EUGLYCEMIC DIABETIC KETOACIDOSIS AND REFEEDING SYNDROME IN A PATIENT WITH ACUTE STROKE: A CASE REPORT

Euglycemic diabetic ketoacidosis (euDKA) is a rare but serious complication characterized by significant ketoacidosis (pH <7.3, bicarbonate <18 mmol/L, ketonemia or ketonuria) with serum glucose <250 mg/dL. Its incidence is increasing with wider use of Sodium-Glucose Cotransporter-2 (SGLT2) inhibitors in diabetes and cardiorenal disease. By promoting glucosuria and lowering insulin levels, SGLT2 inhibitors increase ketogenesis even in euglycemia. Refeeding syndrome (RFS), a life-threatening shift in fluids and electrolytes upon nutritional replenishment, further complicates recovery but is seldom reported alongside euDKA. We present a unique case of SGLT2 inhibitor-induced euDKA complicated by RFS, with emphasis on fluid-electrolyte management in a nephrology-relevant context.

A comprehensive review of the patient's medical records, including clinical presentation, laboratory findings, treatment, and outcome.

A 51-year-old Filipino male with hypertension presented with an acute left thalamic infarct and was initiated on nasogastric feeding due to dysphagia. Laboratory workup revealed an HbA1c of 14.2%, indicating previously undiagnosed diabetes. Despite modest capillary glucose readings (108–185 mg/dL), dapagliflozin was initiated without insulin. On day seven, the patient developed somnolence and tachypnea. Arterial blood gas showed high anion gap metabolic acidosis (pH 7.26, bicarbonate 3.7 mmol/L, anion gap 37), with ketonuria and glucosuria—consistent with euDKA. Dapagliflozin and metformin were discontinued, and insulin with IV fluids initiated. Electrolyte disturbances followed: hypophosphatemia (0.5 mg/dL), hypokalemia (2.97 mmol/L), hypernatremia (154 mmol/L), and hyperchloremia, driven by insulin shifts and isotonic saline. Septic shock from hospital-acquired pneumonia required vasopressor support.

Due to unavailability of IV phosphate, oral phosphate tablets, phosphate enemas, and calcitriol were used. Each FLEET® enema contains approximately 59 mmol of phosphate, and was administered as a retention enema to enhance absorption. Additionally, Coke Zero® (approx. 0.55–1.60 mmol phosphate per can) was used as a supplemental phosphate source. As caloric intake was slowly advanced from 900 kcal/day, serum phosphate and potassium initially normalized with repletion. However, a second significant decline in both electrolytes occurred during ongoing refeeding, strongly suggestive of developing RFS. Nutritional intake was cautiously titrated. A bicarbonate infusion was used to correct non-anion gap acidosis from hyperchloremia. With electrolyte stabilization, the patient was weaned off vasopressors and transitioned to subcutaneous insulin and oral hypoglycemics. He was discharged in stable condition with plans for outpatient nephrology and endocrinology follow-up.

This case highlights the importance of appropriate SGLT2 inhibitor use, particularly in insulin-naïve patients with poorly controlled diabetes and acute illness. euDKA should be suspected in SGLT2-treated patients with metabolic acidosis and near-normal glucose. In the nephrology setting, fluid and electrolyte shifts must be vigilantly monitored, especially during insulin therapy and refeeding. RFS can complicate DKA recovery, requiring careful caloric advancement and innovative electrolyte repletion strategies in resource-limited settings. Multidisciplinary care is essential to prevent morbidity in overlapping metabolic emergencies such as euDKA and RFS.