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REASONING GP · Clinical algorithm · Quick reference
Hyponatraemia in adults — triage and diagnostic approachThe commonest electrolyte abnormality in primary care. Symptoms and speed of onset decide urgency, not the number alone; volume status decides the cause; and the correction rate is itself a safety issue.
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| Trigger / red flag | Leading concern · destination | Do now · do not delay |
|---|---|---|
| Any neurological feature at any sodium level: seizure, drowsiness, reduced GCS, confusion, agitation, severe headache, vomiting or unsteadiness. | Cerebral oedema — needs hypertonic saline and monitoring Emergency admission now |
Symptoms, not the number, define severity: a symptomatic patient at 128 needs admission while an asymptomatic patient at 128 may not. Do not fluid-restrict a symptomatic patient at home or wait for a repeat. Send the previous sodium values and dates so the receiving team can judge the tempo and set a safe correction rate. |
| Na⁺ below 125 mmol/L, however well the patient seems; or a rapid fall — more than 10 mmol/L in 48 hours, or a fall from a normal recent result. | Severe or acute hyponatraemia · risk of seizure and herniation Emergency admission now |
Wellness is not reassurance below 125, and a rapid fall is dangerous at a level that would be tolerated if chronic. Stop the likely culprit drug now — usually a thiazide or an SSRI — and say what was stopped. Do not start fluid restriction and review in a week. |
| Hypovolaemic with hypotension: systolic BP below 90, tachycardia, postural collapse, ongoing vomiting, diarrhoea or high stoma output, or a patient unable to drink. | Hypovolaemic hyponatraemia with circulatory compromise Emergency admission now |
These patients need IV saline with monitoring, not oral fluids at home. Assess postural BP and mucous membranes. Do not fluid-restrict a hypovolaemic patient — the treatment is the opposite, and this is the commonest management error in hyponatraemia. |
| Low sodium with a high potassium, postural hypotension, fatigue, weight loss, pigmentation, hypoglycaemia, or after stopping long-term steroids. | Adrenal insufficiency · adrenal crisis 999 if hypotensive, vomiting or unwell Same-day endocrine advice and a 9 am cortisol |
Each number looks mild alone, which is why this is missed — hyponatraemia plus hyperkalaemia in an unwell patient is an adrenal crisis until excluded. Take a 9 am cortisol but do not wait for it before treating a crisis. Never stop long-term steroids abruptly. |
| Na⁺ 125–129 mmol/L asymptomatic, or any fall that is clearly progressive on serial results. | Moderate hyponatraemia — needs assessment today Same-day clinical assessment and bloods |
Assess volume status face to face; a remote review cannot do it. Send paired serum and urine osmolality with a urine sodium, plus TFTs, 9 am cortisol, glucose, lipids and potassium, before starting any treatment — once fluid restriction or a drug change begins, the diagnostic window closes. Stop or hold the culprit drug. Repeat within 24–48 hours. |
| Hypervolaemic hyponatraemia: oedema, raised JVP, ascites or crackles with heart failure, cirrhosis or advanced CKD; or worsening sodium after a diuretic increase. | Decompensated heart failure · cirrhosis · nephrotic syndrome · advanced CKD Same-day assessment; specialist advice before changing diuretics |
The sodium is a marker of the underlying disease severity and a poor prognostic sign — treat the disease, not the number. Do not simply increase the diuretic, and do not give saline. Seek cardiology, hepatology or renal advice on the diuretic balance; fluid restriction is appropriate here but needs the specialist's dose. |
| Acute water loading: marathon or endurance event, MDMA or ecstasy use, psychogenic polydipsia, excessive water intake, or a recent colonoscopy bowel preparation — particularly with headache, vomiting or confusion. | Acute dilutional hyponatraemia · exercise-associated hyponatraemia Emergency admission if any symptom Same-day assessment if asymptomatic |
This is acute hyponatraemia — the brain has had no time to adapt, so seizures occur at levels a chronic patient tolerates. Do not give further hypotonic fluid. Ask directly about water intake, energy drinks and recreational drugs; the history will not appear in the notes otherwise. |
| Euvolaemic hyponatraemia with a cancer feature: a smoker or ex-smoker with unexplained cough, weight loss, haemoptysis, chest pain or breathlessness; clubbing; supraclavicular nodes; or unexplained SIADH at any age. | SIADH from small-cell lung cancer, or another malignancy Urgent chest X-ray within 2 weeks · NICE NG12 |
