In DKA, describe the relationship between serum potassium, total body potassium status, and insulin therapy.

• A. Serum potassium is always low; total body potassium is high; insulin raises potassium.
• B. Serum potassium may be high or normal due to acidosis; total body potassium is depleted; insulin drives potassium into cells, risking hypokalemia; monitor and replace.
• C. Both serum and total body potassium are depleted; insulin has no effect on potassium.
• D. Serum potassium is high; total body potassium is high; insulin decreases potassium.

Answer: (B)

In DKA, the potassium story is paradoxical: the total body potassium is usually depleted, even though the serum potassium can be normal or elevated. The body loses potassium in urine during osmotic diuresis, and acidosis plus lack of insulin push potassium out of cells, elevating or normalizing the extracellular (serum) level. When insulin therapy starts, potassium shifts back into cells as insulin activates the sodium–potassium pump, which can cause the serum potassium to fall rapidly—potentially producing dangerous hypokalemia if not watched and corrected. Because of this, potassium management is a central part of treating DKA: measure baseline potassium, and replace it as needed during insulin therapy. If the serum potassium is low (below about 3.3 mEq/L), insulin is held until potassium is corrected; if it’s in the normal to high range (roughly 3.3–5.2 mEq/L), insulin is started with potassium supplementation so that serum potassium is kept in a safe range (around 4–5 mEq/L). The key idea is that while total potassium is depleted, insulin therapy can lower serum potassium, so careful monitoring and proactive replacement are essential.