Hyponatraemia — Diagnosis & Management
UK primary care pathway · Adults only (excludes pregnancy/peripartum) · Na⁺ <135 mmol/L · GP trainees & early-career GPs · SCA-ready
Progress0 / 9
1
Safety
Red Flags — Identify Life-Threatening Hyponatraemia First
Hyponatraemia (Na⁺ <135 mmol/L) kills through cerebral oedema. Symptom severity drives urgency — not sodium level alone. Screen for these before any other workup.
Seizures / status epilepticus New-onset seizure with low Na⁺ → 999. Cerebral oedema causing cortical irritation.
Severe acute hyponatraemia (<48h) Rapid fall with any neurological symptom → 999 (emergency admission). Fastest fall = worst risk.
Postoperative hyponatraemia Within 3–5 days surgery + neurological symptoms → 999. IV hypotonic fluids common cause.
Na⁺ <120 mmol/L (any) Urgent same-day hospital/acute medical assessment is generally appropriate, even without symptoms, because of the risk of deterioration and the need for monitored correction. Emergency transfer (999) if neurological symptoms, haemodynamic instability, acute onset or a rapidly falling sodium.
Severe dehydration / shock HR >120, SBP <90, postural collapse with low Na⁺ → 999. Hypovolaemic emergency.
Suspected adrenal crisis Low Na⁺ with hypotension, vomiting, collapse or raised K⁺ → 999. Give IM or IV hydrocortisone immediately if trained and authorised; do not delay treatment for cortisol testing. Think of it after stopping long-term steroids — never stop them abruptly.
⚠️ Acute vs chronic: Symptoms <48h = acute (high risk). Symptoms >48h or insidious onset = chronic (lower immediate risk, but correcting TOO quickly causes osmotic demyelination syndrome).
⚠️ Scope: This pathway applies to adults only. Pregnancy and peripartum hyponatraemia are excluded — follow obstetric guidance (NICE NG235) and seek specialist advice.
Acute hyponatraemia causes cerebral oedema as water shifts intracellularly — the brain cannot adapt fast enough. Untreated seizures from severe acute hyponatraemia can be fatal. The European Clinical Practice Guidelines (Spasovski 2014, endorsed by ESICM/ERA-EDTA; international) mandate immediate hypertonic saline (3% NaCl) for any seizure or GCS deterioration regardless of baseline sodium. Na⁺ <120 mmol/L in apparently asymptomatic patients still represents critical danger — subtle symptoms (nausea, gait disturbance) predict imminent decompensation. Over-rapid correction (more than 10 mmol/L in the first 24h, then 8 mmol/L in each further 24h; slower still in high-risk patients) risks osmotic demyelination syndrome (formerly central pontine myelinolysis), which is irreversible. Never normalise Na⁺ rapidly — it is more dangerous than the hyponatraemia itself.
Measured serum osmolality is preferred where available. Calculated plasma osmolality ≈ 2×Na⁺ + glucose + urea (mmol/L). Effective osmolality (tonicity) ≈ 2×Na⁺ + glucose — urea is an ineffective osmole. Normal 275–295 mOsm/kg.
Low (<275): True hypotonic hyponatraemia — usually water excess relative to sodium
Normal (275–295): Isotonic — consider pseudohyponatraemia (severe hypertriglyceridaemia or hyperproteinaemia, particularly with indirect ion-selective electrode methods)
High (>295): Hypertonic (translocational) — hyperglycaemia, mannitol or other effective osmoles
Symptom severity
Moderate symptoms: Nausea (no vomiting), confusion, headache Severe symptoms: Vomiting, cardiorespiratory distress, seizure, GCS ≤14, coma Symptoms trump sodium level for urgency
Duration
Acute: onset known <48h. Chronic: >48h or unknown. Always assume chronic if uncertain — safer correction rate.
Exclude pseudohyponatraemia
Severe hypertriglyceridaemia (lipid displaces water in sample) or hyperproteinaemia (myeloma) — measured osmolality normal. Hyperglycaemia causes translocational (hypertonic) hyponatraemia, not pseudohyponatraemia; glucose correction factors vary by glucose range and laboratory method, so do not apply a single fixed factor.
