Printed on 3/17/2026
For informational purposes only. This is not medical advice.
When blood glucose is elevated, water shifts from the intracellular to the extracellular space, diluting serum sodium and producing a 'pseudohyponatremia.' The corrected sodium formula estimates what the sodium would be if the glucose were normal. The most commonly used correction adds 1.6 mEq/L to the measured sodium for every 100 mg/dL increase in glucose above 100 mg/dL (Katz, 1973). This calculation is a staple of ER, ICU, and endocrinology practice, particularly in DKA and HHS management.
Formula: Corrected Na = Measured Na + 1.6 × ((Glucose − 100) / 100)
When blood glucose is elevated, glucose is an osmotically active solute that cannot freely cross cell membranes. This creates an osmotic gradient that draws water from inside cells (intracellular fluid) into the bloodstream (extracellular fluid). The additional water dilutes the sodium concentration in the blood, making the measured sodium appear falsely low. This is pseudohyponatremia — the total body sodium content is normal, but it's diluted by the glucose-driven water shift. Correcting for this effect reveals the patient's true sodium status.
The standard correction adds 1.6 mEq/L to the measured sodium for every 100 mg/dL increase in glucose above 100 mg/dL. Formula: Corrected Na = Measured Na + 1.6 × ((Glucose − 100) / 100). For example, if measured sodium is 128 mEq/L and glucose is 500 mg/dL: Corrected Na = 128 + 1.6 × ((500 − 100) / 100) = 128 + 1.6 × 4 = 128 + 6.4 = 134.4 mEq/L. This corrected value (134.4) represents the patient's actual sodium status. Some sources suggest using a factor of 2.4 instead of 1.6 for glucose >400 mg/dL, but 1.6 remains the standard.
If corrected sodium is normal (135-145 mEq/L), the apparent hyponatremia is entirely due to glucose dilution. Treat the hyperglycemia with insulin and isotonic saline — sodium will normalize as glucose falls. If corrected sodium is high (>145 mEq/L), the patient has true hypernatremia masked by glucose dilution, indicating significant free water deficit (common in HHS). Use hypotonic fluids cautiously and monitor closely. If corrected sodium is low (<135 mEq/L), true hyponatremia coexists with hyperglycemia. Investigate other causes (SIADH, adrenal insufficiency, excessive hypotonic fluids).
Emergency physicians, endocrinologists, intensivists
A patient with DKA presents with glucose 550 mg/dL and measured sodium 130 mEq/L. Corrected sodium is 130 + 1.6 × ((550 − 100) / 100) = 130 + 7.2 = 137.2 mEq/L (normal). The apparent hyponatremia is entirely from glucose dilution. Treatment: isotonic saline (0.9% NaCl) initially for volume resuscitation, then insulin to lower glucose. As glucose falls, measured sodium should rise toward 137 mEq/L. If sodium doesn't rise appropriately, suspect excessive free water administration or concurrent SIADH. Corrected sodium guides fluid choice and prevents cerebral edema. Also [calculate anion gap](/tools/anion-gap) to confirm DKA diagnosis.
Emergency physicians, intensivists, endocrinologists
An elderly patient with altered mental status has glucose 1100 mg/dL and measured sodium 132 mEq/L. Corrected sodium is 132 + 1.6 × ((1100 − 100) / 100) = 132 + 16 = 148 mEq/L (elevated). This reveals severe hypernatremia masked by glucose dilution, indicating profound free water deficit (often 8-10 liters). These patients require careful rehydration with hypotonic fluids (0.45% NaCl) after initial isotonic resuscitation. Monitor corrected sodium closely — too-rapid correction as glucose falls can cause cerebral edema. HHS mortality is ~15%, partly from osmotic complications.
Emergency physicians, hospitalists
A patient with known diabetes arrives with nausea, vomiting, and glucose 420 mg/dL. Labs show sodium 133 mEq/L. Corrected sodium is 133 + 1.6 × ((420 − 100) / 100) = 133 + 5.1 = 138.1 mEq/L (normal). The patient's sodium status is normal despite the low measured value. Start isotonic saline and insulin. If measured sodium had been reported without correction, you might have been misled into thinking hyponatremia was present, potentially affecting fluid management decisions. Always correct sodium when glucose is elevated.
Intensivists, critical care nurses
A mechanically ventilated patient with sepsis and stress hyperglycemia has glucose 350 mg/dL and sodium 136 mEq/L. Corrected sodium is 136 + 1.6 × ((350 − 100) / 100) = 136 + 4 = 140 mEq/L (high-normal). While measured sodium looks fine, corrected sodium is trending high, suggesting evolving free water deficit from osmotic diuresis and insensible losses. Consider reducing isotonic fluid rate and adding free water via enteral route or switching to 0.45% NaCl. Serial corrected sodium calculations detect subtle volume status changes before they become clinically significant.
