• 🍒Hyperosmolar hyperglycaemia is under-recognised and has a higher mortality rate than DKA
• Pathophysiology
  • Hyperglycaemia osmotically pulls water from the cells
  • Kidney excretes glucose at extremes of hyperglycaemia which osmotically pulls water into the urine ⇒ water loss (osmotic diuresis)
  • Water loss ⇒ concentration of solutes increases → hyperosmolarity
  • Presence of insulin inhibits ketogenesis resulting in limited metabolic acidosis
• Clinical presentation
  • Hyperglycaemia
  • Fatigue + weight loss
  • Thirst + frequent urination
  • Signs of dehydration: hypotension with reflex tachycardia
  • Confusion and altered mental status
• Management
  • IV rehydration
    • Intravenous potassium replacement can be started when the serum potassium concentration is less than 5 mmol/L
      • The goal is to maintain serum potassium concentrations between 3.5 and 4.5 mmol/L
  • IV insulin
    • An intravenous insulin infusion is not started until the blood glucose concentrations stop falling after initial fluid replacement
    • An intravenous insulin infusion should be given slowly (0.05 units/kg/hour) using short-acting insulin
    • Blood glucose concentration should be lowered at a rate between 4 to 6 mmol/L per hour; a reasonable target is 10 to 15 mmol/L
  • Rapid change in serum osmolality must be avoided
  • 🍒What is the management of hyperosmolar hyperglycaemic non-ketotic state?
  • 🍒Patients with hyperosmolar hyperglycaemia have a very high risk of developing arterial and venous thrombosis::vascular complication