The corrected sodium value represents your estimated true serum sodium concentration after accounting for the dilutional effect of hyperglycemia. If the corrected sodium is within the normal range (135-145 mEq/L), the apparent hyponatremia on the lab report is likely due entirely to the glucose-driven water shift, and the patient's actual sodium balance is normal. Treatment should focus on managing the hyperglycemia, and sodium is expected to normalize as glucose is corrected.

If the corrected sodium is elevated (above 145 mEq/L), this indicates concurrent hypernatremia masked by the dilutional effect of high glucose. This finding is common in hyperosmolar hyperglycemic state (HHS) and indicates significant free water deficit requiring careful fluid replacement. These patients are at higher risk of neurological complications.

If the corrected sodium remains low (below 135 mEq/L) despite correction, this suggests true hyponatremia coexisting with the hyperglycemia, which may require additional workup for causes such as SIADH, adrenal insufficiency, or excessive hypotonic fluid administration. Monitoring the corrected sodium trend during treatment is essential — sodium should rise as glucose falls, and a sodium that fails to rise appropriately may indicate excessive free water administration.

This calculator should be used whenever a serum sodium level is being evaluated in the setting of hyperglycemia, particularly when the glucose is above 200 mg/dL. It is most critical in the management of diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS), where glucose levels can exceed 600-1000 mg/dL and the dilutional effect on sodium is substantial.

The corrected sodium should also be calculated when making fluid management decisions in hyperglycemic patients, as the choice between isotonic and hypotonic fluids depends on the true sodium status. Monitoring the corrected sodium during insulin and fluid therapy helps guide the rate of glucose correction and prevents overly rapid changes in serum osmolality, which can cause cerebral edema.

The standard correction factor of 1.6 mEq/L per 100 mg/dL glucose above 100 is an approximation derived from theoretical calculations and may not be accurate for all patients. Some evidence suggests that a correction factor of 2.4 mEq/L is more appropriate when glucose levels exceed 400 mg/dL, though this remains debated. The true relationship between glucose and sodium may not be perfectly linear.

This formula assumes that hyperglycemia is the sole cause of the osmotic water shift. Other causes of pseudohyponatremia (such as severe hyperlipidemia or hyperproteinemia) are not accounted for and would require separate evaluation. The formula also does not account for concurrent sodium losses from osmotic diuresis, vomiting, or other mechanisms commonly present in diabetic emergencies.

The corrected sodium is an estimate and should be used to guide clinical decision-making rather than as a precise measurement. Serial monitoring of both measured sodium and glucose, along with clinical assessment of volume status, remains essential for safe management of hyperglycemic emergencies.