Electrolytes
Hyponatremia Calculator — v4.1
A guided clinical tool for evaluating low sodium with safety guardrails.
This tool does not replace clinical judgement and is meant to assist in decision-making. Always verify calculations and consider patient-specific factors.
Required Labs
Select Volume Status
Hypovolemia: tachycardia/hypotension, ↓ turgor, dry mucosa, flat neck veins.
Hypervolemia: edema/ascites, JVD, crackles.
Neurologic Symptoms (Severity)
Severe: seizures, coma, obtundation, severe confusion.
Moderate: HA, lethargy, dizziness.
Mild: none of the above.
Select Pertinent Medical History
Optional: Renal Indices (FENa / FEUrea)
FENa auto-calculates when inputs are present. With diuretics, FEUrea is often more reliable.
Results
- Select Volume Status
- Select Neurologic symptoms (severity)
- Select Pertinent Medical History (or "None of the above")
Created and maintained by Yasmine Abbey, MD, MSc · Last reviewed:
Educational decision-support for clinicians. Not medical advice — verify all outputs against your clinical judgment, institutional protocols, and current guidelines.
How this hyponatremia workup calculator works
Hyponatremia — a serum sodium below 135 mEq/L — is the most common electrolyte abnormality in hospitalized patients, and one of the easiest to manage badly. The dangers run in both directions: untreated severe hyponatremia can cause cerebral edema, seizures, and death, while correcting chronic hyponatremia too quickly can cause osmotic demyelination syndrome (ODS), a devastating and largely irreversible neurologic injury.
This calculator walks through the same stepwise workup taught in nephrology: confirm that the hyponatremia is truly hypotonic, use urine osmolality to establish whether ADH is acting, then combine urine sodium, volume status, and history to reach a working etiology. Along the way it computes the glucose-corrected sodium, FENa, and FEUrea for you, applies severity-based safety guardrails, and can draft a chart-ready assessment and plan you can edit and paste into your note.
Step 1 — Confirm true hypotonic hyponatremia
Not every low sodium is a water problem. A measured serum osmolality below 275 mOsm/kg confirms hypotonic hyponatremia. If the osmolality is normal or high, look for another explanation before treating.
Hyperglycemia is the most common culprit: glucose holds water in the extracellular space and dilutes sodium. The calculator applies the Hillier correction — add roughly 2.4 mEq/L to the measured sodium for every 100 mg/dL of glucose above 100 mg/dL. A corrected sodium in the normal range means you are treating hyperglycemia, not hyponatremia. Pseudohyponatremia (a laboratory artifact from severe hyperlipidemia or paraproteinemia) and other effective osmoles such as mannitol are the other classic mimics.
Step 2 — Use urine osmolality to ask: is ADH acting?
A urine osmolality below 100 mOsm/kg means the kidney is appropriately diluting urine and ADH is suppressed — the problem is water or solute intake. Think primary polydipsia, beer potomania, or the 'tea and toast' pattern of very low solute intake.
A urine osmolality of 100 mOsm/kg or higher means ADH is active despite hypotonicity. The rest of the workup is about deciding whether that ADH release is appropriate (true or effective volume depletion) or inappropriate (SIADH and its mimics).
Step 3 — Urine sodium and volume status point to the etiology
With ADH active, a urine sodium below about 30 mEq/L suggests the kidney is avidly retaining sodium: true hypovolemia (vomiting, diarrhea, bleeding, third-spacing) or the reduced effective circulating volume of heart failure and cirrhosis. A urine sodium of 30 mEq/L or higher in a euvolemic patient points toward SIADH — after excluding adrenal insufficiency, severe hypothyroidism, and recent diuretic use.
Diuretics muddy the urine sodium. When a patient is on chronic diuretics, the calculator offers the fractional excretion of urea (FEUrea) instead: values below about 45% still suggest a hypovolemic, prerenal physiology even when the urine sodium is uninterpretable.
Diagnosing SIADH: the essential criteria
SIADH is a diagnosis of exclusion. Once established, hunt for the cause: medications (SSRIs, carbamazepine, antipsychotics, chemotherapy), pulmonary disease, CNS disease or surgery, malignancy (classically small-cell lung cancer), pain, and nausea are the recurring offenders.
- Hypotonic hyponatremia (serum osmolality < 275 mOsm/kg)
- Urine osmolality > 100 mOsm/kg despite hypotonicity
- Urine sodium > 30 mEq/L on normal salt and water intake
- Clinical euvolemia — no edema, ascites, or signs of volume depletion
- Normal thyroid and adrenal function, and no recent diuretic use
Correction limits and osmotic demyelination syndrome (ODS)
In chronic hyponatremia (present or presumed for more than 48 hours), the brain has adapted by shedding intracellular osmoles. Raising the serum sodium faster than the brain can re-adapt drives water out of neurons and can cause osmotic demyelination syndrome — classically appearing days after the overcorrection, with dysarthria, dysphagia, quadriparesis, or locked-in syndrome.
Practical guardrails, reflected in this tool's output: aim for a rise of 4–6 mEq/L in 24 hours, and do not exceed 8 mEq/L in any 24-hour period in patients at high risk for ODS (serum sodium ≤ 105 mEq/L, hypokalemia, alcohol use disorder, malnutrition, or advanced liver disease). Watch for an unexpected water diuresis — as the underlying stimulus for ADH resolves, sodium can climb rapidly. If correction overshoots, re-lower the sodium with D5W with or without desmopressin.