Urine Na⁺ + osmolality
Both essential for classification. Spot urine Na⁺Urine osmolality — order at same time as blood results.
Treating the wrong type of hyponatraemia is dangerous. Giving IV fluids to SIADH will worsen hyponatraemia. Giving fluid restriction to hypovolaemic hyponatraemia will cause haemodynamic collapse. Plasma osmolality is the gating test: only hypotonic hyponatraemia (low plasma osmolality) represents true hyponatraemia requiring management. Pseudohyponatraemia due to extreme hyperlipidaemia or hyperproteinaemia requires no treatment. The symptom-based severity classification (European Guidelines 2014) replaced the older sodium-threshold-based approach because symptoms predict clinical risk more accurately than absolute sodium values. A patient with Na⁺ 128 mmol/L who is seizuring is an emergency; a patient with Na⁺ 118 mmol/L who is ambulant and chronic still needs urgent same-day hospital assessment, but not necessarily an ambulance.
3
Diagnose
Classification — Volume Status & Urine Results Determine the Cause
Once true hypotonic hyponatraemia is confirmed, use urine osmolality first: ≤100 mOsm/kg suggests primary polydipsia, low solute intake or excess water intake; >100 mOsm/kg indicates non-suppressed vasopressin activity — then interpret a contemporaneous urine sodium (≤30 mmol/L: reduced effective arterial volume likely; >30 mmol/L: consider SIAD, renal salt loss, adrenal insufficiency, diuretics). Then use clinical assessment, medication history and renal function to refine the diagnosis — clinical volume assessment alone is often inaccurate.
Hypovolaemic (Low volume)
Urine Na⁺ ≤30 mmol/L: Extra-renal losses — diarrhoea, vomiting, sweating, burns Urine Na⁺ >30 mmol/L: Renal losses — diuretics (thiazides esp.), Addison's, salt-wasting nephropathy, cerebral salt wasting Treat: oral rehydration if stable; IV saline in hospital
Euvolaemic (Normal volume)
Most common cause of hyponatraemia in primary care.
Urine osmolality >100 mOsm/kg + urine Na⁺ >30 = SIADH (most likely)
Also: hypothyroidism, glucocorticoid deficiency, polydipsia Check: TFTs, 9am cortisol, serum osmolality
Hypervolaemic (Excess volume)
Urine Na⁺ ≤30 mmol/L: Heart failure, liver cirrhosis, nephrotic syndrome
Urine Na⁺ >30 mmol/L: CKD/AKI with impaired water excretion Usually requires specialist input
SIADH diagnosis
A diagnosis of exclusion. Consider when all or most are present: hypotonic hyponatraemia + urine osmolality >100 mOsm/kg + urine Na⁺ usually ≥30 mmol/L with normal dietary intake + apparent euvolaemia + normal renal function (or no renal explanation) + no clinically significant adrenal insufficiency + no clinically relevant hypothyroidism + no recent diuretic effect sufficient to explain the findings. Do not diagnose SIAD solely from a low sodium, low serum osmolality and concentrated urine. Common causes: Malignancy (SCLC), CNS disease, pulmonary disease, drugs
Drug causes (Always review)
Thiazide diuretics — most common drug cause in elderly
SSRIs/SNRIs, carbamazepine, oxcarbazepine, tricyclics, PPIs, NSAIDs, opioids, antipsychotics, DDAVP, cyclophosphamide Review ALL medications — stop offending drug if safe
📊 Urine sodium caveat: Urine sodium is a helpful discriminator but is not diagnostic in isolation. Diuretics, CKD, recent saline, vomiting and dietary sodium intake can substantially alter the result. In people taking diuretics, consider the diuretic as a potential cause, review the timing of the last dose, and seek specialist advice if the diagnosis remains unclear. Fractional uric acid excretion may sometimes help but is not a routine primary-care test.
