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PH-EN03

Diabetic ketoacidosis

How insulin deficiency and stress hormones release fatty acids that the liver turns into ketoacids, causing a raised anion gap metabolic acidosis, severe dehydration and dangerous shifts in potassium.

By the end, you can

  • Explain how insulin deficiency and raised counter-regulatory hormones switch metabolism to fat breakdown and ketone production.
  • Describe hepatic ketogenesis and why ketoacids cause a metabolic acidosis with a raised anion gap.
  • Explain how osmotic diuresis and vomiting cause dehydration and electrolyte loss.
  • Explain why serum potassium may be normal or high despite a large total-body deficit.
  • Relate the mechanism to Kussmaul breathing, abdominal pain and reduced consciousness.
  • Recognise the diagnostic criteria, severity and key numbers of DKA, tell it apart from the hyperosmolar state and other ketoacidoses, and explain how fluids, insulin, glucose and potassium act on the mechanism.

What it is

Diabetic ketoacidosis (DKA) is an acute, life-threatening complication of diabetes in which severe insulin deficiency, with raised counter-regulatory hormones, causes ketonaemia (raised blood ketones), a metabolic acidosis with a raised anion gap and, usually, hyperglycaemia with dehydration. It is most common in type 1 diabetes, at diagnosis or with illness or missed insulin, but it can occur in type 2 diabetes.

3 types to tell apart
Typical DKA
Marked hyperglycaemia with ketoacidosis and dehydration.
Euglycaemic DKA
Ketoacidosis with near-normal glucose, for example with SGLT2-inhibitor medicines, in pregnancy or after prolonged starvation: glucose is lost in the urine or made less, while ketone production continues.
Hyperosmolar hyperglycaemic state (contrast)
Not DKA: very high glucose and osmolality with little ketosis, mainly in type 2 diabetes, because residual insulin restrains ketone production. Mixed pictures occur.

US spelling: ketonaemia → ketonemia, hyperglycaemia → hyperglycemia.

Normal function

Fasting fuel: a little ketone, kept in check

Between meals, falling insulin and rising glucagon let fat cells release fatty acids, which most tissues burn directly. The takes up fatty acids too and breaks them down in its mitochondria to acetyl-CoA. When acetyl-CoA is plentiful, the liver joins it into the ketone bodies acetoacetate and beta-hydroxybutyrate; acetone forms from acetoacetate on its own.

Ketones are a useful fuel for the heart, muscle and, in prolonged fasting, the brain; the liver cannot use them itself. In health, insulin is never fully absent, even in a long fast. It restrains fatty-acid release and ketone production, so blood ketones stay low.

Ketone bodies are acids. Blood pH is held at 7.35–7.45, mainly by the bicarbonate buffer, with the lungs adjusting carbon dioxide and the kidneys excreting acid and reclaiming bicarbonate.

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