Hyponatraemia — Diagnosis & Management
UK primary care pathway · Na⁺ <135 mmol/L · GP trainees & early-career GPs · SCA-ready
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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 dehydration / shock HR >120, SBP <90, postural collapse with low Na⁺ → 999. Hypovolaemic emergency.
⚠️ Acute vs chronic: Symptoms <48h = acute (high risk). Symptoms >48h or insidious onset = chronic (lower immediate risk, but correct TOO slowly and cause osmotic demyelination syndrome).
Acute hyponatraemia causes cerebral oedema as water shifts intracellularly — the brain cannot adapt fast enough. Mortality from severe acute hyponatraemia can reach 50% if seizures develop untreated. The European Clinical Practice Guidelines (Spasovski 2014, endorsed by ESICM/ERA-EDTA) 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 (>8–10 mmol/L/24h) risks osmotic demyelination syndrome (formerly central pontine myelinolysis), which is irreversible. Never normalise Na⁺ rapidly — it is more dangerous than the hyponatraemia itself.
Calculate: 2×Na⁺ + glucose + urea (mmol/L). Normal 275–295 mOsm/kg.
Low (<275): True hyponatraemia — hypotonic
Normal (275–295): Pseudohyponatraemia (high lipids/protein) or hyperglycaemia
High (>295): Hypertonic — hyperglycaemia, mannitol, contrast
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
High triglycerides (lipid displaces water in sample), hyperproteinaemia (myeloma), hyperglycaemia (every 1 mmol/L rise in glucose lowers Na⁺ by ~1.6 mmol/L)
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 needs careful outpatient correction.
3
Diagnose
Classification — Volume Status & Urine Results Determine the Cause
Once true hypotonic hyponatraemia is confirmed, classify by clinical volume status and urine sodium/osmolality. This defines the underlying cause and treatment.
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
All of: Na⁺ <135 + plasma hypo-osmolality <275 + urine osmolality >100 mOsm/kg + urine Na⁺ >30 mmol/L + clinically euvolaemic + normal TFTs + normal cortisol 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
📊 Quick classification rule: Urine Na⁺ <30 = kidney conserving salt (extra-renal loss OR dilutional). Urine Na⁺ >30 = kidney wasting salt inappropriately (renal cause or SIADH).
The volume status classification is the cornerstone of hyponatraemia management because it completely reverses treatment priorities. 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 defines volume status (treatment-critical) 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 determines which intravenous fluid (if any) is appropriate. 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: ataxia or confusion in a patient with mild sodium (e.g. 128 mmol/L) warrants 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.
Spot urine Na⁺ — <30 = appropriate conservation; >30 = inappropriate loss (SIADH or renal) Urine osmolality — <100 = psychogenic polydipsia / beer potomania; >100 = SIADH or renal cause 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, consider 2WW referral 2WW if weight loss + SIADH ≥40 years
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
If chronic stable mild hyponatraemia being managed in primary care: recheck U&Es every 4 weeks until stable, then 3-monthly.
