11/13/2025
November is National Diabetes Awareness Month
DKA Awareness
Insulin deficiency—often brought on by missed doses, infection, or other stressors—leads to unchecked hepatic (liver) gluconeogenesis and glycogenolysis, causing significant hyperglycemia. Simultaneously, the lack of insulin and excess of counterregulatory hormones (glucagon, cortisol, growth hormone, catecholamines) stimulate lipolysis (fat breakdown) increasing free fatty acids delivered to the liver, where they are converted to ketone bodies (acetoacetate, β-hydroxybutyrate). The accumulation of these organic acids produces a high anion gap metabolic acidosis.
Also, an osmotic (water) diuresis from hyperglycemia leads to severe dehydration and loss of sodium, potassium, and other important electrolytes. Potassium may be depleted overall, even if serum levels are normal or elevated due to acidosis and insulin deficiency shifting potassium extracellularly from inside cells, where most of our potassium resides. Volume depletion further impairs renal clearance of glucose and ketones, aggravating acidosis and hyperosmolarity (lower water content in the blood).
Acid-base derangements evolve through phases: initial loss is in the form of ketone salts and bicarbonate, development of hyperchloremic (excess chloride) normal-gap acidosis, and progression to high anion gap acidosis as ketone retention (ketones are acidic) increases with worsening dehydration and reduced glomerular filtration rate (water output). During recovery, acidosis may revert to a hyperchloremic (excess chloride in the blood) pattern as ketone excretion resumes and sodium chloride (salt) is retained.