Volume status matters because it can reverse treatment priorities — but clinical assessment of volume is often inaccurate, so urine osmolality and urine sodium are interpreted first and examination is used to refine the diagnosis. In hypovolaemic hyponatraemia (e.g. thiazide + diarrhoea), the kidney is maximally retaining sodium — treating with fluid restriction would be catastrophic. In hypervolaemic states (heart failure, cirrhosis), the kidney is correctly retaining sodium but water is in excess — giving IV saline worsens oedema and congestion. SIADH accounts for the majority of hyponatraemia seen in hospital and increasingly in primary care due to widespread SSRI and thiazide prescribing. Distinguishing SIADH from hypothyroid or adrenal causes is essential: thyroid and cortisol deficiency both mimic SIADH biochemically but require hormone replacement, not fluid restriction. Drug review is the single highest-yield intervention in primary care — stopping thiazide diuretics in elderly patients frequently normalises sodium within 2–4 weeks without further intervention.
4
Diagnose
Targeted Examination — Volume Status & Systemic Disease Clues
Examination helps estimate volume status (often inaccurate — interpret alongside urine osmolality, urine sodium and drug history) and may reveal the underlying cause. Aim to complete in under 3 minutes.
Vital signs
BP supine + standing (postural drop >20 mmHg systolic = hypovolaemia). HR, RR, SpO₂, temp. Shocked patient → 999.
Volume status
Hypovolaemic: Dry mucous membranes, reduced skin turgor, sunken eyes, cool peripheries, tachycardia Euvolaemic: Normal JVP, no oedema, no ascites Hypervolaemic: Raised JVP, peripheral oedema, bibasal crackles, ascites
Compare to previous. Rapid gain = fluid retention (HF, cirrhosis). Rapid loss = malignancy, Addison's.
Clinical volume assessment informs which fluid strategy (if any) is appropriate, but is often inaccurate on its own. Getting this wrong is one of the most common cause of iatrogenic harm in hyponatraemia management. A postural BP drop is the single most useful bedside test for hypovolaemia and takes 2 minutes. Skin hyperpigmentation is pathognomonic of primary adrenal insufficiency (Addison's disease), which presents with hyponatraemia, hyperkalaemia, hypotension and fatigue — it is a medical emergency if in crisis. Neurological findings change the pathway immediately: confusion in a patient with mild sodium (e.g. 128 mmol/L) needs emergency admission, and ataxia or new falls at least same-day assessment, regardless of other findings. Weight trend is often overlooked in primary care but provides crucial objective evidence of fluid shifts that the clinical examination may miss.
Order these systematically. Urine sodium and osmolality are the most underutilised but highest-yield tests — always request alongside bloods.
First-line bloods
U&Es Na⁺, K⁺, urea, creatinine (eGFR), bicarbonate Serum osmolality measured preferred (effective osmolality ≈ 2×Na + glucose) Glucose exclude hyperglycaemia shifting sodium LFTs + albumin cirrhosis, nephrotic syndrome TFTs hypothyroidism mimics SIADH 8–9 am cortisol if adrenal insufficiency is possible, provided this will not delay treatment. Interpret using the local laboratory assay and NICE NG243 thresholds; intermediate results need endocrinology advice and/or dynamic testing. Do not diagnose or exclude adrenal insufficiency on a single value without considering exogenous steroids, timing, clinical features and assay-specific ranges
Urine (essential)
Spot urine Na⁺ — interpret if urine osmolality >100: ≤30 = reduced effective arterial volume likely; >30 = consider SIAD, renal salt loss, adrenal insufficiency or diuretics (unreliable with diuretics, CKD or recent saline) Urine osmolality (first discriminator) — ≤100 = primary polydipsia, low solute intake (e.g. beer potomania) or excess water intake; >100 = non-suppressed vasopressin activity Urine K⁺ if available Collect before any IV fluids change the result
If SIADH confirmed with no other cause → exclude occult malignancy.
