A 60-year-old woman is transferred from an outpatient surgery facility to the emergency department due to diffuse abdominal pain, nausea, and vomiting. She developed these symptoms while waiting to be discharged following a routine colonoscopy. The patient has type 2 diabetes mellitus, which is managed with sitagliptin, canagliflozin, and insulin detemir; the insulin was held the night before the procedure. She was previously treated with metformin but was switched to canagliflozin due to persistent diarrhea. Since that time, the patient has had significant weight loss and an improvement in blood glucose levels. Other medical issues include hypertension and hyperlipidemia, for which she takes losartan, hydrochlorothiazide, and atorvastatin. Blood pressure is 110/70 mm Hg, pulse is 100/min, respirations are 24/min, and oxygen saturation is 99% on room air. BMI is 34 kg/m². Oral mucous membranes are dry, but the remainder of the physical examination is unremarkable. Laboratory results are as follows: Which of the following is the most likely cause of this patient's laboratory findings?

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Explanation: 11ec2b69_beb1_8cbd_8f63_f73a02d3eef5_MD0005_00 This patient has acute anion gap metabolic acidosis associated with abdominal pain, nausea, and vomiting. In light of the positive urine ketone screen, this most likely represents euglycemic diabetic ketoacidosis (euDKA), a recognized complication of sodium-glucose cotransporter-2 (SGLT2) inhibitor (eg, canagliflozin) therapy. SGLT2 inhibitors lower blood glucose by reducing reabsorption of glucose in the kidney, which leads to a low insulin-to-glucagon ratio because high blood glucose levels are the primary stimulus for insulin release. euDKA in patients taking SGLT2 inhibitors can be triggered by prolonged fasting, major illness, intense exercise, excessive alcohol intake, or an abrupt reduction in concurrent insulin dose. These conditions further lower the insulin-to-glucagon ratio and exacerbate relative insulin deficiency to the point of stimulating ketogenesis. In contrast to typical DKA, which is associated with very high glucose levels, blood glucose in SGLT2-associated euDKA is usually <250 mg/dL due to the increased excretion of glucose in the urine. Management includes aggressive hydration, discontinuation of the drug, and control of blood glucose with insulin. (Choice A) The primary acid-base disorder in hyperventilation is respiratory alkalosis. This patient has metabolic acidosis, and the tachypnea is due to the resulting respiratory compensation. (Choice C) Lactic acidosis is a potential complication of metformin therapy, particularly in patients with underlying renal insufficiency. This patient's creatinine is normal, and her metformin has been discontinued. She also does not appear to have significant hypotension that could lead to tissue hypoperfusion. (Choice D) Renal tubular acidosis causes non-anion gap acidosis. The anion gap [sodium − (chloride + bicarbonate)] in this patient is 20 mEq/L (normal: 10-14). (Choice E) Vomiting is a common manifestation of ketoacidosis. The primary acid-base abnormality associated with vomiting is metabolic alkalosis. Educational objective: Patients treated with sodium-glucose cotransporter-2 inhibitors can develop diabetic ketoacidosis with normal or only minimally elevated blood glucose levels. Manifestations may include abdominal pain, nausea, vomiting, tachypnea, and metabolic acidosis. References: SGLT2 inhibitor-associated diabetic ketoacidosis: clinical review and recommendations for prevention and diagnosis. (http://www.ncbi.nlm.nih.gov/pubmed/28003053)

A 60-Year-Old Woman Is Transferred from an Outpatient Surgery Facility