Epidemiology

4.5 to 8 episodes per 1,000 patients with diabetes

Mortality has fallen in last 20 years from 7.96% to 0.67%

Pathophysiology

Ketones are made by the liver, by conversion of fatty acids as a fuel source when glucose and glycogen stores are exhausted. in normal patients they are buffered so the blood does not become acidotic, in T1DM this can cause a state of extreme hyperglycaemic ketosis resulting in metabolic acidosis that is life threatening - this is DKA.

When does it happen - where a person who has T1DM is not producing enough insulin, not injecting themselves and thus can't process glucose and use it in cells for energy. the main problems are:

• Ketoacidosis - cells have no fuel, ketone levels continue to rise, initially bicarbonate levels counteract the acidity in the blood but over time the ketone acids use up the bicarbonate and the blood start to become acidic

Main ketone bodies produces are acetate, acetoacetate (this is smelt in the breath) and 3-beta-hydroxybutyrate (what we measure for)

• Dehydration - Due to hyperglycamia overwhelming the kidneys causing osmotic diuresis = polyuria and polydipsia (polyuria stimulates thirst centres)
• Potassium Imbalance - No insulin to drive into cells, and hydrogen ions complete with K to enter cells. Serum K is high/normal but total body K levels are low as no K is stored in cells so patient can develop severe hypokalaemia quickly and can lead to arrhythmias.

The most important biochemical abnormality in DKA is not the hyperglycaemia but the uncontrolled lipolysis in adipose tissue and uncontrolled ketogenesis in the liver

Precipitating factors

• Inadequate insulin treatment or non-compliance
• New onset diabetes (20-25%)
• Acute illness (30-40%) - infection (patient may ba apyretic), MI, CVA, acute pancreatitis
• Drugs - Olanzapine, Cocaine, Lithium, SGLT2 inhibitors

PC: