Hyponatraemia
Most common electrolyte disorder, defined as serum sodium <135 mmol/L, requiring systematic assessment of volume status and osmolality to guide management.
Key Facts
Hyponatraemia (Na <135 mmol/L) is the most common electrolyte disturbance in hospitalised patients, affecting up to 30% Classified by volume status: hypovolaemic, euvolaemic (most commonly SIADH), hypervolaemic (heart failure, cirrhosis, nephrotic syndrome) SIADH is the most common cause of euvolaemic hyponatraemia; diagnose by exclusion (normal thyroid, adrenal, renal function) Acute symptomatic hyponatraemia (<48h): treat urgently with hypertonic saline (3% NaCl) to raise Na by 1-2 mmol/L/hour initially Chronic hyponatraemia: correct no faster than 8-10 mmol/L in 24 hours to avoid osmotic demyelination syndrome (ODS) Fluid restriction (750-1000mL/day) is first-line for SIADH Common causes: thiazide diuretics, SSRIs, SIADH (lung/CNS pathology), Addison disease, hypothyroidism
Overview
Key Facts
Hyponatraemia is the most frequently encountered electrolyte abnormality in clinical practice. It ranges from mild and asymptomatic to acutely life-threatening. A systematic approach to diagnosis based on osmolality and volume status is essential.
Epidemiology
- Present in 15-30% of hospitalised patients (mild); 5% have Na <130 mmol/L
- More common in elderly, patients on diuretics, and those with chronic diseases
- Associated with increased hospital length of stay and mortality
Aetiology
Hypovolaemic (low total body water and sodium):
- Vomiting, diarrhoea
- Thiazide diuretics (most common drug cause)
- Addison disease (adrenal insufficiency)
- Cerebral salt wasting
- Burns
Euvolaemic (excess water relative to sodium):
- SIADH (most common cause of euvolaemic hyponatraemia)
- Hypothyroidism (severe)
- Psychogenic polydipsia
- Drugs: SSRIs, carbamazepine, cyclophosphamide
Hypervolaemic (excess total body water > sodium):
- Heart failure
- Cirrhosis
- Nephrotic syndrome
- CKD
Pathophysiology
- Hyponatraemia reflects relative excess of water to sodium
- True hyponatraemia is associated with low serum osmolality (<275 mOsm/kg)
- Pseudohyponatraemia: normal osmolality with high lipids/proteins
- Hypertonic hyponatraemia: high osmolality due to glucose (each 5.6 mmol/L glucose rise → ~2.4 mmol/L fall in sodium)
- In SIADH: ADH secretion is inappropriate → water retention, dilutional hyponatraemia, concentrated urine
Clinical Presentation
Mild Hyponatraemia (130-134 mmol/L)
- Often asymptomatic
- Subtle cognitive impairment, increased fall risk in elderly
- May have gait disturbance
Moderate Hyponatraemia (125-129 mmol/L)
- Nausea, headache
- Confusion, disorientation
- Muscle cramps, weakness
Severe Hyponatraemia (<125 mmol/L)
- Seizures
- Reduced consciousness, coma
- Respiratory arrest (brainstem herniation)
Red Flags
- Acute symptomatic hyponatraemia (<48h with seizures/reduced consciousness) → medical emergency
- Post-operative hyponatraemia → common and potentially dangerous
- Features of adrenal crisis (hypotension, hyperkalaemia) → urgent Synacthen test
- Rapid correction → risk of osmotic demyelination syndrome (ODS)
Differential Diagnosis
| Diagnosis | Key Features | Investigation |
|---|---|---|
| SIADH | Euvolaemic, concentrated urine, low serum osmolality | Paired serum/urine osmolality, urinary Na |
| Addison disease | Hyperkalaemia, postural hypotension, hyperpigmentation | Short Synacthen test |
| Hypothyroidism | Fatigue, weight gain, dry skin | TFTs |
| Heart failure | Dyspnoea, oedema, raised JVP | BNP, echocardiography |
| Cirrhosis | Jaundice, ascites, spider naevi | LFTs, USS liver |
| Psychogenic polydipsia | Psychiatric history, low urine osmolality (<100) | Fluid balance, urine osmolality |
Diagnosis / Investigation
Bedside