CXR (SCLC), CT chest/abdomen/pelvis if high suspicion; suspected cancer pathway referral if chest X-ray suggests lung cancer, or aged 40+ with unexplained haemoptysis. Hyponatraemia/SIADH alone is not an NG12 criterion but lowers the threshold for chest imaging Urgent CXR (NG12) aged 40+ with ≥2 of cough, fatigue, breathlessness, chest pain, weight loss, appetite loss — or ≥1 if ever smoked
When NOT to investigate
Do NOT measure ADH (AVP) — not routinely available or clinically useful in primary care
Do NOT order bone marrow biopsy in primary care
Avoid delay: treat first, investigate concurrently if severely symptomatic
Monitoring sodium
Monitoring frequency should depend on the sodium level, symptoms, cause, treatment and rate of change. Recheck promptly after stopping a likely causative medicine, changing fluid intake or starting treatment. Na⁺ <130 mmol/L, unexplained hyponatraemia, recurrent falls, symptoms or a falling trend need closer follow-up and usually specialist advice.
The combination of urine Na⁺ and urine osmolality defines the differential when interpreted alongside clinical volume status — this is the diagnostic workup for hyponatraemia. TFTs and 9am cortisol are mandatory in euvolaemic hyponatraemia: hypothyroidism and adrenal insufficiency both cause dilutional hyponatraemia and are potentially life-threatening if missed but entirely treatable. Serum urate below 0.24 mmol/L is a supportive criterion for SIADH because ADH promotes urate excretion. SCLC (small cell lung cancer) is a classic cause of SIADH via ectopic ADH production and must be screened for with CXR in all new SIADH without obvious cause — SIADH is not itself an NG12 criterion, but the NICE NG12 (updated April 2026) urgent chest X-ray and lung cancer referral routes apply if there are associated symptoms or X-ray findings. Collecting urine before IV saline is critical: even one litre of IV fluid washes out the urine sodium result, making it uninterpretable.
6
Refer
Referral Criteria — When to Escalate & to Whom
Most moderate/severe hyponatraemia requires hospital management. Only mild chronic stable cases with clear reversible cause are suitable for primary care alone.
999
Seizures, GCS ≤14, respiratory distress, signs of herniation
Na⁺ <120 mmol/L with neurological symptoms, acute onset or a rapidly falling sodium
Haemodynamic instability (SBP <90 or postural collapse)
Acute hyponatraemia (<48h) with neurological features
Suspected adrenal crisis
Moderately severe symptoms attributable to hyponatraemia at any sodium level (confusion, headache, nausea without vomiting) — emergency admission
Symptomatic postoperative, exercise-associated, MDMA-associated, bowel-preparation-associated or water-intoxication hyponatraemia
Same-day medical admission
Na⁺ <120 mmol/L (even if asymptomatic) — urgent same-day hospital/acute medical assessment
Na⁺ <125 mmol/L, even if well (NICE CKS); rapidly falling sodium or known onset within 48 hours
Inability to maintain oral intake (vomiting or postural collapse → 999, as above)
Significant hypokalaemia, malnutrition, alcohol dependence or liver disease alongside hyponatraemia
Recurrent or worsening hyponatraemia despite stopping an offending drug
Suspected adrenal insufficiency (postural hypotension, hyperpigmentation, K⁺ elevated) — 999 if adrenal crisis
Acute-on-chronic hyponatraemia with worsening trajectory
Hypervolaemic hyponatraemia (HF, cirrhosis, nephrotic) — complex fluid management
Urgent (days–1 week)
Na⁺ 120–124 mmol/L: same-day hospital assessment even if stable, chronic and asymptomatic (NICE CKS; see same-day list above)
Na⁺ 125–129 mmol/L: same-day face-to-face assessment, with bloods sent before any treatment and specialist advice; repeat Na⁺ within 24–48 hours — hospital assessment if symptomatic, acute, worsening, significant comorbidity or cause unclear; stable chronic cases may be managed with specialist advice and close follow-up
New SIADH with no obvious cause — urgent to rule out malignancy
Intermediate 8–9 am cortisol (interpret against NICE NG243 and local assay) → endocrinology advice and/or dynamic testing
Severe hypothyroidism suspected as the cause (check TSH and free T4)
Suspected cancer route — NICE NG12 (updated April 2026)
Aged 40+ → urgent chest X-ray with ≥2 of cough, fatigue, shortness of breath, chest pain, weight loss or appetite loss, or ≥1 if ever smoked; consider urgent chest X-ray for persistent/recurrent chest infection, clubbing, supraclavicular/persistent cervical lymphadenopathy, chest signs suggestive of lung cancer or thrombocytosis. Hyponatraemia/SIADH alone is not an NG12 criterion but lowers the threshold for chest imaging
