Euglycaemic diabetic ketoacidosis in a 43-year-old woman with type 2 diabetes mellitus on SGLT-2 inhibitor (empagliflozin)

Abstract

We report a case of euglycaemic diabetic ketoacidosis (EDKA) in a 43-year-old woman with type 2 diabetes mellitus who presented to the emergency department with problems of vomiting, cough, shortness of breath and generalised weakness after following a ketogenic diet for 2 weeks. Therapy with sodium glucose transport protein-2 empagliflozin had been started 2 months prior. Initial evaluation revealed high anion gap metabolic acidosis with blood glucose level of 169 mg/dL. Treatment for EDKA with fluid resuscitation, intravenous insulin and dextrose resolved her acidosis and symptoms in less than 24 hours. Empaglifozin was discontinued on discharge. This entity represents a diagnostic challenge since the differential diagnosis is broad with a potentially misleading clinical presentation that can result in delayed diagnosis and adverse outcomes including acute kidney injury, multiple electrolyte abnormalities, cerebral oedema, acute respiratory distress syndrome, shock and death.

Postoperatory Euglycemic Diabetic Ketoacidosis: A Not So Rare Complication of Sglt2 Inhibitors

“…This situation leads to a glucagon release that causes an elevation of the glucagon to insulin ratio, increasing the gluconeogenesis, lipolysis and ketogenesis [3]. This mechanism can be exacerbated because of the dehydration caused by the natriuretic and osmotic effect on glucose and sodium cotransporter that SGLT2 has, which leads to a secondary osmotic effect on reabsorption of water [8].…”

“…The process by which can produce EDKA is not other than the main mechanism of action of the drug: to enhance excretion and block reabsorption of glucose in the proximal convoluted tubule, leading to a loss of urinary glucose which develops a state of carbohydrate starvation and boosting a glucagon/insulin ratio disbalance. Additionally, it has been found that SGLT2 inhibitors can also stimulate the release of glucagon from the pancreas, worsening the dysregulation above mentioned by maintaining euglycemia [8].…”