Diabetic Ketoacidosis (DKA)

Diabetic ketoacidosis (DKA) may be a complication of existing type 1 diabetes mellitus or be the first presentation, accounting for around 6% of cases. Rarely, under conditions of extreme stress, patients with type 2 diabetes mellitus may also develop DKA.

Whilst DKA remains a serious condition, mortality rates have decreased from 8% to under 1% in the past 20 years.

Pathophysiology

• DKA is caused by uncontrolled lipolysis (not proteolysis) which results in an excess of free fatty acids that are ultimately converted to ketone bodies
• Absolute or relative insulin deficiency, together with increased counter-regulatory hormones (especially glucagon), drives hepatic gluconeogenesis and glycogenolysis → hyperglycaemia
• Hyperglycaemia exceeds the renal threshold → glycosuria → osmotic diuresis
  • Leads to loss of water and electrolytes (including potassium), explaining the dehydration, tachycardia, and hypotension seen clinically
• Uncontrolled lipolysis releases free fatty acids → hepatic ketogenesis
  • Produces 3-beta-hydroxybutyrate, acetoacetate, and acetone (responsible for fruity breath)
• Accumulation of ketones → metabolic acidosis
  • Drives Kussmaul respiration and contributes to nausea, vomiting, and abdominal pain
• Potassium imbalance:
  • Total body potassium is depleted due to urinary losses from osmotic diuresis and vomiting
  • Serum potassium may initially be normal or raised due to acidosis and insulin deficiency shifting potassium out of cells
  • Potassium levels often fall rapidly with treatment (especially insulin), creating a risk of arrhythmias

Pathophysiology

Most Common Precipitating Factors of DKA

• Acute infection 40%
• Missed Insulin or Incompliance 25%
• Newly diagnosed DM 15%
• Others 20%

Features