Weight loss + new hyponatraemia (SCLC, pancreatic, other)
Unexplained visible haematuria aged 45+ (NG12 renal/bladder criterion)
Chest X-ray suggesting lung cancer (mass / lymphadenopathy) → suspected cancer pathway (NG12)
Aged 40+ with unexplained haemoptysis → suspected cancer pathway (NG12)
Clinically well, mild, stable, usually chronic hyponatraemia (Na⁺ generally ≥130 mmol/L), no neurological symptoms, clear reversible cause (e.g. stop offending drug)
Overt hypothyroidism — treat according to the thyroid-disease pathway; recheck Na⁺
Post-gastroenteritis recovery, clearly reversible cause, Na⁺ normalising Requires reliable follow-up, a documented repeat blood-test plan and clear safety net
The referral thresholds are based on the European Clinical Practice Guidelines (Spasovski et al. 2014, international), which stratify management by symptom severity, not sodium level alone. Na⁺ <120 mmol/L generally warrants urgent same-day hospital assessment because the risk of deterioration, and of rapid correction causing osmotic demyelination syndrome (ODS), requires careful monitored correction that cannot be delivered safely in primary care. The urgent CXR threshold reflects SCLC's strong association with SIADH — it is the most common paraneoplastic cause. Confirmed new SIADH in a smoker over 40 should be treated as SCLC until proven otherwise. Addisonian crisis is life-threatening and requires immediate IM or IV hydrocortisone — if suspected, do not wait for cortisol results.
7
Treat
Treatment Pathway — Tailored to Cause & Severity
Treatment is entirely cause-specific. There is no universal approach. Correction rate is the most critical factor — in chronic or unknown-duration hyponatraemia avoid a rise of more than 10 mmol/L in the first 24 hours, then 8 mmol/L in each further 24 hours (18 mmol/L in 48 hours); slower still if high risk (SfE 2022). These are maximum limits, not targets.
Severe symptoms (seizure/coma) — Hospital
3% NaCl (Hypertonic saline) Hospital only
Severe or moderately severe neurological symptoms attributable to hyponatraemia: 150 mL IV over 20 min according to the local emergency protocol, in a monitored setting (resus/HDU/ICU). May be repeated (European guideline: up to twice), with reassessment after each bolus, until symptoms improve or Na⁺ rises by about 5 mmol/L. The aim is symptom improvement, not normalisation. 999 is the transfer route — never given in primary care.
Hypovolaemic — Dehydration / GI loss
Oral rehydration (stable) / IV crystalloid in hospital 1st line
If shocked or haemodynamically unstable, call 999 and transfer for monitored IV crystalloid resuscitation. In a stable patient who can drink, oral rehydration may be appropriate while arranging urgent assessment. Stop thiazide diuretic. Once volume is restored, suppressed vasopressin may cause a brisk water diuresis and rapid sodium correction — monitor closely.
SIADH — Mild–moderate, chronic
Fluid restriction 1st line
Commonly first-line for persistent SIAD when clinically appropriate. Individualise to urine output, urine osmolality, comorbidity, thirst, nutritional intake and the likely ability to achieve a negative electrolyte-free water balance — not a generic 500 mL/day instruction without specialist input. Advise patient this includes all drinks. Remove offending drug first.
Hypervolaemic (HF/cirrhosis)
Treat underlying cause (specialist-led) Specialist
Treat the underlying heart failure, cirrhosis, nephrotic syndrome or renal failure with specialist input. Avoid reflexive IV fluids. Diuretic and fluid strategies must be individualised to renal function, congestion and specialist plans.
Step 1Remove the cause: Stop thiazide, SSRI, or other offending drug. Check TSH and free T4 and treat overt hypothyroidism according to the thyroid-disease pathway — do not prescribe a standard levothyroxine dose solely to correct sodium without considering age, cardiac disease, TSH/free T4 and specialist advice. Suspected adrenal crisis is an emergency: give IM or IV hydrocortisone immediately if trained and authorised, arrange ambulance transfer, and treat shock with IV 0.9% sodium chloride according to the emergency protocol — do not delay treatment for cortisol testing. Review and stop unnecessary PPIs, carbamazepine.
