Overview
Hyponatraemia
1. Clinical Overview
Summary
Hyponatraemia is defined as Serum Sodium less than 135 mmol/L. It is the most common electrolyte abnormality in hospitalised patients (up to 30%). The clinical approach is based on Volume Status (Hypovolaemic, Euvolaemic, Hypervolaemic) and Osmolality. Severe hyponatraemia causes cerebral oedema and can be fatal. However, overly rapid correction can cause Osmotic Demyelination Syndrome (ODS), also known as Central Pontine Myelinolysis (CPM). [1,2]
Clinical Pearls
Pseudohyponatraemia: Always check serum osmolality first. If osmolality is normal or high, the low sodium is "fake". Causes include severe hyperlipidaemia (milky serum) or hyperproteinaemia (Myeloma), or presence of osmotically active substances (Glucose, Mannitol).
The Beer Potomania Patient: Chronic alcoholics who drink huge volumes of low-solute fluids (beer) develop hyponatraemia. Their kidneys cannot excrete the water because the dietary solute load is too low to generate urine. They need solutes (protein, salt), not fluid restriction.
"Sodium doesn't drop, Water rises": In most cases of true hyponatraemia, the problem is excess water relative to sodium, not actual sodium loss. The treatment is often to restrict water, not give salt.
The 10/8 Rule for Correction: Maximum safe correction is 10 mmol/L in the first 24 hours and 8 mmol/L in each subsequent 24-hour period. Exceeding this risks ODS.
2. Epidemiology
Demographics
- Prevalence: Present in up to 30% of hospitalised patients.
- Incidence: 5-7% of inpatients have clinically significant hyponatraemia (less than 130).
- Mortality: Severe hyponatraemia is associated with significantly increased mortality.
Risk Factors
- Elderly: Reduced total body water, impaired thirst, comorbidities.
- Medications: Thiazides, SSRIs, Carbamazepine, Desmopressin, Opioids.
- Chronic Disease: Heart Failure, Cirrhosis, CKD.
- Psychogenic Polydipsia: Psychiatric patients.
- Post-Operative: SIADH post-surgery is common.
3. Pathophysiology
Mechanism
- Sodium is the Major Extracellular Cation: It determines plasma osmolality and therefore fluid shifts.
- Low Sodium = Low Osmolality: Water moves from plasma (low osmolality) into cells (higher osmolality).
- Cerebral Oedema: Brain cells swell as water enters them. The skull is rigid, so swelling causes raised ICP, herniation, and death.
- Brain Adaptation: Over 48 hours, the brain adapts by extruding organic osmolytes (Taurine, Glutamate). This protects against further swelling.
- Danger of Rapid Correction: If sodium is corrected too fast, water rapidly exits brain cells, which have lost their osmolytes. The cells shrink excessively, damaging the myelin sheath, particularly in the Pons (Osmotic Demyelination Syndrome).
Classification by Volume Status
| Volume Status | TBW | TBNa | ECF | Common Causes | Urine Na |
|---|---|---|---|---|---|
| Hypovolaemic | ↓ | ↓↓ | ↓ | Diarrhoea, Vomiting, Diuretics (Thiazides), Addison's, Salt-wasting Nephropathy | less than 20 (Extrarenal loss) or >40 (Renal loss) |
| Euvolaemic | ↑ | ↔ | ↔ | SIADH, Hypothyroidism, Glucocorticoid deficiency, Psychogenic Polydipsia | Usually >40 |
| Hypervolaemic | ↑↑ | ↑ | ↑ (Oedema) | Heart Failure, Cirrhosis, Nephrotic Syndrome | less than 20 (Kidney holding onto Na) |
4. Differential Diagnosis (Approach to Hyponatraemia)
| Condition | Osmolality | Volume | Key Features |
|---|---|---|---|
| SIADH | Low | Euvolaemic | Low Urine Osmolality >100, Urine Na >40, No oedema. Exclude Hypothyroid/Addison's first. |
| Diuretic-Induced | Low | Hypovolaemic | Usually Thiazides. Urine Na high. |
| Hyperglycaemia | High | Variable | Corrected Na = Measured Na + 2.4 x (Glucose-5.5)/5.5. |
| Heart Failure | Low | Hypervolaemic | Oedema, raised JVP, Urine Na less than 20. |
| Cirrhosis | Low | Hypervolaemic | Ascites, Jaundice, Urine Na less than 20. |
| Addison's (Adrenal Insufficiency) | Low | Hypovolaemic | Hyperkalaemia, Postural hypotension, Pigmentation. Low Cortisol. |
| Hypothyroidism | Low | Euvolaemic | Fatigue, bradycardia. High TSH. |
| Psychogenic Polydipsia | Low | Euvolaemic | Psychiatric history. Urine Osm very low (less than 100). Massive water intake. |
5. Clinical Presentation
Symptoms (Severity Dependent)
Signs
Mild (130-135)
Often asymptomatic.
