approach to hyponatraemia

Na⁺ <135 mmol/L. The algorithm is: confirm true hyponatraemia (exclude pseudohyponatraemia and translocational) → assess volume status → measure urine Na and urine osmolality. Most cases are either SIADH (euvolaemic, concentrated urine, urine Na >30) or diuretic-induced (hypovolaemic, urine Na >20 from the diuretic itself). Correction speed is more dangerous than the sodium itself.

do not miss

seizures or obtundation → give 100 mL 3% NaCl bolus over 10 min, repeat up to 3× — do not wait for labs
Na⁺ <120 mmol/L with any neurological symptom → hypertonic saline urgently
overcorrection (>10 mmol/L in 24 h) → osmotic demyelination syndrome; re-lower with D5W ± desmopressin if overcorrecting

the algorithm

step 1 — confirm true hypotonic hyponatraemia

Measure serum osmolality
Low (<275 mOsm/kg) → true hypotonic hyponatraemia → proceed
Normal (275–295) → pseudohyponatraemia (hyperproteinaemia, hyperlipidaemia — lab artefact with indirect ion-selective electrode methods)
High (>295) → translocational — glucose or mannitol pulling water into the ECF. Corrected Na⁺ = measured Na⁺ + 2.4 × (glucose − 5.5) / 5.5 (SI units, mmol/L glucose)

step 2 — assess volume status

hypovolaemic	euvolaemic	hypervolaemic
orthostasis, dry mucosae, tachycardia, ↑ urea:Cr ratio	clinically euvolaemic (no oedema, no dehydration)	oedema, ascites, JVP elevated
GI losses, diuretics, adrenal insufficiency, cerebral salt wasting	SIADH, hypothyroidism, cortisol deficiency, low solute intake (“tea and toast”)	heart failure, cirrhosis, nephrotic syndrome, advanced CKD

volume status is hard

Clinical assessment of volume status is inaccurate in ~50% of cases. Urine Na and urine osmolality are more reliable discriminators than clinical exam alone — always send them.

step 3 — urine studies

	urine osmolality	urine Na
SIADH	>100 mOsm/kg (inappropriately concentrated)	>30 mmol/L
hypovolaemic	>500 mOsm/kg (maximally concentrated)	<20 mmol/L (renal Na conservation)
diuretic-induced	variable	>20 mmol/L (diuretic effect — misleading)
hypervolaemic (HF, cirrhosis)	>300 mOsm/kg	<20 mmol/L (low effective circulating volume)
low solute intake	<100 mOsm/kg (dilute)	<20 mmol/L

SIADH — the most common cause in hospital

Diagnosis requires: hypotonic hyponatraemia, urine osmolality >100, urine Na >30, euvolaemia, normal thyroid and cortisol, no diuretics.

Common causes: malignancy (lung small cell), CNS (SAH, meningitis, trauma), drugs (SSRIs, carbamazepine, cyclophosphamide, oxytocin), pulmonary disease (pneumonia, TB), post-operative (pain, nausea, anaesthesia all stimulate ADH).

management

severe symptoms (seizures, obtundation)

Hypertonic saline (3% NaCl) — 100 mL IV bolus over 10 min. Can repeat twice at 10-min intervals (total 300 mL). Target: raise Na⁺ by 4–6 mmol/L in the first 1–2 h to arrest symptoms.

correction rate limits

≤10 mmol/L in 24 h and ≤18 mmol/L in 48 h — European guidelines suggest ≤8 mmol/L per 24 h for high-risk patients (Na⁺ <120, hypokalaemia, alcoholism, malnutrition, liver disease)
If overcorrecting → D5W infusion ± desmopressin 2 µg IV q8h to re-lower sodium

by cause

Hypovolaemic → isotonic saline. Na⁺ often self-corrects rapidly once volume restored — monitor closely for overcorrection.
SIADH → fluid restriction (typically <1 L/day). If refractory: salt tablets ± loop diuretic (increases free water excretion), or consider tolvaptan. EMPA-SIAD (JAMA 2023) showed empagliflozin raised sodium by ~5 mmol/L via osmotic diuresis — a potential alternative, though not yet guideline-endorsed.
Hypervolaemic → treat the underlying cause (diuresis for HF, sodium and fluid restriction for cirrhosis). Fluid restriction.

tolvaptan risk

Vaptans carry a risk of overly rapid correction. Do not use in hypovolaemic hyponatraemia (worsens volume depletion). Requires inpatient initiation with frequent Na⁺ monitoring (q6h for first 24 h). Hepatotoxicity limits long-term use — avoid in liver disease.

traps

Diuretic-induced hyponatraemia looks euvolaemic — thiazides are worse than loops because they impair free water excretion without washing out the medullary gradient. A “SIADH” diagnosis in a patient on hydrochlorothiazide is often wrong.
Cortisol deficiency mimics SIADH perfectly — always check a morning cortisol before diagnosing SIADH. ADH is tonically inhibited by cortisol; without it, ADH rises.
Hypothyroidism as a cause is overstated — only severe myxoedema causes hyponatraemia. Mild TSH elevation is not the explanation for a low sodium.
Saline can worsen SIADH — isotonic saline in a patient with SIADH and urine osmolality >500 leads to net free water retention and a further drop in Na⁺. The kidneys keep the urine concentrated and excrete the Na⁺, retaining the water.
Rapid K⁺ correction raises Na⁺ — potassium is an effective osmole. Aggressive K⁺ repletion counts toward the Na⁺ correction rate. A patient getting 40 mmol/h KCl plus hypertonic saline can overcorrect before you notice.

hyponatraemia