The combination of urine Na⁺ and urine osmolality defines the differential with 85–90% accuracy 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) causes SIADH in up to 10–15% of cases via ectopic ADH production and must be screened for with CXR in all new SIADH without obvious cause — this is a NICE 2WW trigger. 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 ANY symptoms
Haemodynamic instability (SBP <90 or postural collapse)
Acute hyponatraemia (<48h) with neurological features
Same-day medical admission
Na⁺ <120 mmol/L (even if asymptomatic)
Moderate symptoms (nausea, confusion, headache) with any sodium level
Suspected Addisonian crisis (postural hypotension, hyperpigmentation, K⁺ elevated)
Acute-on-chronic hyponatraemia with worsening trajectory
Hypervolaemic hyponatraemia (HF, cirrhosis, nephrotic) — complex fluid management
Urgent (days–1 week)
Na⁺ 120–129 mmol/L, asymptomatic, chronic — urgent endocrine / medical OPA
New SIADH with no obvious cause — urgent to rule out malignancy
9am cortisol 100–400 nmol/L → urgent endocrine for short synacthen test
Suspected hypothyroidism causing hyponatraemia (TSH >10)
2WW Cancer Referral
SIADH in patient ≥40 years without clear benign cause
Weight loss + new hyponatraemia (SCLC, pancreatic, other)
Haematuria + hyponatraemia (renal cell carcinoma)
Abnormal CXR (mass / lymphadenopathy)
The referral thresholds are based on the European Clinical Practice Guidelines (2014) and NICE guidance, which stratify management by symptom severity, not sodium level alone. Na⁺ <120 mmol/L requires hospital admission universally because the risk of rapid correction causing osmotic demyelination syndrome (ODS) requires careful supervised correction that cannot be delivered safely in primary care. The 2WW threshold reflects SCLC's strong association with SIADH — it is the most common paraneoplastic cause, present in 5–15% of SCLC cases. Confirmed new SIADH in a smoker over 40 should be treated as SCLC until proven otherwise. Addisonian crisis is life-threatening and requires immediate 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 — never exceed 8–10 mmol/L per 24 hours (maximum 18 mmol/L in 48 hours) to avoid osmotic demyelination syndrome.
Severe symptoms (seizure/coma) — Hospital
3% NaCl (Hypertonic saline) 999
150 mL IV bolus over 20 min. Repeat up to 3× until symptoms improve. Target: raise Na⁺ by 5 mmol/L acutely. ICU/HDU monitoring. Do NOT use in primary care.
Hypovolaemic — Dehydration / GI loss
0.9% NaCl IV / oral rehydration 1st line
Replace fluid deficit. 0.9% NaCl IV if unable to take orally. Stop thiazide diuretic. Sodium corrects as volume restored. Monitor 4–6 hourly.
SIADH — Mild–moderate, chronic
Fluid restriction 1st line
500–1000 mL/day total fluid intake. Advise patient this includes all drinks. Takes days to weeks to work. Remove offending drug first.
Hypervolaemic (HF/cirrhosis)
Treat underlying cause + fluid restriction Specialist
HF: optimise diuretics (specialist-guided). Cirrhosis: terlipressin + albumin if hepatorenal. Tolvaptan consideration in hospital only.
Step 1Remove the cause: Stop thiazide, SSRI, or other offending drug. Treat hypothyroidism (levothyroxine 25–50 mcg OD, titrate). Replace cortisol if Addisonian (hydrocortisone 10 mg AM / 5 mg noon / 5 mg PM). Review and stop unnecessary PPIs, carbamazepine.
Step 2SIADH — Fluid restriction: 500–1000 mL/day total. 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. Evidence from European Guidelines. Cheap, effective, well-tolerated. Specialist initiation recommended
Step 4SIADH refractory — Demeclocycline: 300–600 mg BD (reduces renal response to ADH). Used less often due to nephrotoxicity risk. Monitor renal function. 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. Ongoing specialist monitoring required.
⚠️ Rate of correction rule: Raise Na⁺ by maximum 8–10 mmol/L per 24 hours. In high-risk patients (alcoholism, malnutrition, hypokalaemia) limit to 6–8 mmol/L per 24 hours. Exceeding this 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) reduced the 24-hour correction limit from 12 to 8 mmol/L based on case series data. 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 is increasingly favoured in Europe as a second-line option before 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) 500–1000 mL/day TOTAL intake. 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. Advise: eat sodium-containing foods with fluid intake. Full-fat milk, vegetable juice have higher solute load.
Dietary sodium optimisation Do NOT restrict salt in SIADH patients. Adequate dietary sodium supports correction. Hypovolaemic patients: actively encourage salty foods, electrolyte drinks during recovery.
Alcohol reduction Beer potomania: beer is extremely hypotonic (<3 mOsm/L). 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 isotonic sports drinks, not excess water, during prolonged exercise (>4 hours).
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. Isotonic fluid preferred.
