The mechanisms and management strategies for diabetic ketoacidosis are discussed elsewhere, as one of the scenarios in critical care endocrinology.

Rather than get bogged down in thick endocrinology (thereby duplicating content from the Endocrinology section) I offer this brief summary, aimed at answering the short ABG interpretation questions rather than the long "how'd you manage this ketoacidosis" or "critically evaluate something" questions. 

Ketoacidosis-asociated ABG interpretation questions include the following:

Just like in real life, the ketoacidosis in these questions if often paired with some sort of hyperglycaemic hyperosmolar state. Calculation of corrected sodium is occasionally called for.

A brief summary of different ketoacidosis subvarieties follows:

The Varieties of Ketoacidosis
  Starvation ketoacidosis Alcoholic ketoacidosis Diabetic ketoacidosis
  • Prolonged starvation: ~3 days
  • Starvation following a binge
  • Inadequate insulin supplementation in the face of increased requirements. eg. sepsis
  • Diminished intake of carbohydrates leads to decreased insulin levels, and thus ketogenesis
  • Ketogenesis occurs in the absence of adequate hepatic glycogen stores
  • Diminished intake of carbohydrates leads to decreased insulin levels, and thus ketogenesis
  • Hepatic metabolism of ethanol depletes NAD+ and increases NADH levels, favouring conversion of acetoacetate into β-hydroxybutyrate
  • In the absence of insulin, and the presence of stress hormones and glucagin, hepatic lipid metabolism switches to ketogenesis
Characteristic features
  • mild acidosis
  • Low ketone levels
  • Anion gap may be normal
  • BSL is frequently low
  • Patient is neither a diabetic nor an alcoholic
  • moderate acidosis
  • β-hydroxybutyrate is the most prevalent ketone species
  • BSL is frequently low
  • Severe acidosis
  • May be mixed high and normal anion gap (ketones are excreted along with strong cations; SID decreases as a result)
  • Severe dehydration
  • Recommencement of nutrition results in a release of insulin
  • Refeeding syndrome may occur
  • Recommencement of nutrition results in a release of insulin
  • Severe acidosis - usually requires insulin/dextrose infusion
  • Refeeding syndrome may occur
  • Insulin/dextrose infusion
  • Volume replacement:
    • Water deficit: 100ml/kg
  • Electrolyte replacement:
    • Na+: 7-10mmol/kg
    • K+ deficit: 3-5mmol/kg
    • Cl- deficit: 3-5mmol/kg
    • PO4 deficit: 1-1.5mmol/kg
    • Mg2+ deficit: 1-1.5mmol/Kg
    • Ca2+ deficit: 1-2mmol/Kg

Points to note:

  • Starvation ketoacidosis typically is not especially acidotic, and with lowish ketone levels
  • β-hydroxybutyrate is the prevalent ketone in ketoacidosis; the normal ratio of beta-hydroxybutyrate and acetoacetate is 3:1, and it can rise to 10:1 in diabetic ketoacidosis. Acetone is the least abundant.
  • In alcoholic ketoacidosis, β-hydroxybutyrate is even more prevalent
  • Urine dipstick ketone tests rely on the reaction between acetoacetate or acetone and sodium nitroprusside; this means beta-hydroxybutyrate will not be detected.
  • Conversely, the point-of-care capillary fingerprick ketones test detects only beta-hydroxybutyrate.


UpToDate has a nice summary of this topic for the paying customer.

Oh's Intensive Care manual: Chapter 58  (pp. 629) Diabetic  emergencies  by Richard  Keays

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Basnet, Sangita, et al. "Effect of Normal Saline and Half Normal Saline on Serum Electrolytes During Recovery Phase of Diabetic Ketoacidosis." Journal of intensive care medicine 29.1 (2014): 38-42.

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