Paediatric DKA Cerebral Edema

Diabetic ketoacidosis (DKA) begins with too little effective insulin. Without insulin, glucose cannot be used normally by insulin-dependent tissues, while glucagon, catecholamines, cortisol, and growth hormone drive hepatic glucose release. Hyperglycemia pulls water into the urine, causing osmotic diuresis, sodium and water losses, and progressive intravascular depletion. At the same time, unrestrained lipolysis produces beta-hydroxybutyrate and acetoacetate. These ketoacids consume bicarbonate and create a high-anion-gap metabolic acidosis. The child breathes deeply and rapidly to lower carbon dioxide and partially compensate for the acid load; this is Kussmaul respirations, not simply anxiety. Potassium is a dangerous paradox in DKA. Acidosis and insulin deficiency shift potassium out of cells, so the initial serum potassium may be normal or elevated. Yet urinary losses have depleted total-body potassium. Once insulin and fluids are started, potassium moves back into cells and the serum value can fall quickly enough to cause weakness, dysrhythmia, or cardiac arrest. Cerebral injury, often called cerebral edema, is the most feared complication of paediatric DKA. It is uncommon, affecting roughly 0.3% to 1% of episodes, but it causes substantial death and...