Nursing care
Sodium Level Interpretation: reading the number and acting on it
Written and reviewed by Dana Whitfield, RN, MSN · 4 min read · Updated September 2026
Short answer
Normal serum sodium is 135 to 145 mEq/L. A low or high result only means something once it's read against the patient's fluid status, because sodium disturbances track total body water, not just salt. Correct hyponatraemia no faster than 8 to 10 mEq/L in 24 hours; faster correction can cause osmotic demyelination syndrome.
Why this value is ordered
Sodium is checked whenever a patient presents with confusion, seizure, lethargy, or unexplained weakness, and it's part of every basic metabolic panel. It's the main determinant of serum osmolality, so it moves whenever water balance shifts, even when total body sodium hasn't changed at all.
It's also ordered to monitor patients on diuretics, those receiving IV fluids or tube feeds, anyone with heart failure or cirrhosis, and postoperative patients who've had large volume shifts. In practice you'll see it trended daily on anyone at risk of SIADH, diabetes insipidus, or fluid overload.
Interpreting the number in context
Normal serum sodium is 135 to 145 mEq/L. Below 135 is hyponatraemia; above 145 is hypernatraemia. The number alone tells you nothing about the cause, so pair it with volume status: is the patient hypovolaemic, euvolaemic, or hypervolaemic?
A hypovolaemic hyponatraemic patient has lost both salt and water, usually through vomiting, diarrhoea, or diuretic use, and needs isotonic fluid. A euvolaemic hyponatraemic patient, often with SIADH, is retaining free water and needs fluid restriction, not saline. A hypervolaemic hyponatraemic patient, as in heart failure or cirrhosis, is diluted despite excess total sodium. Reading the number without the volume assessment leads to the wrong treatment every time.
Critical values and what to do
A sodium below 120 mEq/L or above 160 mEq/L is a critical value and warrants an immediate call to the provider. Severe hyponatraemia causes cerebral oedema; severe hypernatraemia causes cellular dehydration and can precipitate seizures in both directions.
The correction rule matters more than the diagnosis: correct hyponatraemia no faster than 8 to 10 mEq/L in 24 hours. Correcting too quickly pulls water out of brain cells faster than they can adapt, and it demyelinates the pons, producing osmotic demyelination syndrome with irreversible quadriparesis and dysarthria. Hold or slow any hypertonic saline infusion if the rate of rise looks too steep, and recheck sodium every 2 to 4 hours during active correction.
Related tests read alongside it
Serum osmolality confirms whether hyponatraemia is truly hypotonic or a lab artefact from hyperglycaemia or hyperlipidaemia. Urine sodium and urine osmolality distinguish SIADH from other causes and guide whether fluid restriction or saline is appropriate.
Potassium, chloride, and BUN/creatinine are drawn on the same panel and help characterise volume status and renal function. In a patient on diuretics, checking magnesium alongside sodium and potassium catches concurrent electrolyte losses that would otherwise be missed.
Nursing implications
Assess neurological status before and during correction; a change in level of consciousness, new headache, or seizure activity is an emergency in either direction. Track strict intake and output and daily weights, since fluid balance drives the sodium far more than dietary salt does.
Never bolus hypertonic saline without a written rate and a plan for frequent recheck labs. If a patient is fluid-restricted for SIADH, explain why plain water is the problem, not salt, so they don't reach for more fluids to feel better.
What patients ask about it
Patients often ask whether they need to eat more salt, assuming low sodium means dietary deficiency. Most hospital hyponatraemia is dilutional, from excess water intake or impaired water excretion, not from too little salt in the diet.
They also ask why fluids are being restricted when they feel thirsty. Explaining that the kidneys can't clear free water fast enough in SIADH, and that drinking more will worsen the labs, helps with adherence far more than a blanket instruction to limit fluids.
The next step on this is the same as on everything else here: answer questions and read the rationales. Our dosage calculation and lab values practice questions are the closest set to what this page covers.
Common questions
What causes hyponatraemia in a hospitalised patient?
Common causes include SIADH, diuretic use, heart failure, cirrhosis, and excess hypotonic IV fluids. The cause determines treatment, so volume status assessment always comes before deciding whether to restrict fluids or give saline.
How fast can you correct hyponatraemia?
No faster than 8 to 10 mEq/L in 24 hours. Faster correction risks osmotic demyelination syndrome, a permanent neurological injury, so recheck levels frequently during active treatment.
Why does an NCLEX question about low sodium usually mention confusion or seizures?
Sodium moves water across cell membranes, so low levels cause cerebral oedema and neurological symptoms first. Expect questions to test whether you recognise a change in mental status as the priority finding, not just the lab number.
What's the difference between isotonic and hypertonic saline for hyponatraemia?
Isotonic (0.9%) saline is used for hypovolaemic hyponatraemia to replace lost volume. Hypertonic (3%) saline is reserved for severe or symptomatic hyponatraemia and is given cautiously with strict rate limits because of the demyelination risk.
Can hyperglycaemia cause a falsely low sodium reading?
Yes. High glucose pulls water into the vascular space and dilutes sodium, a phenomenon called translocational hyponatraemia. Correcting the measured value for glucose (roughly 1.6 mEq/L drop in sodium per 100 mg/dL rise in glucose above normal) gives the true picture.
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