Step 2SIADH — Fluid restriction: Individualised volume (not a fixed 500–1000 mL/day without specialist input). Explain clearly to patient — include tea, coffee, soup, fruit juice. Review response at 1 week. If Na⁺ not improving consider urine-to-plasma osmolality ratio (if >1, restriction alone unlikely to work).
Step 3SIADH refractory — Urea (oral): 15–30 g daily in water or juice. Increases solute excretion, allows water loss. May be considered by renal/endocrine specialists when fluid restriction is ineffective or poorly tolerated. Requires monitoring for over-correction and tolerability. Specialist only
Step 4SIADH refractory — Demeclocycline: Not a routine primary-care treatment — avoid initiating it in primary care; discuss with renal/endocrine medicine if considered. The European guideline advises against it in chronic SIAD (variable efficacy, nephrotoxicity) and the local formulary restricts it for new patients. Specialist only
Step 5Vaptans (Tolvaptan): Selective V2-receptor antagonist. Rapidly raises Na⁺ in SIADH/hypervolaemic. Hospital initiation ONLY — risk of over-rapid correction. Never initiate in primary care. Specialist initiation, close early sodium monitoring, hepatotoxicity considerations and local commissioning restrictions apply. Not a treatment for emergency symptomatic hyponatraemia.
🏥 Over-correction (hospital only): If sodium is rising faster than intended or exceeds the correction limit — stop active sodium-raising treatment; seek urgent renal/endocrine/critical-care advice; consider electrolyte-free water (usually IV dextrose) and/or desmopressin to stop ongoing water diuresis; monitor sodium and urine output frequently.
⚠️ Correction limits (maximum, not targets): In chronic or unknown-duration hyponatraemia avoid a rise in Na⁺ of more than 10 mmol/L in the first 24 hours or 18 mmol/L in the first 48 hours. In patients at high risk of osmotic demyelination (alcohol dependence, malnutrition, advanced liver disease, hypokalaemia or very low sodium) correct more slowly still, with specialist oversight (SfE 2022: no more than 10 mmol/L in the first 24 hours, then 8 mmol/L in each further 24 hours). For chronic mild hyponatraemia, active correction may offer no proven benefit and can cause harm — treat the cause. Exceeding these limits risks osmotic demyelination syndrome — irreversible brainstem injury, quadriplegia, locked-in syndrome.
The rate-of-correction rule is the single most important principle in hyponatraemia management. Osmotic demyelination syndrome (ODS) occurs when chronically hyponatraemic cells (which have adapted by extruding osmoles) are suddenly exposed to rising osmolality — myelin sheaths are destroyed, particularly in the central pons. The mortality is 10–25% and survivors often have permanent disability. The European Guidelines (2014) set maximum limits of 10 mmol/L in the first 24 hours and 18 mmol/L in 48 hours. For SIADH, fluid restriction remains first-line because it addresses the core pathophysiology (impaired water excretion) without the risks of drug therapy. However, compliance is poor (only ~50% effective) and it takes 1–2 weeks to show effect — urea may be considered by specialists as a second-line option, while the European guideline advises against demeclocycline. Tolvaptan is effective but was associated with hepatotoxicity in trials and must never be used in primary care. Drug review is cost-free and highly effective — SSRIs cause hyponatraemia in up to 0.5% of users, disproportionately elderly women.
Lifestyle modification is primary treatment in SIADH and preventive strategy in all causes. Patient education dramatically reduces re-admission rates.
Fluid restriction (SIADH) Individualised TOTAL daily limit agreed with the clinician (specialist input before very tight restriction). Include all fluids — water, tea, coffee, soup, fruit. Write it down, use a measured jug. Reduces Na⁺ dilution. Most effective when urine:plasma osmolality ratio <1.
Avoid hypotonic drinks Water, squash, fruit juice are hypotonic — worsen SIADH. Full-fat milk, vegetable juice have higher solute load.
