DKA

Diabetic ketoacidosis (DKA) results from absolute or relative insulin deficiency combined with counter-regulatory hormone excess (glucagon, cortisol, catecholamines, GH). Without insulin, glucose cannot enter cells, triggering hepatic gluconeogenesis and glycogenolysis (causing severe hyperglycemia) and unregulated lipolysis (releasing free fatty acids from adipose tissue). In the liver, fatty acids undergo beta-oxidation to acetyl-CoA, which is converted to ketone bodies (acetoacetate, beta-hydroxybutyrate, acetone) by ketogenesis — a process driven by glucagon excess and insulin deficiency. Ketone bodies are strong organic acids that consume bicarbonate buffers, causing high anion gap metabolic acidosis (AG = Na - Cl - HCO3; normal 8-12; DKA typically > 20). Hyperglycemia causes osmotic diuresis (glycosuria pulls water and electrolytes), leading to profound dehydration (average 5-9 L deficit), total body potassium depletion (despite possible initial hyperkalemia from transcellular shift due to acidosis and insulin deficiency), and electrolyte derangement. Cerebral edema is the most feared complication in children, occurring in 0.5-1% of pediatric DKA cases.