Diabetic ketoacidosis (DKA) is a serious complication of diabetes mellitus, and consists of the biochemical triad of ketosis, hyperglycaemia and acidaemia. DKA usually occurs as a result of an absolute or relative insulin deficiency and an increase in counter-regulatory hormones, such as glucagon, cortisol, growth hormone and catecholamines. This hormone imbalance enhances glycogenolysis and gluconeogenesis, resulting in hyperglycaemia. Increased lipolysis increases free fatty acid levels, which are metabolised to ketones as an alternative energy source. This results in the accumulation of ketone bodies (acetoacetate (AcAc), β-hydroxybutyrate (β-OHB) and acetone) and a consequent metabolic acidosis. Acetone is formed by spontaneous decarboxylation of AcAc and is excreted by the lungs, and is responsible for the sweet odour on the breath of DKA patients. β-OHB is the dominant ketone in DKA.

β-Hydroxybutyrate at the Bedside

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