- Volume status assessment: JVP, skin turgor, mucous membranes, oedema, postural BP
- Fluid balance chart review
- Drug history: thiazides, SSRIs, carbamazepine
Bloods
- Serum sodium: confirm hyponatraemia and severity
- Serum osmolality: low (<275 mOsm/kg) confirms true hyponatraemia
- Urine osmolality: >100 mOsm/kg suggests impaired water excretion
- Urine sodium: >30 mmol/L suggests renal sodium loss (SIADH, diuretics, Addison); <30 mmol/L suggests extrarenal loss (vomiting, diarrhoea)
- TFTs: exclude hypothyroidism
- 9am cortisol/Short Synacthen test: exclude adrenal insufficiency
- Glucose: exclude hyperglycaemic hyponatraemia
- Lipid profile, protein: exclude pseudohyponatraemia
Special Tests
- Paired serum and urine osmolality with urine sodium: essential for aetiological diagnosis
- BNP/NT-proBNP: if heart failure suspected
- CT head/chest: if SIADH suspected (identify underlying cause – lung cancer, CNS pathology)
SIADH Diagnostic Criteria
- Serum osmolality <275 mOsm/kg
- Urine osmolality >100 mOsm/kg (inappropriately concentrated)
- Urine sodium >30 mmol/L (usually >40)
- Euvolaemic
- Normal thyroid, adrenal, renal function
- No diuretics
Management
Acute Symptomatic Hyponatraemia (seizures, reduced consciousness)
- Hypertonic saline (3% NaCl): 100-150mL IV over 20 minutes, can repeat x2
- Aim to raise Na by 4-6 mmol/L in first 6 hours (sufficient to reduce cerebral oedema)
- Monitor Na every 2-4 hours
- Do not exceed 8-10 mmol/L correction in 24 hours
Chronic/Asymptomatic Hyponatraemia
Treat underlying cause:
- Hypovolaemic: IV 0.9% NaCl (restore volume)
- Euvolaemic (SIADH):
- Fluid restriction 750-1000 mL/day (first-line)
- Demeclocycline 600-1200mg daily (ADH antagonist – rarely used now)
- Tolvaptan 15mg OD (vasopressin V2 receptor antagonist – specialist initiation only, monitor Na closely due to risk of overcorrection)
- Treat underlying cause of SIADH
- Hypervolaemic: fluid restriction + treat underlying cause (diuretics for HF, spironolactone for cirrhosis)
- Drug-induced: withdraw offending drug (thiazides, SSRIs)
- Adrenal insufficiency: hydrocortisone replacement
Preventing Osmotic Demyelination Syndrome (ODS)
- Correct Na by ≤8-10 mmol/L in first 24 hours and ≤18 mmol/L in first 48 hours
- High-risk patients (Na <105, alcoholism, malnutrition, hypokalaemia): limit to 6 mmol/L in 24 hours
- If over-corrected: desmopressin 2 mcg IV + 5% dextrose to lower Na back down
Referral Criteria
- Severe or symptomatic hyponatraemia → acute medicine/ITU
- Persistent SIADH requiring tolvaptan → endocrinology
- Suspected underlying malignancy → oncology
Prognosis
- Mild hyponatraemia: associated with increased fall risk and fractures in elderly, longer hospital stays
- Severe acute hyponatraemia: mortality up to 50% if untreated
- ODS: can cause permanent neurological damage (locked-in syndrome, quadriparesis) – develops 2-7 days after overly rapid correction
- SIADH prognosis depends on underlying cause (drug-induced = excellent; malignancy = poor)
- Chronic mild hyponatraemia associated with osteoporosis and cognitive impairment in elderly
Other Relevant Information
Diagnostic Algorithm
| Step | Test | Finding | Interpretation |
|---|---|---|---|
| 1 | Serum osmolality | <275 | True hyponatraemia |
| 2 | Urine osmolality | >100 | Impaired water excretion |
| 3 | Volume status | Clinical assessment | Hypo/eu/hypervolaemic |
| 4 | Urine sodium | >30 or <30 | Renal vs extrarenal loss |
Common Causes of SIADH
| Category | Examples |
|---|---|
| Malignancy | Small cell lung cancer (most common), lymphoma, pancreatic |
| CNS | Meningitis, encephalitis, SAH, head injury, stroke |
| Pulmonary | Pneumonia, TB, COPD, positive pressure ventilation |
| Drugs | SSRIs, carbamazepine, cyclophosphamide, PPIs, NSAIDs |
| Post-operative | Pain, nausea, anaesthetic agents |