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 not merely advisory — it is the primary pharmacological-equivalent treatment for SIADH. A Cochrane review found that strict fluid restriction (≤1 L/day) is the most effective non-drug intervention for chronic SIADH. However, adherence in practice is only ~50%, which is why patient education is critical. The falls risk associated with hyponatraemia is often underappreciated: a systematic review (Kinsella 2010) demonstrated that chronic mild hyponatraemia (Na⁺ 130–135 mmol/L) is independently associated with 3× increased fall rate, impaired attention and gait stability — equivalent to being intoxicated. 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 correction if Na⁺ rises faster than 10 mmol/L/24h. If over-corrected → DDAVP + D5W to re-lower Na⁺
Post-hospital discharge
U&Es within 1 week of discharge. Then weekly until Na⁺ stable. Confirm cause has been addressed. Summarise correction rate achieved.
Drug-induced (mild, primary care)
U&Es at 2 weeks after stopping offending drug. If normalised → 3-monthly for 1 year. If persistent → investigate SIADH cause.
Stable chronic SIADH
U&Es every 4 weeks initially, then 3-monthly once Na⁺ stable >130 mmol/L. Annual review of underlying cause.
Hypothyroidism-related
Recheck Na⁺ and TFTs at 4–6 weeks after starting levothyroxine. Na⁺ should normalise with euthyroid state.
Cortisol-related
Recheck U&Es at 2 weeks after starting hydrocortisone. Na⁺ should normalise. Ensure patient has sick-day rules card and wears medical alert bracelet.
Heart failure / cirrhosis
Monitor U&Es monthly minimum. Diuretic changes require U&Es within 1 week. Weight diary. Specialist team lead.
Monitoring targets
Acceptable: Na⁺ rising 4–8 mmol/L per 24h Stop/reduce correction if: Na⁺ rises >10 mmol/L per 24h in hospital Target range (chronic stable): Na⁺ 130–135 mmol/L — do not push to normal if risk of ODS
999 — Safety net New seizure, GCS drop, inability to rouse, respiratory arrest. Any acute neurological deterioration after treatment started.
Same-day GP / 999 — Safety net Severe vomiting preventing fluid intake, postural collapse, confusion worsening, muscle cramps (may indicate electrolyte crisis).
Urgent same-day GP — Safety net New severe headache, worsening nausea, new falls, acute thirst with urine output stopping.
Re-refer if Na⁺ falls below 125 mmol/L again, new neurological symptoms appear, suspected malignancy emerges, cause remains unexplained after 3 months of primary care workup.
📋 Discharge checklist: Written summary of cause, lowest Na⁺ achieved, maximum correction rate used, target monitoring schedule, and which symptoms require emergency attendance. Medication changes documented in summary letter.
Hyponatraemia has a documented 30-day hospital readmission rate of up to 20% — predominantly in elderly patients on thiazides, SSRIs, or with HF/cirrhosis. Structured follow-up at 1 week post-discharge significantly reduces re-admission (NICE guidance on managing chronic disease). 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 every 2–4 weeks ensures 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 community study (Kinsella et al., BMJ 2010) demonstrated that even asymptomatic mild hyponatraemia significantly increases fracture risk through falls, making this a bone health issue as much as a metabolic one.
The full reasoning pathway — symptom severity (not the number) drives urgency; confirm the result, screen the emergency, then work serum osmolality → urine osmolality → volume status → urine sodium to a named cause, treat, exclude SIADH-related lung cancer, and safety-net.StartDecisionInvestigateActionReferStop / Admit
PresentationConfirmed Na⁺ <135 mmol/L
Repeat U&Es to exclude error / drip-arm contamination. Note onset (<48h = acute) and review the full drug list.
<125 = profound → ADMIT (or any symptoms: seizure, reduced GCS, vomiting, cardiorespiratory distress, acute fall). Mild 130–134 · moderate 125–129. If serum Na⁺ is dropping on repeat → discuss with medics with a view to admission.
