein 30 mg/dl, urine glucose >500 mg/dl. CT abdomen and pelvis with contrast: questionable regional colitis of ascending colon with prominent distended stomach, and possible functional obstruction, such as diabetic gastroparesis, and fatty infiltration of liver. An insulin infusion per DKA protocol was started. Over the next few days, she continued with high anion gap and low CO2; requiring bicarbonate drip. By day 3, laboratory results finally improved. Symptoms completely resolved, and the patient was started on a carbohydrate restricted diet with insulin pump therapy, and discharged home after intensive education by the diabetes team. Discussion: Euglycemic diabetic ketoacidosis is a rare, but serious complication of DM, characterized by glucose values ≤200 mg/L, ketosis and metabolic acidosis. Possible risk factors include decreased caloric intake, keto diet, heavy alcohol consumption, change in insulin regimen, chronic liver disease, pregnancy, and sodium glucose cotransporter 2 (SGLT2) inhibitors. This case highlights the complex interplay between type 1 DM, a keto diet, in combination with SGLT-2 inhibitor therapy, which may result in euglycemic diabetic ketoacidosis, and also demonstrates the importance of patient education regarding risks of ketoacidosis in the setting of SGLT-2 inhibitor therapy, in conjunction with low calorie intake and diets, such as the keto diet. Reference: (1) Julio Rosenstock, et al. Empagliflozin as Adjunctive to Insulin Therapy in Type 1 Diabetes: The EASE Trials. Diabetes Care 2018 Dec; 41(12): 2560–2569.

Euglycemic Diabetic Ketoacidosis Secondary to SGLT2-inhibitor Use in Combination With a Ketogenic Diet

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.

The optimal medical therapy for glycemic control in covid-19

Diabetes is highly linked to the severity of coronavirus disease 2019 (COVID-19). My recent meta-analysis also suggested a higher prevalence of diabetes in severe COVID-19 as compared with non-severe COVID-19. Recent observational studies have shown that hyperglycemia was significantly associated with severity of COVID-19 in both diabetic and non-diabetic patients. To prevent worse outcome of COVID-19, more tight glucose control is required. I studied the association between hyperglycemia and worse outcome of COVID-19, the putative beneficial and harmful effects, and clinical outcomes of oral hypoglycemic drugs and insulin use in glycemic control among COVID-19 patients, by searching literatures. Although there were some negative studies, the meta-analysis reported that the treatment using metformin was associated with reduction in mortality due to COVID-19. One study showed that treatment with sitagliptin, one of dipeptidyl peptidase-4 (DPP4) inhibitors, during hospitalization was associated with reduction of mortality, with a clinical improvement as compared with patients on the standard care. There were no clinical studies showed effects of glucagon-like peptide-1 receptor agonists, pioglitazone and sulfonylurea on COVID-19 outcomes. Regarding sodium-glucose cotransporter 2 (SGLT2) inhibitors, a case of euglycemic diabetic ketoacidosis (DKA) associated with COVID-19 and a case of DKA that was difficult to distinguish from COVID-19 were reported. COVID-19 patients who need hospital care may deteriorate rapidly, an early and appropriate initiation of insulin therapy in hyperglycemic COVID-19 patients may be to be encouraged. J Endocrinol Metab. 2021;11(1):1-7 doi: https://doi.org/10.14740/jem718