Moderate (125-129)
Nausea, headache, confusion.
Severe (less than 125)
Vomiting, seizures, obtundation, coma.
6. Investigations
Essential First Steps
- Serum Sodium: Confirm.
- Serum Osmolality: Low (less than 280 mOsm/kg) = True (Hypotonic) Hyponatraemia. Normal/High = Pseudohyponatraemia or Translocational (e.g., Hyperglycaemia).
- Urine Osmolality: High (>100 mOsm/kg) = Kidneys are concentrating inappropriately (SIADH, Heart Failure, Cirrhosis etc.). Low (less than 100) = Appropriately dilute urine (Polydipsia).
- Urine Sodium: less than 20 mmol/L = Sodium avid state (Hypovolaemia, Oedematous states). >40 mmol/L = Renal salt wasting (Diuretics, Addison's, SIADH).
Second Line
- TFTs: Exclude Hypothyroidism.
- 9am Cortisol / Short Synacthen Test: Exclude Addison's.
- Glucose: Exclude hyperglycaemia.
7. Management
Management Algorithm
HYPONATRAEMIA CONFIRMED (less than 135)
↓
CHECK SERUM OSMOLALITY
┌────────────────┼────────────────┐
NORMAL/HIGH LOW (less than 280)
(Pseudohypo) (True Hypotonic)
- Glucose Assess VOLUME STATUS
- Lipids ↓
┌───────────┼───────────┐
HYPOVOLAEMIC EUVOLAEMIC HYPERVOLAEMIC
(Dehydrated) (Normal) (Oedema)
↓ ↓ ↓
SALINE (0.9%) FLUID RESTRICT FLUID RESTRICT
Rehydration (750-1500ml/d) + Diuretics
↓ ↓ ↓
Exclude: SIADH? Treat HF/Cirrhosis
Addison's Hypothyroid?
Addison's?
↓
IF SEVERE / SYMPTOMATIC
(Seizures, GCS drop)
↓
HYPERTONIC SALINE (3%)
- 100ml IV over 10-20 mins
- Repeat if needed
- MAX Correction 10mmol/24h
(Risk ODS!)
1. Severity Assessment
- Acute (less than 48 hours): Brain has NOT adapted. More symptomatic. Safer to correct faster.
- Chronic (>48 hours or unknown): Brain HAS adapted. Risk of ODS with fast correction.
2. Symptomatic / Severe (less than 120 with Seizures/Coma)
- Hypertonic Saline (3%): 100-150ml IV bolus over 10-20 mins. May repeat 2-3 times.
- Aim: Raise Na by 4-6 mmol/L in first few hours to stop seizures.
- Then SLOW DOWN: Maximum 10 mmol/L in 24 hours total.
3. Chronic / Asymptomatic
- Hypovolaemic: Normal Saline (0.9% NaCl). Treat cause (e.g., Stop Thiazide).
- Euvolaemic: Fluid Restriction (e.g., 750-1000ml/day). Treat cause (Hypothyroid/Addison's). If SIADH confirms, consider Demeclocycline or Tolvaptan.
