Sodium Correction for Hyperglycemia Calculator
Glucose pulls water into the vascular space and drags measured sodium down. Correct it with both the classic 1.6 and empirically derived 2.4 factors — and see why the neurologic stakes of getting this wrong run in both directions.
Reviewed by Zaka Ahmed, MD Clinical reference · 3 min read
Sodium Correction for Hyperglycemia
Enter the measured sodium and glucose. Both standard correction factors are shown — 1.6 mEq/L (Katz) and 2.4 mEq/L (Hillier) per 100 mg/dL of glucose above 100.
Corrected sodium by both factors appears here.
Educational tool only. Correction factors are approximations of a nonlinear relationship; serial measured values during treatment outrank any single corrected number. This does not replace clinical judgment or in-person evaluation.
Clinical notes & interpretation Scoring guidance, pitfalls, FAQs, and references
Why measured sodium lies when glucose is high
Glucose is an effective osmole: at high concentrations it pulls intracellular water into the extracellular space, diluting sodium without changing total body sodium or water balance — translocational (factitious) hyponatremia. The classic Katz correction adds 1.6 mEq/L per 100 mg/dL of glucose above 100; Hillier's experimental data suggested ~2.4 is more accurate at glucose above roughly 400. Showing both brackets the truth better than either alone.
The neurologic stakes run both ways
Get this wrong in one direction and you treat a hyponatremia that does not exist; the danger is compounded during DKA/HHS treatment, where falling glucose shifts water back and measured sodium rises — a corrected-sodium trend that climbs too fast flags an osmotic trajectory that risks demyelination in susceptible patients. Get it wrong in the other direction and you miss true hypertonicity: in HHS the corrected sodium is often frankly high, the effective osmolality explains the encephalopathy, and the free-water deficit is the treatment target. On a neuro service the practical habits are: calculate corrected sodium on every significantly hyperglycemic chemistry before attributing encephalopathy or seizures to "hyponatremia," follow effective osmolality (2×Na + glucose/18) in HHS — and remember hyperglycemia is also independently bad for the injured brain, worsening infarct evolution and hemorrhagic transformation risk after stroke.
Frequently asked questions.
Which factor should I use — 1.6 or 2.4?
1.6 (Katz) is the traditional default; Hillier's data support ~2.4 when glucose exceeds ~400 mg/dL. Treat them as a bracket, and let serial measured values during treatment adjudicate.
Is translocational hyponatremia dangerous itself?
The tonicity, not the sodium number, is what the brain feels — and in hyperglycemia tonicity is high or normal, not low. The danger is mismanagement: giving hypertonic saline for a pseudo-low sodium, or failing to anticipate the sodium rise as glucose falls.
How does this interact with stroke care?
Admission hyperglycemia predicts worse outcomes in ischemic stroke and ICH, and osmotic shifts complicate cerebral edema management. When an edema patient on hyperosmolar therapy is also hyperglycemic, corrected sodium and measured osmolality — not raw sodium — are the numbers to steer by.