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Printed on 6/29/2026
For informational purposes only. This is not medical advice.
Hyperglycemia causes osmotic water shift from intracellular to extracellular space, diluting serum sodium. The Katz correction (Na + 1.6 × (glucose − 100)/100) estimates the true sodium level if glucose were normal. This is essential in DKA and HHS management. For full sodium workup, calculate [Serum Osmolality Calculator](/tools/serum-osmolality) to check osmolar gap. For DKA, also calculate [Anion Gap](/tools/anion-gap) to quantify metabolic acidosis. Check ABG interpretation for acid-base context with [ABG Interpreter](/tools/abg-interpreter). Monitor renal function during DKA/HHS treatment with [eGFR Calculator](/tools/egfr-calculator).
Formula: Corrected Na = Measured Na + 1.6 × (Glucose − 100) / 100
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Glucose is an osmotically active solute that cannot freely cross most cell membranes. Elevated blood glucose creates an osmotic gradient drawing water from the intracellular space into the extracellular space (bloodstream). This water dilutes the sodium concentration, producing a factitious hyponatremia — sometimes called pseudohyponatremia or dilutional hyponatremia from hyperglycemia. The true total body sodium content is unchanged; it is simply diluted by the glucose-driven water shift.
Corrected Na = Measured Na + 1.6 × (Glucose - 100) / 100. For each 100 mg/dL elevation in glucose above 100 mg/dL, add 1.6 mEq/L to the measured sodium. Example: measured Na 128 mEq/L, glucose 500 mg/dL — Corrected Na = 128 + 1.6 × (500 - 100)/100 = 128 + 6.4 = 134.4 mEq/L. Note: some authorities (Hillier et al. 1999) recommend using 2.4 instead of 1.6 for glucose above 400 mg/dL, as 1.6 underestimates correction at extreme hyperglycemia.
Corrected Na 135-145 mEq/L: apparent hyponatremia is entirely from glucose dilution; treat with insulin and isotonic fluids. As glucose falls, measured sodium will rise toward corrected value. Corrected Na above 145 mEq/L: patient has underlying true hypernatremia masked by dilution — indicates significant free water deficit (classic in HHS). Corrected Na below 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 has glucose 550 mg/dL and measured sodium 130 mEq/L. Corrected sodium = 130 + 1.6 × (550 - 100)/100 = 137.2 mEq/L (normal). Treatment: isotonic saline initially for volume, then insulin. As glucose corrects, measured sodium should rise toward 137 mEq/L. Failure of measured sodium to rise during treatment suggests excessive free water administration or concurrent SIADH. Track corrected sodium at each glucose check to guide fluid management.
Emergency physicians, endocrinologists
HHS typically shows higher corrected sodium than DKA, reflecting more profound dehydration and less acidosis. Corrected sodium in HHS is often 145-155 mEq/L or higher, confirming massive free water deficit. The degree of hypernatremia predicts fluid deficit magnitude (each 1 mEq/L above 140 represents approximately 1-2 L free water deficit in a 70 kg patient). HHS osmolality is often above 320-340 mOsm/kg — calculate with the Serum Osmolality Calculator.
Endocrinologists, ICU nurses, hospitalists
As insulin lowers glucose during DKA treatment, the osmotic water shift reverses — water moves back into cells, and measured sodium rises. The corrected sodium predicts the endpoint sodium. If corrected sodium is 140 mEq/L, the measured sodium should approach 140 as glucose normalizes. Monitor sodium every 2-4 hours. Rapid sodium rise (above 2 mEq/L/hour) suggests the patient is receiving too little free water; stable or falling corrected sodium suggests adequate or excessive hydration.
ICU physicians, endocrinologists
A patient with uncontrolled diabetes and altered mental status has measured Na 142 mEq/L (appears normal) and glucose 900 mg/dL. Corrected sodium = 142 + 1.6 × (900-100)/100 = 142 + 12.8 = 154.8 mEq/L (markedly elevated). This patient has severe underlying hypernatremia masked by glucose dilution. As insulin is given, the measured sodium will spike dramatically unless adequate free water is co-administered. This calculation prevents potentially dangerous hypernatremia during DKA/HHS treatment.
Intensivists, anesthesiologists
In any critically ill patient receiving insulin infusions for hyperglycemia, corrected sodium guides appropriate fluid selection. Isotonic saline raises sodium and treats hyperglycemia-driven dilution. Half-normal saline (0.45% NaCl) provides free water and is appropriate when corrected sodium is elevated. Tracking corrected sodium prevents both under-treatment of true hypernatremia and over-treatment causing hyponatremia during glucose correction.
The traditional Katz 1.6 correction factor was derived theoretically and validated in mild-to-moderate hyperglycemia. Hillier et al. (Ann Intern Med 1999) demonstrated that 1.6 underestimates correction by approximately 40% at glucose levels above 400 mg/dL. The empirically derived correction factor of 2.4 mEq/L per 100 mg/dL glucose elevation is more accurate in severe hyperglycemia (glucose above 400 mg/dL, common in DKA and HHS).
During DKA treatment with insulin, glucose falls and measured sodium rises — this is expected and not concerning if corrected sodium remains stable. An appropriate response is measured sodium rising 1-2 mEq/L for every 100 mg/dL glucose decrease. If measured sodium rises faster (corrected sodium increases), the patient is relatively dehydrated — increase free water. If corrected sodium is falling, the patient may be receiving too many hypotonic fluids.
