A 17-year-old girl admitted with diabetic ketoacidosis has a serum potassium of 5.4 mEq/L. After 6 hours of insulin infusion and fluids her potassium falls to 3.0 mEq/L. The initial hyperkalaemia despite a large total body potassium deficit is best explained by:

• A Haemoconcentration artefactually elevating the measured serum value
• B Excessive oral potassium intake before admission masking the deficit
• C Reduced renal potassium excretion caused by volume depletion
• D Extracellular shift of potassium driven by acidosis and insulin deficiency ✓

Explanation

Insulin stimulates Na-K ATPase and drives potassium into cells, while hydrogen ion excess promotes K-H exchange across cell membranes. Insulin lack plus acidosis therefore shifts potassium out of cells, raising the serum level even though total body stores are severely depleted. Once insulin is given, uptake resumes and the true deficit emerges as hypokalaemia, which is why replacement begins once urine output is confirmed. Haemoconcentration contributes marginally but is not the dominant mechanism.

Reference: Williams Textbook of Endocrinology, 14th ed.

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Written and medically reviewed by the StethoPrep medical team.