YES — <125 or symptoms
Stop · AdmitADMIT for IV fluids + solutes
Do not attempt correction in the community; increasing oral fluids at home risks worsening hyponatraemia. Profound <125 / symptomatic
Send serum osmolality, urine osmolality and urine sodium on the same sample. Moderate 125–129 — consider discussing with medics.
Step 3 · interpret serum osmolality
≥ 275 mosm/kg
Discuss with medics todayNot true (hypotonic) hyponatraemia
High glucose, lipids or protein. Hyperglycaemia may signal a diabetic emergency — discuss with medics today.
< 275 — hypotonic
Investigate · Urine osmolalityUrine osm ≤100 vs >100
Urine osm ≤100: consider primary polydipsia / high water–low solute intake (anorexia, very restricted diet, beer potomania). >100: now look at urine sodium.
Investigate · Primary-care work-up (mild/moderate, stable, well)Treat & look for the underlying cause
If managing in primary care: stop non-essential fluids and fluid restrict (0.5–1.5 L/day), stop contributing medications, and repeat sodium (e.g. at 2 weeks if mild, well and medication altered — be guided by presentation; if not improving, refer). Bloods: U&Es, TFTs, LFTs, glucose/HbA1c, lipids, 9am cortisol, BNP, myeloma screen; urinalysis, CXR, consider CT chest/abdomen/pelvis.
new unexplained SIADH
Refer · Cancer exclusion 2WWNICE NG12Unexplained SIADH → exclude lung cancer (SCLC)
SIADH is a recognised paraneoplastic flag for small-cell lung cancer.
Offer an urgent direct-access chest X-ray (within 2 weeks) in people aged 40 and over with unexplained SIADH, unexplained weight loss, or other NG12 lung features (haemoptysis, persistent cough, chest signs, clubbing) — especially ever-smokers.
Refer via the suspected lung cancer pathway (2-week-wait) if the CXR suggests lung cancer, or for anyone aged 40+ with unexplained haemoptysis.
Consider CT chest if CXR normal but suspicion persists.
➕ Step 8 · Lifestyle & modifiable factors: in chronic SIADH/euvolaemic hyponatraemia, reinforce the agreed fluid restriction (0.5–1.5 L/day) and review high water–low solute patterns (anorexia, very restricted diets, beer potomania). Review and rationalise culprit drugs — SSRIs/SNRIs, thiazides, carbamazepine, PPIs, desmopressin. In the elderly, falls-risk review (hyponatraemia causes unsteadiness and fractures). Sick-day rules: hold thiazides/diuretics during D&V.
🔁 Step 9 · Monitoring & safety-net: recheck Na⁺ after the intervention (e.g. ~2 weeks if mild, well and a drug has been changed; sooner if borderline). Same-day / 999 if headache, nausea/vomiting, confusion, drowsiness, unsteadiness or seizure. If sodium keeps dropping despite measures → discuss with medics with a view to admission. Always recheck a fresh, non-drip-arm sample before acting on an unexpected result.
⚠️ Worsening triggers escalation (GEMS): Na⁺ <125 or symptoms → ADMIT; 125–129 → discuss with medics; serum osmolality ≥275 → discuss with medics today (?diabetic emergency). In hospital, raise Na⁺ by a maximum of 8–10 mmol/L per 24 h (6–8 if high-risk) to avoid osmotic demyelination. Increasing oral fluids at home risks worsening hyponatraemia.
Educational use only. Pathway based on: European Clinical Practice Guidelines for Hyponatraemia (Spasovski et al. 2014, endorsed ESICM/ERA-EDTA) · NICE CKS: Hyponatraemia · NICE CG108 (Chronic kidney disease) · BNF UK drug guidance · Kinsella et al. BMJ 2010 (falls & hyponatraemia). Always adapt to individual patient context and local formulary. Drug-induced hyponatraemia: consult local endocrine/renal guidelines. Version 1.0 · Reasoning GP 2024.