Hyponatraemia
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Direct answer
Serum sodium below 135 mmol/L defines hyponatraemia, and the classification that matters at the bedside is by volume status and urine indices — hypovolaemic, euvolaemic and hypervolaemic — with the euvolaemic syndrome of inappropriate antidiuretic hormone secretion (SIADH) the commonest in practice. Severe symptomatic hyponatraemia with seizures or coma is treated with a bolus of 3 per cent hypertonic saline, while correction in any chronic case must not exceed about 8 to 10 mmol/L in 24 hours to avoid osmotic demyelination syndrome.
What you must remember
- First check serum osmolality: exclude pseudohyponatraemia (hyperlipidaemia, paraproteinaemia — normal osmolality) and translocational hyponatraemia of hyperglycaemia — correct sodium by about 2 mmol/L for every 100 mg per dL glucose above normal.
- Hypovolaemic (vomiting, diarrhoea, diuretics): urine sodium below 20 mmol/L suggests extrarenal loss, above 20 renal loss (diuretics, cerebral salt wasting); treat with isotonic saline.
- Euvolaemic: SIADH — urine osmolality above 100 mOsm/kg and urine sodium above 40 mmol/L with normal volume status; causes: small-cell lung carcinoma, CNS disease, pneumonia, SSRIs, carbamazepine; also hypothyroidism and adrenal insufficiency; primary polydipsia gives dilute urine below 100.
- Hypervolaemic: heart failure, cirrhosis, nephrotic syndrome — treat the primary disorder with salt restriction and diuretics.
- SIADH management: fluid restriction, salt with a loop diuretic if needed, tolvaptan for refractory cases; treat the cause.
- Severe symptomatic: 3 per cent saline 100 to 150 mL bolus over 10 to 20 minutes, repeated up to three times, for a prompt 4 to 6 mmol/L rise to stop seizures.
- Correction limit 8 to 10 mmol/L in 24 hours in chronic cases; if overcorrected, relower with desmopressin and 5 per cent dextrose.
One sodium value, three questions in sequence
A 60-year-old with small-cell lung carcinoma is found drowsy with sodium 116 mmol/L. Question one: is the plasma truly hypotonic? Check serum osmolality — pseudohyponatraemia gives normal osmolality, and hyperglycaemia causes translocational dilution, corrected by about 2 mmol/L for every 100 mg per dL glucose above normal. Hers is low, so the hyponatraemia is real. Question two: her low uric acid and urea would support it, and thyroid and adrenal function must be normal before the label sticks. Contrast the other lanes: a dry patient with urine sodium below 20 is extrarenal hypovolaemic — isotonic saline; urine sodium above 20 in a dry patient suggests renal loss or cerebral salt wasting, also treated with saline. The oedematous lanes — heart failure, cirrhosis, nephrotic syndrome — are hypervolaemic, treated by treating the primary disorder; primary polydipsia shows urine osmolality below 100. Question three: how fast? She is chronic and symptomatic but not seizing: controlled correction within the 8 to 10 daily ceiling, fluid restriction, tolvaptan only if refractory. Had she seized, 100 to 150 mL of 3 per cent saline over 10 to 20 minutes, repeated up to three times for a 4 to 6 rise — and if someone overshoots, relower with desmopressin and 5 per cent dextrose.
Where students slip
SIADH versus cerebral salt wasting is the classic pair and the viva favourite: both show urine sodium and osmolality inappropriately high, but SIADH patients are euvolaemic and treated with fluid restriction, whereas cerebral salt wasting patients are hypovolaemic and need saline — the volume examination decides. The other recurring errors: treating pseudohyponatraemia, missing glucocorticoid deficiency behind an "SIADH" label, and correcting too fast — the osmotic demyelination that follows is iatrogenic and largely irreversible, which is why the numbers 135, 100, 40, the 2-per-100 glucose rule, the 4 to 6 acute target and the 8 to 10 ceiling carry the marks.
Frequently asked questions
How do you classify hyponatraemia at the bedside?
By volume status with urine sodium and osmolality: hypovolaemic (saline-responsive), euvolaemic (SIADH, endocrine causes) and hypervolaemic (oedematous states), after confirming hypo-osmolality.
What are the diagnostic criteria for SIADH?
Hypotonic hyponatraemia with inappropriately concentrated urine (above 100 mOsm/kg), urine sodium above 40 mmol/L, euvolaemia, normal thyroid, adrenal and renal function, and no diuretics.
How does hyperglycaemia lower measured sodium?
Glucose draws water out of cells, diluting extracellular sodium; correct by about 2 mmol/L per 100 mg per dL glucose above normal.
Why is correction limited to 8 to 10 mmol/L per day?
Rapid osmolality rises demyelinate pontine and extrapontine neurons (osmotic demyelination syndrome), especially in malnourished or alcoholic patients.
What is the treatment of hyponatraemic seizures?
A 100 to 150 mL bolus of 3 per cent hypertonic saline, repeated if needed, for a prompt 4 to 6 mmol/L rise, then controlled correction.
How do SIADH and cerebral salt wasting differ?
Both show high urine sodium, but SIADH is euvolaemic and needs fluid restriction, while cerebral salt wasting is hypovolaemic and needs isotonic saline.