MON-663 - Dulaglutide Associated Euglycemic Ketoacidosis in A Patient with Type 2 Diabetes: A Case Report

Introduction:

Euglycemic diabetic ketoacidosis (EDKA) is characterized by diabetic ketoacidosis with blood glucose levels typically below 250 mg/dL, accompanied by anion gap metabolic acidosis and ketosis. This atypical presentation often delays diagnosis due to the absence of marked hyperglycemia. The incidence of EDKA has increased significantly with SGLT2 inhibitors and GLP-1receptor agonists. Other precipitants include pregnancy, prolonged fasting, heavy alcohol use, and acute illness. We report a case of euglycemic DKA following dulaglutide administration in a patient with type 2 diabetes mellitus.

Case presentation:

A 69-year-old female with type 2 diabetes mellitus, chronic kidney disease stage IIIb, hypertension, seizure disorder, recent L3-L4 osteomyelitis, Candida psoas muscle abscess, non-small cell lung cancer with bone metastases, obstructive sleep apnea, and right total hip arthroplasty presented with fatigue and vomiting. Laboratory evaluation revealed severe high anion gap metabolic acidosis with bicarbonate 5 mmol/L, anion gap 26 mEq/L, beta-hydroxybutyrate 1.9 mmol/L, serum glucose 163 mg/dL, and creatinine 1.8 mg/dL. Arterial blood gas showed pH 7.32, pCO2 15 mmHg, and pO2 120 mmHg. Her diabetes medications included dulaglutide (last dose four days prior), insulin glargine, and insulin lispro.

She was diagnosed with euglycemic diabetic ketoacidosis and started on continuous insulin infusion at 7 units/hour with intravenous fluid resuscitation. The course was complicated by hypoglycemia (blood glucose 60 mg/dL), requiring reduction of insulin infusion to 3 units/hour and initiation of dextrose infusion. She briefly required sodium bicarbonate infusion for severe acidosis. Her anion gap gradually closed, and she was transitioned to subcutaneous insulin glargine and lispro once metabolic acidosis resolved. Her acute kidney injury improved with fluid resuscitation, and she was discharged in stable condition.

Conclusion:

The temporal association between dulaglutide administration and the subsequent development of euglycemic DKA supports a potential causal relationship. GLP-1 receptor agonists promote ketogenesis through relative insulin deficiency, particularly in patients with limited endogenous insulin reserve, combined with suppressed glucagon reducing hepatic glucose output. Gastrointestinal side effects leading to reduced oral intake can precipitate starvation ketosis. While EDKA remains a rare complication, clinicians should maintain heightened awareness, particularly in patients with additional risk factors such as acute illness, reduced caloric intake, insulin dose reductions, or concurrent SGLT2 inhibitor use.

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