Endocrinologists, hospitalists
A patient with small cell lung cancer and known SIADH develops hyperglycemia (glucose 380 mg/dL, sodium 120 mEq/L). Corrected sodium is 120 + 1.6 × ((380 − 100) / 100) = 120 + 4.5 = 124.5 mEq/L (still low). Even after correction, significant hyponatremia persists, confirming that SIADH is present independent of glucose effects. Treatment requires both glucose management (insulin) and hyponatremia management (fluid restriction, hypertonic saline if symptomatic). The correction distinguishes true hyponatremia from pseudohyponatremia.
Pediatric emergency physicians, pediatric intensivists
A child with DKA has glucose 650 mg/dL and measured sodium 127 mEq/L. Corrected sodium is 127 + 1.6 × ((650 − 100) / 100) = 127 + 8.8 = 135.8 mEq/L (normal). During treatment, measured sodium should rise as glucose falls (~1-2 mEq/L per 100 mg/dL glucose drop). If measured sodium fails to rise or falls, suspect excessive hypotonic fluid administration, increasing cerebral edema risk. Monitoring corrected sodium trend is critical in pediatric DKA, where cerebral edema is a major cause of morbidity and mortality (~1% incidence, 20-40% mortality when it occurs).
The dilutional effect becomes clinically significant when glucose exceeds 200 mg/dL. At glucose 400 mg/dL, sodium is diluted by approximately 5 mEq/L. At 800 mg/dL, ~11 mEq/L. Don't rely on measured sodium alone in hyperglycemic patients — always calculate and trend the corrected value.
In DKA/HHS, expect measured sodium to increase by approximately 1-2 mEq/L for every 100 mg/dL decrease in glucose. If sodium doesn't rise appropriately, you're giving too much free water (switch to isotonic fluids). If sodium rises too quickly, consider adding hypotonic fluids. Serial measurements (every 2-4 hours) guide fluid management.
If corrected sodium is normal or low: start with isotonic saline (0.9% NaCl) for volume resuscitation. If corrected sodium is high (>145 mEq/L): after initial isotonic bolus for perfusion, switch to hypotonic fluids (0.45% NaCl) to address free water deficit. Never use hypotonic fluids in a volume-depleted patient — always resuscitate with isotonic first.
HHS patients with corrected sodium >150 mEq/L have higher mortality and greater risk of neurological complications. These patients have severe hyperosmolality (often >350 mOsm/kg) and require meticulous fluid management. Aim to reduce serum osmolality gradually — no more than 3-8 mOsm/kg/hr to minimize cerebral edema risk.
Some evidence suggests that when glucose exceeds 400 mg/dL, a correction factor of 2.4 mEq/L per 100 mg/dL is more accurate than 1.6. However, 1.6 remains the standard used in most protocols. Be aware of this debate when glucose is extremely elevated (>800 mg/dL) — the corrected sodium may be slightly underestimated with the 1.6 factor.
If measured sodium stays flat or falls as glucose improves, the patient is receiving too much free water. Common sources: D5W, 0.45% NaCl, excessive oral intake, hypotonic tube feeds. Switch to isotonic fluids. In DKA, this is a key warning sign of impending cerebral edema, especially in children.
In HHS, measured sodium of 135 mEq/L might seem reassuring, but with glucose 1000 mg/dL, corrected sodium is 135 + 14.4 = 149.4 mEq/L (severe hypernatremia). These patients need aggressive free water replacement. Don't be fooled by a normal measured sodium in severe hyperglycemia.
Insulin lowers glucose, which reverses the osmotic water shift. Water moves back into cells, concentrating sodium. If you're giving hypotonic fluids simultaneously, you can cause rapid sodium changes. Recheck labs every 2-4 hours during acute treatment and adjust fluid composition based on trends.
The correction formula only accounts for dilutional pseudohyponatremia. It doesn't account for actual sodium losses from osmotic diuresis (common in hyperglycemia as kidneys excrete glucose and sodium together). If corrected sodium is rising less than expected or is declining, consider that sodium is being lost in urine and may need replacement.
Calculate effective osmolality: 2 × Na + Glucose/18. Normal is 285-295 mOsm/kg. In DKA, osmolality is mildly elevated (295-320). In HHS, it's markedly elevated (>320, often >350). High osmolality with high corrected sodium confirms severe hyperosmolar state requiring cautious rehydration. Use both metrics together.
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.
For related assessments, see Anion Gap and Corrected Calcium.
Disclaimer: This tool is for educational and informational purposes only. It is not a substitute for professional medical advice, diagnosis, or treatment. Always consult a qualified healthcare provider with questions about your health.
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