## Pseudohyponatremia in DKA **Key Point:** Serum sodium is LOW in DKA despite total body sodium depletion. This apparent paradox is explained by osmotic shifts, not by sodium gain. ### Mechanism of Hyponatremia in DKA **High-Yield:** Hyperglycemia (often >250 mg/dL) creates an osmotic gradient that pulls water from the intracellular compartment into the extracellular space. This dilutes the extracellular sodium concentration, causing **pseudohyponatremia** or **osmotic hyponatremia**. 1. Hyperglycemia increases serum osmolality 2. Water follows osmotic gradient from ICF → ECF 3. ECF volume expands, but sodium concentration is diluted 4. Measured serum Na^+^ falls (typically 125–135 mEq/L) 5. **Corrected sodium** = measured Na^+^ + (glucose − 100)/18 ### Clinical Pearl For every 100 mg/dL rise in glucose above 100, serum sodium drops by approximately **1.6 mEq/L** due to osmotic dilution. This is **not a true sodium deficit** in the sense of total body depletion—it is a concentration effect. ### Key Distinction - **Total body sodium:** Depleted (due to osmotic diuresis and vomiting) - **Serum sodium concentration:** Low (due to osmotic dilution by hyperglycemia) - **Corrected sodium:** Often normal or high when adjusted for glucose **Warning:** Overcorrecting hyponatremia in DKA by giving hypertonic saline can cause hypernatremia and worsening cerebral edema. Treatment is insulin (which lowers glucose and allows water to re-enter cells) plus fluid replacement. [cite:Harrison 21e Ch 397]
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