Diabetic ketoacidosis (DKA) is a life-threatening metabolic emergency caused by absolute or relative insulin deficiency combined with counter-regulatory hormone excess (glucagon, cortisol, catecholamines, growth hormone). Without insulin, glucose cannot enter cells despite hyperglycemia, creating intracellular energy starvation. The liver responds by increasing gluconeogenesis and glycogenolysis, worsening hyperglycemia. Simultaneously, uninhibited lipolysis in adipose tissue releases massive quantities of free fatty acids (FFAs) to the liver, where they undergo beta-oxidation to acetyl-CoA. When acetyl-CoA production exceeds the capacity of the citric acid cycle, the excess is diverted to ketogenesis, producing acetoacetate, beta-hydroxybutyrate, and acetone. These ketone bodies are strong organic acids that overwhelm the bicarbonate buffering system, causing high-anion-gap metabolic acidosis. The resulting hyperglycemia causes osmotic diuresis with massive fluid loss (average 5-7 liters in adults), electrolyte depletion (potassium, sodium, phosphate, magnesium), and hyperosmolarity. Total body potassium is always depleted even when serum K+ appears normal or elevated—because acidosis shifts potassium extracellularly. When insulin is given, potassium shifts back intracellularly, and potentially fatal hypokalemia can occur.