Hypokalemia is a common observation in diabetic ketoacidosis (DKA) and it is usually associated with insulin deficiency. At first, it hinders the inflow of serum potassium (SK) from extra- to intracellular compartments, which triggers hyperkalemia. In the course of progressive DKA, hyperglycemia and ketosis-induced osmotic diuresis increases potassium excretion, contributing to potassium depletion in intracellular compartments. Insulin deficiency–mediated increased catecholamine levels have a relative effect on potassium concentration via β-adrenoceptors. Moreover, potassium loss is increased, as the degree of acidosis worsens. Acidosis has also been associated with changes on electrocardiography similar to those typical of hypokalemia. However, despite a significant potassium loss, patients with DKA present with various degrees of potassium disturbance on admission, which range from normal kalemia to hyperkalemia.