SIADH is a recognised presentation of small-cell lung cancer and is often the first abnormality. Hyponatraemia is not itself an NG12 criterion, but where there is unexplained cough, weight loss, haemoptysis, chest pain or breathlessness, or the patient is 40 or over and has ever smoked, arrange an urgent chest X-ray within 2 weeks and refer on the urgent suspected-cancer route if it suggests cancer (NG12). A normal film with persistent unexplained SIADH still needs investigation — do not stop at "SIADH, cause unknown". |
REASONING GP · Hyponatraemia in adults — triage and diagnostic approach |
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| Drug-induced | The commonest cause in primary care and usually euvolaemic SIADH-like: thiazides and thiazide-like diuretics (indapamide especially), SSRIs and SNRIs, carbamazepine and oxcarbazepine, PPIs, NSAIDs, tricyclics, antipsychotics, desmopressin. Check start and dose-change dates against the sodium trend — the answer is usually there. |
| Hypovolaemic, and hypervolaemic | Hypovolaemic — urine Na⁺ below 20 with postural drop and dry membranes: vomiting, diarrhoea, bleeding, poor intake, high stoma output. Urine Na⁺ above 20 despite hypovolaemia points to renal loss (diuretics, adrenal insufficiency). Treated with salt and water, never fluid restriction. Hypervolaemic — oedema with a low urine sodium: heart failure, cirrhosis, nephrotic syndrome, advanced CKD. The sodium reflects disease severity and carries prognostic weight; treat that disease, with specialist-directed restriction, not saline. |
| SIADH, and the endocrine causes it must not hide | SIADH: euvolaemic, low serum osmolality, inappropriately concentrated urine with urine Na⁺ above 30, normal thyroid and adrenal function, no diuretic. Causes: malignancy (especially small-cell lung), chest disease, CNS disease and stroke, drugs, pain, nausea, surgery. A diagnosis of exclusion that still needs its own cause found. Exclude first: hypothyroidism and adrenal insufficiency — both treatable, and the latter classically pairs a low sodium with a high potassium and postural hypotension. |
| Excess water, and pseudohyponatraemia | Water excess: primary polydipsia, beer potomania, post-marathon or MDMA, excessive hypotonic fluid — dilute urine with a low osmolality. Pseudohyponatraemia: a normal or raised serum osmolality from marked hyperlipidaemia or paraproteinaemia, or translocational hyponatraemia from hyperglycaemia — the sodium is not truly low and needs no correction. |
| Do not conclude by default | "SIADH" without TFTs, a 9 am cortisol and a drug review · "chronic and stable" without finding the previous results · "the thiazide" in a clearly hypovolaemic patient — the mechanism changes the treatment · "unexplained SIADH" in a smoker without a chest X-ray. |
| Send the diagnostic bloods before you treat, then change the drug | Bloods first: paired serum and urine osmolality with a urine sodium, TFTs, 9 am cortisol, glucose, lipids and total protein — all before fluid restriction or stopping the drug. Once treatment starts the results become uninterpretable and the cause is lost, which turns a solvable problem into "SIADH, cause unknown". Then the drug: stop the thiazide and choose another antihypertensive class, and do not restart it; for an SSRI, weigh the mental-health risk — stop, switch class or reduce with a plan, and recheck the sodium at 1–2 weeks after any change. Review carbamazepine, PPIs, NSAIDs and tricyclics. |
| Match the treatment to the volume status | Hypovolaemic: oral salt and water, treat the loss — never fluid restriction. Euvolaemic (SIADH): fluid restriction, typically 1–1.5 L/24 h, with written advice on what counts as fluid, and only after the osmolalities are sent. Hypervolaemic: treat the underlying disease, with restriction at the specialist's dose. Tolvaptan and demeclocycline are specialist-only. |
| Correct slowly, then recheck — both are safety limits | Correction: no more than 8–10 mmol/L in 24 hours, slower still where the hyponatraemia is chronic, or in alcohol excess, malnutrition, liver disease or hypokalaemia — over-rapid correction causes osmotic demyelination, irreversible and iatrogenic. A sodium rising faster than this needs urgent advice, not congratulation. Recheck: U&E at 3–7 days after any change (sooner if below 130), then widening intervals once stable, with the thresholds written down: any confusion, drowsiness, seizure or vomiting, or Na⁺ below 125 → emergency admission; 125–129 → same-day assessment. |
| What not to do | Do not fluid-restrict a hypovolaemic patient, or give saline to a hypervolaemic one. Do not treat before the osmolalities. Do not accept one low sodium without the previous values. Do not restart the thiazide that caused it. Do not file a sodium of 128 as "borderline" with no plan and no reviewer. |