The Optimal Medical Therapy for Glycemic Control in COVID-19

Diabetes is highly linked to the severity of coronavirus disease 2019 (COVID-19). My recent meta-analysis also suggested a higher prevalence of diabetes in severe COVID-19 as compared with non-severe COVID-19. Recent observational studies have shown that hyperglycemia was significantly associated with severity of COVID-19 in both diabetic and non-diabetic patients. To prevent worse outcome of COVID-19, more tight glucose control is required. I studied the association between hyperglycemia and worse outcome of COVID-19, the putative beneficial and harmful effects, and clinical outcomes of oral hypoglycemic drugs and insulin use in glycemic control among COVID-19 patients, by searching literatures. Although there were some negative studies, the meta-analysis reported that the treatment using metformin was associated with reduction in mortality due to COVID-19. One study showed that treatment with sitagliptin, one of dipeptidyl peptidase-4 (DPP4) inhibitors, during hospitalization was associated with reduction of mortality, with a clinical improvement as compared with patients on the standard care. There were no clinical studies showed effects of glucagon-like peptide-1 receptor agonists, pioglitazone and sulfonylurea on COVID-19 outcomes. Regarding sodium-glucose cotransporter 2 (SGLT2) inhibitors, a case of euglycemic diabetic ketoacidosis (DKA) associated with COVID-19 and a case of DKA that was difficult to distinguish from COVID-19 were reported. COVID-19 patients who need hospital care may deteriorate rapidly, an early and appropriate initiation of insulin therapy in hyperglycemic COVID-19 patients may be to be encouraged. J Endocrinol Metab. 2021;11(1):1-7 doi: https://doi.org/10.14740/jem718

A case of euglycemic diabetic ketoacidosis (EDKA) after appendectomy due to a sodium-glucose cotransporter-2 (SGLT2) inhibitor

A case of euglycemic diabetic ketoacidosis (EDKA) after appendectomy due to a sodium-glucose cotransporter-2 (SGLT2) inhibitor

438: A Hidden Issue in Plain Sight: A Case of Euglycemic DKA in the Setting of Pancreatitis

438: A Hidden Issue in Plain Sight: A Case of Euglycemic DKA in the Setting of Pancreatitis

The case of euglycemic diabetic ketoacidosis associated with sodium-glucose cotransporter 2 inhibitors application

The case of euglycemic diabetic ketoacidosis associated with sodium-glucose cotransporter 2 inhibitors application

Euglycemic DKA as an Initial Presentation of Immunotherapy-Induced Insulin-Dependent Diabetes

New onset insulin dependent diabetes (DM) has been reported in cancer patients (pts) receiving immunotherapy (IO). Typically, pts have Grade 3 hyperglycemia (CTCAE) and sometimes DKA. Euglycemic DKA has been reported in pts on empagliflozin (Empa). We present a unique case of euglycemic DKA as initial presentation for immunotherapy induced insulin dependent DM. Pt is a 68 year old man without preexisting DM started on nivolumab for metastatic prostate cancer. Following 2 doses of nivolumab, he developed fatigue, weight loss and Grade 2 hyperglycemia for which he was started on metformin, glipizide, and Empa by his outside physician. His BG levels ranged from 130-200 mg/dL on these therapies. Nivolumab treatment was stopped due to significant adverse effects. On return visit to our clinic, approximately 3 months after initial hyperglycemia, pt complained of persistent fatigue, weight loss and a new fruity odor in his breath. Labs revealed BG of 134mg/dl, bicarb of 19 mEq/L (23-30mEq/L), anion gap (AG) of 17mEq/L (4-14mEq/L). Urine ketones were positive and c-peptide level was 0.3ng/ml (0.8- 3.85ng/ml). Pt was advised to immediately stop Empa and follow-up with local ER. When he presented to local ER, approximately 4 days later, he was hyperglycemic with glucose 316 mg/dL, and labwork consistent with classic DKA. Pt was initiated on basal bolus insulin regimen and had resolution of DKA.IO mediated DM results from immune mediated islet cell destruction leading to rapidly progressive insulin deficiency. When suspected, these pts should be evaluated for beta cell dysfunction and insulin should be used for glycemic control. This case highlights that SGLT2 therapy should be used with caution in patients with hyperglycemia on immunotherapy as it could mask the diagnosis of DKA. In addition, this case shows that patients taken off of immunotherapy may develop delayed glycemic complications and may need long term monitoring. Disclosure P. Iyer: None. S.N. Thosani: Consultant; Spouse/Partner; Boston Scientific Corporation, Medtronic. Speaker's Bureau; Spouse/Partner; AbbVie Inc..