- Hypervolaemic: Treat underlying cause (Diuretics for HF, Spironolactone for Cirrhosis). Fluid Restrict.
4. Monitoring
- Check Sodium every 2-4 hours during active treatment.
- If over-correcting: Give Dextrose 5% IV or Desmopressin (DDAVP) to re-lower sodium.
8. Complications
Of Severe Hyponatraemia
- Cerebral Oedema: Raised ICP, Herniation, Death.
- Seizures: Generalised tonic-clonic.
Of Overly Rapid Correction
- Osmotic Demyelination Syndrome (ODS): Also known as Central Pontine Myelinolysis (CPM) or Extrapontine Myelinolysis (EPM).
- Mechanism: Myelin sheath in Pons (and elsewhere) is damaged by rapid osmotic shifts.
- Timing: Symptoms appear 2-6 days after rapid correction.
- Features: Dysarthria, Dysphagia, Quadriparesis ("Locked-in syndrome").
- Risk Factors: Chronic hyponatraemia, Alcoholism, Malnutrition, Hypokalaemia.
- Prognosis: Often irreversible and devastating.
9. Prognosis and Outcomes
- Prognosis depends heavily on underlying cause, severity, and speed of correction.
- Mild chronic hyponatraemia may have minimal direct impact but is a marker of poor health.
- Severe hyponatraemia with appropriate management has good neurological outcomes if ODS is avoided.
10. Evidence and Guidelines
Key Guidelines
| Guideline | Organisation | Key Recommendations |
|---|---|---|
| Hyponatraemia | European (2014) | Defines Acute vs Chronic. Max correction 10mmol/24h (limit 8mmol if high ODS risk). |
| Hyponatraemia | UpToDate | Pragmatic approach based on symptoms. |
Landmark Evidence
1. Osmotic Demyelination (Sterns, 1987)
- Seminal paper describing ODS following rapid correction of hyponatraemia.
- Impact: Established the need for slow, controlled correction.
11. Patient and Layperson Explanation
What is Hyponatraemia?
It means your blood has too little sodium (salt). Sodium helps control the amount of water in your body. When sodium is low, water gets drawn into your cells, making them swell.
Why is it dangerous?
If the sodium drops quickly or very low, the brain cells swell. The brain is enclosed in a rigid skull, so swelling causes pressure, leading to confusion, seizures, or even coma.
How is it treated?
- Find the Cause: We check if you are dehydrated, have a hormone problem, or have heart/liver issues.
- Fluids: If you are dehydrated, we give salt water (saline) through a drip. If you are overloaded, we restrict your fluid intake.
- Slowly: We raise your sodium slowly and carefully. If we do it too fast, it can damage part of the brain.
12. References
Primary Sources
- Spasovski G, et al. Clinical practice guideline on diagnosis and treatment of hyponatraemia. Eur J Endocrinol. 2014.
- Sterns RH, et al. Osmotic demyelination syndrome following correction of hyponatremia. N Engl J Med. 1986.
13. Examination Focus
Common Exam Questions
- Diagnosis: "Urine Na >40, Euvolaemic?"
- Answer: SIADH (or Diuretics/Addison's). Must exclude Hypothyroid/Addison's first.
- Complication: "Rapid correction risk?"
- Answer: Osmotic Demyelination Syndrome (Central Pontine Myelinolysis).
- Management: "Max correction rate?"
- Answer: 10 mmol/L in 24 hours (some guidelines say 8 if high risk for ODS).
- Pharmacology: "Drug for SIADH?"
- Answer: Tolvaptan (V2 receptor antagonist / Vaptan) or Demeclocycline.
Viva Points
- SIADH Criteria: Hypo-osmolar serum, Inappropriately concentrated urine (Osm >100), Euvolaemia, Urine Na >40, Normal Renal/Adrenal/Thyroid function. It is a diagnosis of exclusion.
- "Sodium doesn't drop, Water rises": Explain the concept that water excess causes dilutional hyponatraemia.
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