Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a state of insulin deficiency with excess counterregulatory hormones—glucagon, catecholamines, cortisol, and growth hormone. It can occur with type 1 or type 2 diabetes. Infection, missed insulin, pump failure, myocardial infarction, pancreatitis, corticosteroids, pregnancy, alcohol use, and SGLT2 inhibitors are among the recognized triggers. Without enough insulin, glucose remains in the bloodstream while cells cannot use it normally. The liver responds to the hormonal signal by making and releasing still more glucose through gluconeogenesis and glycogenolysis. At the same time, fat is broken down without restraint. The liver converts free fatty acids into the ketoacids beta-hydroxybutyrate and acetoacetate. These acids consume bicarbonate and lower the blood pH. The same excess glucose draws water into the urine. This osmotic diuresis removes water, sodium, potassium, chloride, and phosphate. The patient becomes intravascularly depleted, tachycardic, hypotensive, and at risk for reduced renal perfusion. Potassium requires particular caution. DKA commonly produces a total-body potassium deficit of approximately 2–5 mmol/kg, even though the first serum potassium may be normal or high. Acidosis and insulin deficiency move potassium out of cells into...