A Case of Euglycemic Diabetic Ketoacidosis due to Canagliflozin Complicated by Takotsubo Cardiomyopathy

Sodium-glucose co-transporter-2 (SGLT-2) inhibitor is the latest class of anti diabetic medication that improves glycemic control in insulin independent fashion by increasing urinary loss of filtered glucose. Since its introduction in 2013, several cases of euglycemic DKA have been reported in patients being treated with SGLT-2 inhibitors. Blood glucose levels in range lower than expected for DKA makes the diagnosis challenging if clinical suspicion for euglycemic DKA is not high. We report a case of a patient being treated with canagliflozin who presented with DKA, AKI and mild hyperglycemia that was complicated by stress-induced cardiomyopathy.

Euglycemic Diabetic Ketoacidosis Secondary to Dapagliflozin Use: A Case Report

BackgroundSodium-glucose co-transporter-2 (SGLT2) inhibitors are a novel class of oral antihyperglycemic agents. They are associated with rare cases of euglycemic diabetic ketoacidosis (DKA), which presents a diagnostic challenge in the emergency department (ED) and potentially severe consequences if missed. Case ReportA 53-year-old man with type 2 diabetes mellitus and a recent Roux-en-Y gastric bypass surgery presented to the ED with nausea, vomiting, and generalized abdominal pain. His medications included dapagliflozin. Work-up revealed anion-gap acidosis, which prompted us to send serum ketone levels despite a blood glucose level of 9.8 mmol/L (162 mg/dL). The patient was ultimately diagnosed with euglycemic DKA. Why Should an Emergency Physician Be Aware of This?Patients on SGLT2 inhibitors may present in DKA despite having normal blood glucose levels. It is important for emergency physicians to be aware of this phenomenon in all SGLT2-inhibitor users, as a delay in the diagnosis of DKA can be life threatening.

Prolonged Ketosis in a Patient With Euglycemic Diabetic Ketoacidosis Secondary to Dapagliflozin.

Since the approval of sodium-glucose cotransporter 2 (SGLT2) inhibitors by the US Food and Drug Administration for type 2 diabetes, there have been several reports of euglycemic diabetic ketoacidosis in patients using this class of medication. We present a case of euglycemic diabetic ketoacidosis where ketonemia and glucosuria persisted well beyond the expected effect of dapagliflozin. Our patient is a 50-year-old woman with type 2 diabetes since age 35 who was taking metformin and dapagliflozin. She presented with fatigue, constipation, and 3 days of reduced oral intake. Laboratory data indicated anion gap acidosis, ketonemia, severe hypokalemia, and minimally elevated blood glucose. She was treated with sliding scale short-acting insulin and electrolyte replacement until hospital day 6, when endocrinology was consulted. An insulin drip was initiated due to persistent ketonemia and reopening of the anion gap, despite improved oral intake and normoglycemia. On stopping the insulin drip on day 9, the β-hydroxybutyrate increased again. It finally stabilized within normal range with the initiation of basal subcutaneous insulin. This case indicates that clinical effects of dapagliflozin persist much longer than the reported half-life of 12.9 hours would predict. To prevent this potentially dangerous complication, patients taking SGLT2 inhibitors who become ill should discontinue the medication, undergo ketone evaluation, and start basal insulin, if ketones are positive. In addition, patients should be educated to stop their SGLT2 inhibitor at least 1 week prior to elective procedures.

Euglycemic Diabetic Ketoacidosis in a Patient with Cocaine Intoxication.

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.

Misleading presentation of euglycemic diabetic ketoacidosis: Implication for low-mid-income communities

Misleading presentation of euglycemic diabetic ketoacidosis: Implication for low-mid-income communities