Dietary sodium Ensure a normal dietary sodium and solute intake in SIADH, but do not advise increased salt as a universal intervention — it may not correct SIAD and can worsen oedema or hypertension in heart failure/cirrhosis. Hypovolaemic patients: oral rehydration and electrolyte drinks during recovery.
Alcohol reduction Beer potomania: beer is very low in solute. Heavy beer drinkers develop severe hyponatraemia from low solute intake + high fluid load. Reduce alcohol and ensure adequate nutrition.
Medication review Lifestyle action: do not restart stopped thiazide without sodium monitoring. Carry a medication list. Inform all future prescribers of hyponatraemia history before adding new medications.
Fall prevention Hyponatraemia doubles the risk of falls — even mild chronic hyponatraemia causes gait instability and cognitive impairment. Refer to falls service if Na⁺ <130 mmol/L and falls history.
Exercise caution Marathon runners and endurance athletes: overhydration with water is a major cause of acute severe hyponatraemia. Advise drinking to thirst, not to a schedule, during prolonged exercise — sports drinks are still hypotonic and do not prevent hyponatraemia if drunk in excess.
MDMA awareness MDMA causes SIADH + polydipsia — most common cause of acute severe hyponatraemia in young people. Non-judgemental advice: do not drink excessive water on MDMA — sip fluids rather than drinking large volumes.
Weigh daily (HF/cirrhosis) Daily weights allow early detection of fluid retention. Advise: if weight increases by >2 kg in 2 days → contact GP same day.
Patient information card Provide written information about hyponatraemia, correction rate risks, and symptoms to report. Hyponatraemia UK patient resources available. Especially important if taking vaptans or post-hospital discharge.
Fluid restriction is commonly first-line treatment for persistent SIAD when clinically appropriate, but it should be individualised according to urine output, urine osmolality, comorbidity, thirst, nutritional intake and the likely ability to achieve a negative electrolyte-free water balance — not prescribed as a generic fixed volume without specialist input. Adherence is often poor, which is why patient education is critical. The falls risk associated with hyponatraemia is often underappreciated: a case-control study (Renneboog et al., Am J Med 2006) found that 21% of patients with apparently asymptomatic chronic hyponatraemia (mean Na⁺ 126 mmol/L) had fallen, against 5% of controls, with attention and gait deficits comparable to those produced by alcohol. This makes Na⁺ monitoring in elderly fallers a mandatory part of assessment. Beer potomania is increasingly recognised: craft beer consumption has increased and low-protein diets exacerbate the condition. The clinical lesson is that any patient with chronic heavy beer consumption and unexplained hyponatraemia has this diagnosis until proven otherwise.
Monitoring frequency depends on severity and trajectory. Undermonitoring risks missing ODS or worsening hyponatraemia. Safety-netting is mandatory at every contact.
In-hospital correction (specialist)
U&Es every 4–6 hours until stable. Stop active treatment if Na⁺ rises faster than intended or exceeds the correction limit. If over-corrected → expert-directed electrolyte-free fluid and/or desmopressin
Post-hospital discharge
Interval specified in the discharge plan — within 1 week is reasonable for many, but sooner after active correction, a medication change, persistent AKI or ongoing fluid instability. Check the discharge summary's "Cause of hyponatraemia and treatment plan" section — request it from the hospital team if missing. Confirm cause has been addressed. Summarise correction rate achieved.
Drug-induced (mild, primary care)
Recheck U&Es promptly after stopping the offending drug, timed to the sodium level, symptoms and trend. If normalised → periodic review. If persistent → investigate SIADH cause.
Stable chronic SIADH
Frequency individualised to sodium level, symptoms, cause, treatment and rate of change, usually with specialist advice; widen intervals once Na⁺ stable >130 mmol/L. Annual review of underlying cause.
Hypothyroidism-related
Recheck Na⁺ and TFTs after starting levothyroxine, per the thyroid pathway. If Na⁺ does not improve, look for another cause — mild hypothyroidism is an uncommon cause of significant hyponatraemia.
Cortisol-related
Recheck U&Es after starting hydrocortisone, as advised by endocrinology. If Na⁺ does not improve, reconsider the cause. Ensure patient has sick-day rules card and wears medical alert bracelet.
