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Diabetic ketoacidosis (DKA) is a serious acute complication of diabetes characterized by hyperglycemia, high anion gap metabolic acidosis, and ketonemia. It is most common in type 1 diabetes but increasingly recognized in type 2, particularly with SGLT2 inhibitor use.
Absolute or relative insulin deficiency with excess counterregulatory hormones drives unrestrained lipolysis and ketogenesis. Free fatty acids are converted to ketone bodies in the liver, consuming bicarbonate and producing a high anion gap acidosis. Hyperglycemia causes osmotic diuresis with profound volume depletion and electrolyte losses, particularly potassium.
DKA requires the triad: glucose >250, pH <7.3, and positive ketones. Management priorities: IV fluids, insulin infusion, potassium replacement (hold insulin if K <3.5), and identifying the precipitant. The anion gap and bicarbonate track resolution. Euglycemic DKA should be considered in SGLT2 inhibitor users.