In HHS, corrected sodium is typically 145-155 mEq/L or higher, reflecting massive free water deficit. Approximate free water deficit = 0.6 × weight(kg) × (corrected Na/140 - 1). Example: 70 kg patient with corrected Na 155 = 0.6 × 70 × (155/140 - 1) = 42 × 0.107 = 4.5 liters free water deficit. Replace deficit slowly over 24-48 hours to avoid cerebral edema from rapid osmolality changes.
Corrected sodium tools out glucose contribution: if corrected sodium is normal (135-145), the hyponatremia is entirely explained by hyperglycemia. If corrected sodium remains low (below 135) despite correction, SIADH, adrenal insufficiency, hypothyroidism, or other causes must be investigated. Do not assume all hyponatremia in a hyperglycemic patient is from glucose — the corrected sodium reveals if a second disorder is present.
Effective serum osmolality = 2 × Na + Glucose/18 (omit BUN as urea is not osmotically active at membranes). Normal is 275-290 mOsm/kg. Effective osmolality above 320-340 mOsm/kg in HHS drives neurological symptoms (stupor, coma, seizures). Tracking effective osmolality during HHS treatment targets less than 3-8 mOsm/kg/hour reduction to prevent cerebral edema.
Even when corrected sodium reveals underlying hypernatremia in DKA, initial resuscitation uses isotonic saline (0.9% NaCl) to restore intravascular volume and tissue perfusion. Once hemodynamically stable and glucose begins falling, switch to 0.45% NaCl + potassium to provide free water for hypernatremia correction. This sequence prevents both shock (from inadequate initial resuscitation) and renal failure from inadequate volume.
Children with DKA are at higher risk for cerebral edema during treatment than adults. Risk factors include: severe acidosis (pH below 7.1), low PCO2 at presentation, rapid sodium correction (measured sodium should not fall, corrected sodium should remain stable), excessive fluid administration. Monitor for headache, confusion, bradycardia, hypertension, or unequal pupils — early signs of cerebral edema in pediatric DKA requiring immediate hypertonic saline.
Traditional correction factor 1.6 mEq/L per 100 mg/dL from Katz (NEJM 1973). Revised factor 2.4 mEq/L from Hillier et al. (Ann Intern Med 1999) who found 1.6 underestimates by ~40% at glucose above 400 mg/dL. ADA Clinical Practice Standards (2024) recommend monitoring serum sodium during DKA treatment. Cerebral edema risk and sodium trends: Glaser et al. (NEJM 2001). HHS management: Kitabchi et al. (Diabetes Care 2009). Effective serum osmolality formula and HHS outcomes: Bhardwaj et al. (Crit Care Med 2002).
Your corrected sodium value estimates what the serum sodium concentration would be if the blood glucose were at a normal level of 100 mg/dL. If the corrected sodium is within the normal range (135-145 mEq/L), the measured hyponatremia is entirely attributable to the dilutional effect of hyperglycemia, and sodium is expected to normalize as glucose is corrected. If the corrected sodium remains low (below 135 mEq/L), there is a true underlying hyponatremia that needs to be evaluated independently.
Conversely, if the corrected sodium is elevated (above 145 mEq/L), the patient has underlying hypernatremia masked by the dilutional effect of high glucose. This is particularly important in DKA and HHS management because as insulin lowers glucose, water shifts back into cells, and the serum sodium will rise. Failure to recognize underlying hypernatremia can lead to overly rapid sodium changes and risk of osmotic demyelination or cerebral edema.
Use this calculator whenever a patient presents with hyperglycemia (glucose above 100 mg/dL) and an abnormal sodium level, particularly in diabetic ketoacidosis (DKA), hyperosmolar hyperglycemic state (HHS), and other severe hyperglycemic emergencies. It is essential for accurately assessing a patient's true sodium status before and during insulin therapy.
It is also valuable for monitoring sodium trends during DKA or HHS treatment. As glucose falls with insulin therapy, you can predict how sodium will change. If the corrected sodium is stable or rising appropriately, fluid management is on track. If the corrected sodium is falling, the patient may be receiving excessive free water.
The Katz correction factor of 1.6 mEq/L per 100 mg/dL glucose elevation was derived from theoretical modeling and small studies. Some evidence (Hillier 1999) suggests that 2.4 mEq/L per 100 mg/dL is more accurate at glucose levels above 400 mg/dL. Neither correction factor has been rigorously validated in large prospective studies.
The formula assumes a linear relationship between glucose and sodium displacement, which may not hold at extreme glucose levels (above 800-1000 mg/dL). It also does not account for other causes of pseudohyponatremia (such as severe hyperlipidemia or hyperproteinemia) or for concurrent osmotically active substances. In clinical practice, the corrected sodium should be used as a guide alongside serum osmolality, clinical assessment of volume status, and serial monitoring rather than as a standalone decision point.
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.
April 21, 2026 · trust-baseline
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Calculate corrected sodium for hyperglycemia using the Katz formula to estimate true sodium status in DKA, HHS, and severe stress hyperglycemia.
OpenClinicalCalculate serum osmolality from sodium, glucose, and BUN. Normal range: 275–295 mOsm/kg. Osmolal gap >10 suggests toxic alcohol ingestion (methanol, ethylene glycol, isopropanol) or other unmeasured osmoles.
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