Severe symptomatic hyponatremia is an emergency
Seizures, obtundation, or coma attributable to hyponatremia call for immediate hypertonic saline regardless of the cause: a 100–150 mL bolus of 3% NaCl over 10–20 minutes, repeated up to two more times if symptoms persist, targeting a 4–6 mEq/L rise in serum sodium — enough to decompress the brain, while staying inside the 24-hour ceiling. These patients belong in a monitored setting with sodium checks every 2 hours initially, and the calculator's plan output reflects that cadence.
Frequently asked questions
What sodium level defines hyponatremia, and when is it severe?
Hyponatremia is a serum sodium below 135 mEq/L. It is commonly graded as mild (130–134), moderate (125–129), and profound or severe (below 125 mEq/L). Severity of symptoms matters more than the number: any patient with seizures, marked confusion, or coma attributable to hyponatremia is treated as a hypertonic-saline emergency regardless of the absolute value.
How do you correct sodium for hyperglycemia?
Add approximately 2.4 mEq/L to the measured serum sodium for every 100 mg/dL of glucose above 100 mg/dL (the Hillier correction; the older Katz factor of 1.6 underestimates at very high glucose). This calculator computes the corrected value automatically when you enter a glucose.
What is the maximum safe rate of sodium correction?
For chronic hyponatremia, target a rise of 4–6 mEq/L per 24 hours and avoid exceeding 8 mEq/L in 24 hours in patients at high risk of osmotic demyelination — many guidelines allow up to 10 mEq/L in low-risk patients, but staying at or under 8 is the safer default in hospital practice.
What is osmotic demyelination syndrome (ODS)?
ODS is neurologic injury caused by overly rapid correction of chronic hyponatremia, classically central pontine myelinolysis. Symptoms — dysarthria, dysphagia, quadriparesis, behavioral change, locked-in syndrome — typically appear two to six days after overcorrection. Risk is highest when the starting sodium is ≤ 105 mEq/L or the patient has hypokalemia, alcohol use disorder, malnutrition, or advanced liver disease.
How is SIADH diagnosed?
SIADH requires hypotonic hyponatremia with inappropriately concentrated urine (urine osmolality > 100 mOsm/kg), urine sodium > 30 mEq/L, clinical euvolemia, and exclusion of adrenal insufficiency, hypothyroidism, and diuretic effect. It is a diagnosis of exclusion, and finding the underlying cause — drugs, pulmonary or CNS disease, malignancy — is part of the diagnosis.
What does a urine osmolality below 100 mOsm/kg mean?
Maximally dilute urine means ADH is appropriately suppressed and the kidney is doing its job — the problem is intake. Consider primary polydipsia, beer potomania, or very low solute intake ('tea and toast' diet). Treatment centers on the intake problem, and these patients can auto-correct dangerously fast once free-water intake stops.
How do I evaluate hyponatremia in a patient on diuretics?
Diuretics (especially thiazides) both cause hyponatremia and make the urine sodium uninterpretable. The fractional excretion of urea (FEUrea) is less affected: a FEUrea below about 45% suggests a hypovolemic, prerenal physiology. This calculator computes FEUrea when you provide urine urea, BUN, and creatinine values.
What is the Furst formula (urine-to-serum electrolyte ratio)?
The Furst ratio — (urine Na + urine K) ÷ serum Na — predicts whether fluid restriction alone can raise the sodium, because it approximates whether the kidney is excreting any electrolyte-free water. A ratio above 1 means essentially no free water is being excreted and fluid restriction alone is unlikely to work (consider stricter restriction or additional therapy such as salt tabs, urea, or a vaptan). A ratio of 0.5–1 suggests restricting to about 500 mL/day; below 0.5, roughly 1 L/day may suffice.
What should I do if the sodium is correcting too fast?
Stop the active therapy, and re-lower the sodium if the 24-hour limit is exceeded or neurological risk is high: infuse D5W (with desmopressin if a water diuresis is driving the rise). Relowering sodium after overcorrection is guideline-supported and protective against ODS. Involve nephrology early.
Is this calculator a substitute for clinical judgment?
No. It is an educational decision-support and documentation aid for clinicians. It does not account for every clinical scenario, and its output must be verified against your own assessment, your institution's protocols, and current guidelines before any order is placed.
How is this different from a single-formula sodium calculator?
Most online tools compute one number (a sodium deficit or an infusate effect). This tool runs the diagnostic workup — tonicity, ADH activity, volume status, and history — applies severity-based safety rails, and drafts an editable assessment and plan, which is usually the slow part of managing hyponatremia on the wards.
References
- Spasovski G, Vanholder R, Allolio B, et al. Clinical practice guideline on diagnosis and treatment of hyponatraemia. Eur J Endocrinol. 2014;170(3):G1–G47.
- Verbalis JG, Goldsmith SR, Greenberg A, et al. Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. Am J Med. 2013;126(10 Suppl 1):S1–S42.
- Sterns RH. Disorders of plasma sodium — causes, consequences, and correction. N Engl J Med. 2015;372(1):55–65.
- Adrogué HJ, Madias NE. Hyponatremia. N Engl J Med. 2000;342(21):1581–1589.
- Hillier TA, Abbott RD, Barrett EJ. Hyponatremia: evaluating the correction factor for hyperglycemia. Am J Med. 1999;106(4):399–403.
- Furst H, Hallows KR, Post J, et al. The urine/plasma electrolyte ratio: a predictive guide to water restriction. Am J Med Sci. 2000;319(4):240-244.
- Hoorn EJ, Zietse R. Diagnosis and treatment of hyponatremia: compilation of the guidelines. J Am Soc Nephrol. 2017;28(5):1340–1349.