Heart failure / cirrhosis
Monitoring frequency per the specialist plan, renal function and congestion; recheck U&Es promptly after diuretic changes. On ACE inhibitors/ARBs, SPS advises specialist advice if Na⁺ <132 mmol/L. Weight diary. Specialist team lead.
Monitoring targets
Limits, not targets: no more than 10 mmol/L in 24h or 18 mmol/L in 48h (then 8 mmol/L per further 24h; slower still if high risk of ODS) Stop active treatment if: Na⁺ rising faster than intended or exceeds the limit — urgent specialist advice Chronic mild: treat the cause and avoid iatrogenic over-correction — normalisation is not always required
999 — Safety net A fit, collapse or fainting, unusual drowsiness or being hard to wake, new or worsening confusion, a severe headache, vomiting, or breathing difficulty. Any acute neurological deterioration after treatment started.
Same-day GP or 111 — Safety net Feeling sick, dizziness on standing, unsteadiness or new falls, muscle cramps, cannot keep up with fluids (diarrhoea, poor intake).
Urgent same-day GP — Safety net Worsening nausea, very thirsty with little or no urine, sticking to the fluid limit becoming impossible. Attend the repeat blood test even if well.
Re-refer if Na⁺ falls below 125 mmol/L again (same-day assessment), new neurological symptoms appear (999), suspected malignancy emerges (NG12 route), or the cause remains unexplained after the first-line workup (endocrinology).
⚠️ Remote and out-of-hours results: volume status cannot be assessed by telephone, so Na⁺ below 130 mmol/L needs a face-to-face examination. Convert to face-to-face or emergency assessment if the patient cannot attend, has vomiting, diarrhoea or poor intake, a relative reports confusion or other cognitive change, or the result arrives out of hours with no one able to act.
📋 Discharge summary — "Cause of hyponatraemia and treatment plan" section: every discharge summary should contain a dedicated section stating the cause of hyponatraemia and the treatment plan (drugs stopped or changed, any fluid restriction, specialist follow-up) and the interval for the next sodium check. Discharge checklist: lowest Na⁺ achieved, maximum correction rate used, target monitoring schedule, and which symptoms require emergency attendance. Medication changes documented in summary letter.
Readmission after hyponatraemia is common, particularly in elderly patients on thiazides, SSRIs, or with HF/cirrhosis. The post-discharge monitoring interval should be specified in the discharge plan alongside the cause of hyponatraemia and treatment plan — within one week is reasonable for many patients but may be too slow after active correction, a medication change, persistent AKI or ongoing fluid instability. The correction rate monitoring is critical even in the recovery phase: paradoxically, if the underlying cause (e.g. SIADH) resolves rapidly after an intervention (e.g. stopping the offending drug), the sodium may rise too fast on its own. In this situation, patients may require deliberate re-lowering with DDAVP (desmopressin) to slow correction — this happens in hospital. In primary care, monitoring tailored to the sodium level, cause and trend helps ensure that patients with reversible causes do not inadvertently have their Na⁺ over-corrected in the community. The safety-netting around falls is often omitted but is evidence-based: a retrospective study (Kinsella et al., Clin J Am Soc Nephrol 2010) found hyponatraemia associated with fractures independent of osteoporosis — even mild hyponatraemia increases fracture risk through falls, making this a bone health issue as much as a metabolic one.
⚡ Snapshot. The whole pathway on one page: act now, triage, classify, treat today and safety-net. The Steps tab holds the detail.
Educational use only. Pathway based on: European Clinical Practice Guidelines for Hyponatraemia (Spasovski et al. 2014, endorsed ESICM/ERA-EDTA; international) · Society for Endocrinology Endocrine Emergency Guidance (2022) · NICE NG243 (Adrenal insufficiency) · NICE NG12 (Suspected cancer) · NICE CG174 (IV fluids in adults) · Local formulary · Renneboog et al. Am J Med 2006 (falls & hyponatraemia); Kinsella et al. Clin J Am Soc Nephrol 2010 (fractures). Always adapt to individual patient context and local formulary. Drug-induced hyponatraemia: consult local endocrine/renal guidelines. Version 1.0 · Reasoning GP 2024.