Expansion
Insulin deficiency with counter-regulatory excess causes hyperglycaemia and ketogenesis
Expansion
Mechanism
- Insulin deficiency plus excess glucagon, catecholamines, cortisol and growth hormone
- Hyperglycaemia from gluconeogenesis, glycogenolysis and reduced uptake
- Unrestrained lipolysis releases free fatty acids, which the liver converts to ketone bodies: acetoacetate, beta-hydroxybutyrate and acetone
- High anion gap metabolic acidosis, with respiratory compensation (Kussmaul breathing)
- Osmotic diuresis causes profound dehydration and electrolyte loss
Potassium is the classic trap. Acidosis and insulin deficiency move potassium out of cells, so the serum level may be normal or high while total body stores are depleted by 3 to 5 mmol/kg. Giving insulin drives potassium back in and can cause dangerous hypokalaemia, so potassium must be replaced early and monitored closely.
Treatment order follows the physiology: fluid first, then insulin, then potassium, with glucose added once the level falls so that insulin can be continued to switch off ketogenesis. Bicarbonate is rarely indicated.