Euglycemic ketoacidosis following sleeve gastrectomy in a young non-diabetic female: a case report.

INTRODUCTION AND IMPORTANCE: Euglycemic ketoacidosis (EKA) is a rare metabolic emergency characterized by severe metabolic acidosis, elevated ketones, and normal or near-normal blood glucose levels. It is typically associated with factors such as prolonged fasting, low-carbohydrate diets, or sodium-glucose cotransporter-2 (SGLT2) inhibitor use in diabetic patients. Bariatric procedures like sleeve gastrectomy can increase the risk of EKA due to rapid metabolic shifts and reduced caloric intake. However, EKA occurring after sleeve gastrectomy in non-diabetic patients without SGLT2 inhibitor use is extremely uncommon. Its non-specific symptoms - such as shortness of breath and palpitations - can mimic more common postoperative complications, making diagnosis challenging. CASE PRESENTATION: We report a rare case of EKA in a 22-year-old non-diabetic female 1-month post-laparoscopic sleeve gastrectomy for morbid obesity. The patient presented to the emergency department with severe dyspnea, palpitations, and generalized weakness. Laboratory evaluation revealed severe metabolic acidosis (pH: 7.11, bicarbonate: 8.8 mmol/L), elevated serum creatinine (1.6 mg/dL), sodium (137 mmol/L), potassium (3.9 mmol/L), and reduced urine output. Suspected complications such as an anastomotic leak and pulmonary embolism were ruled out via abdominopelvic and pulmonary computed tomography scans, with normal D-dimer levels further supporting the exclusion of pulmonary embolism. Within 6 hours, the patient's condition deteriorated, necessitating hemodialysis for acute kidney injury. Urinalysis confirmed significant ketonuria, and arterial blood gas analysis revealed a high anion gap metabolic acidosis (24 mmol/L), leading to a diagnosis of EKA. Treatment with intravenous insulin, dextrose-containing fluids, and electrolyte correction resulted in complete recovery within 72 hours. This case highlights EKA as a rare but serious complication of sleeve gastrectomy, even in non-diabetic patients without SGLT2 inhibitor use, emphasizing the need for heightened clinical suspicion. CLINICAL DISCUSSION: The pathophysiology of EKA in bariatric surgery patients involves reduced carbohydrate availability, increased lipolysis, and ketone production. Sleeve gastrectomy significantly reduces gastric capacity, leading to restricted caloric and carbohydrate intake, which can decrease hepatic glucose production (gluconeogenesis) and drive the body toward ketogenesis. Additionally, surgical stress and postoperative hormonal changes, such as elevated cortisol and catecholamine levels, may exacerbate lipolysis. In the present case, the absence of diabetes or SGLT2 inhibitor use made EKA an unexpected diagnosis, as these are common triggers for EKA. Reduced caloric intake, potential dehydration, and postoperative physiological stress likely contributed to EKA. The patient's symptoms of dyspnea and palpitations initially suggested common postoperative complications, such as an anastomotic leak or pulmonary embolism. Patient education on maintaining adequate caloric intake and hydration post-surgery is critical to prevent EKA. CONCLUSION: This case illustrates a rare presentation of euglycemic ketoacidosis in a non-diabetic patient following sleeve gastrectomy, highlighting the diagnostic challenges due to nonspecific symptoms and normal glucose levels. Clinicians should consider EKA in the differential diagnosis of patients presenting with dyspnea, palpitations, or metabolic acidosis post-bariatric surgery, even in the absence of diabetes or SGLT2 inhibitor use.