Diabetic ketoacidosis (DKA) is a life-threatening acute metabolic complication of both diabetes mellitus type 1 and type 2 in which the reduced effective action of circulating insulin combined with upregulation of counterregulatory hormones leads to hyperglycemia and uncontrolled oxidation of fatty acids into ketone bodies. This results in hyperosmolality, dehydration, and usually a severe anion gap metabolic acidosis.

Symptoms have a rapid onset (< 24 hours) and include polyuria, polydipsia, lethargy, and abdominal pain. The hyperosmolality can cause neurologic symptoms, such as mental obtundation and coma.

Patients taking sodium-glucose cotransporter 2 (SGLT-2) inhibitors (eg, for diabetes mellitus type 2) may be at increased risk for DKA, especially euglycemic DKA. Approximately 10% of DKA occurs with euglycemia or near normoglycemia. 

The treatment of DKA includes the correction of electrolyte and fluid abnormalities along with the administration of insulin as well as reversal of the underlying stressor leading to the development of DKA. The most common precipitating factors for DKA are inadequate insulin therapy and the presence of infection. Other potential precipitants include acute coronary syndromes, medications (steroids in particular), pulmonary embolism, stroke, and alcohol use disorder.