Hyponatraemia ✅
Hyponatraemia — symptomatic versus chronic
- Recognise / red flags: The severity of neurological symptoms and speed of sodium fall matter more than the absolute sodium concentration alone. Seizures, coma or severe encephalopathy need emergency senior-led treatment.
- Investigate / stratify: Confirm true hypotonic hyponatraemia using glucose, serum osmolality, urine osmolality and urine sodium alongside volume status, medication history and possible adrenal insufficiency.
- Initial management: For severe symptoms, specialist emergency guidance uses 150 mL of 3% hypertonic saline over 20 minutes with immediate sodium rechecking and controlled repetition aiming for an initial rise of about 5 mmol/L. Manage in a setting with frequent biochemical and neurological monitoring; treat the cause.
- Exam pitfall / safety: Initial emergency correction targets are not the same as 24-hour safety ceilings. Avoid exceeding 10 mmol/L in the first 24 hours and 8 mmol/L per 24 hours thereafter under the cited European guidance; stricter individual limits may be needed in high-risk patients. Overcorrection requires urgent specialist management.
Source checked 2026-10-30: Society for Endocrinology emergency guidance / European guideline. Focused teaching summary only; historical material below has not had a full dose-by-dose review. Use current BNF, local guidelines and specialist advice for individual patients.
Related Subjects:
| Sodium Physiology
| Hyponatraemia
| TURP Hyponatraemia syndrome
| Hypernatraemia
| Diabetes Insipidus
| SIADH
⚠️ Hyponatraemia (Na⁺ <135 mmol/L): A clinical emergency when acute or severe.
🧠 Pathophysiology: Low extracellular sodium creates an osmotic gradient that drives water into brain cells, causing cerebral oedema and increased intracranial pressure.
📈 The "Rule of 8": Aim for a correction of 4–6 mmol/L/24h. Absolutely limit rise to <10 mmol/L in 24h to prevent irreversible brain damage (ODS).
| 🚨 Emergency Management (Severe Symptoms) |
|
Definition of Severe Symptoms: Seizures, GCS <8, status epilepticus, or respiratory arrest.
- Immediate Action: 150 mL of 3% Hypertonic Saline IV over 20 minutes.
- Repeat: If symptoms persist, repeat the 150 mL bolus twice (max 3 doses/450 mL).
- Target: A rapid rise of 5 mmol/L in serum sodium is usually enough to reduce brain swelling and stop seizures.
- Monitoring: Check Na⁺ every 2 hours until stable, then every 4 hours.
- Threshold to Stop: Once symptoms improve, or Na⁺ reaches 130 mmol/L, or a total rise of 10 mmol/L is achieved-STOP hypertonic saline.
|
🔬 Deep Dive: Diagnostic Investigations
Diagnosis must follow a logical sequence to avoid incorrect treatment (e.g., giving saline to an SIADH patient, which worsens the drop).
- 1. Confirm True Hyponatraemia:
- Check Serum Osmolality. If >275 mOsm/kg, it is "secondary" (e.g., Hyperglycaemia). If normal, it is "Pseudohyponatraemia" (Hyperlipidaemia/Hyperproteinaemia).
- 2. Assess ADH Activity:
- Check Urine Osmolality. If <100 mOsm/kg, ADH is appropriately suppressed (e.g., Psychogenic Polydipsia or "Tea and Toast" diet). If >100 mOsm/kg, ADH is active and driving the hyponatraemia.
- 3. Differentiate SIADH vs. Hypovolaemia:
- Check Urine Sodium (UNa).
- UNa <30 mmol/L: The kidneys are desperately holding onto salt. This indicates effective volume depletion (Hypovolaemia, Heart Failure, or Cirrhosis).
- UNa >30 mmol/L: The kidneys are losing salt. This suggests SIADH, Diuretics, or Adrenal Insufficiency.
⚖️ SIADH: Formal Diagnostic Criteria
To diagnose SIADH (Syndrome of Inappropriate Antidiuretic Hormone), you must meet all the following:
- Hyponatraemia (Na⁺ <135).
- Low plasma osmolality (<275 mOsm/kg).
- Inappropriately concentrated urine (Urine Osm >100 mOsm/kg).
- Elevated Urine Sodium (>30 mmol/L) with normal salt/water intake.
- Exclusion of adrenal, thyroid, pituitary, or renal dysfunction.
- Exclusion of diuretic use.
⚠️ Osmotic Demyelination Syndrome (ODS) - The Danger Zone
ODS (formerly Central Pontine Myelinolysis) occurs when brain cells, having adapted to a low-sodium environment, are suddenly "shrunk" by rapid sodium replacement. This tears the myelin sheaths off neurons.
- High-Risk Patients (Limit rise to <8 mmol/L/24h):
- Chronic Alcoholism.
- Liver Disease / Malnutrition.
- Hypokalaemia (Low K⁺ increases ODS risk).
- Clinical Presentation: Initially, the patient improves. 2–6 days later, they develop:
- Dysphagia/Dysarthria (difficulty swallowing/speaking).
- Quadriparesis (weakness in all limbs).
- Locked-in Syndrome (total paralysis except for eye movement).
🩺 Management Strategies by Aetiology
| Type |
Common Causes |
NICE/Consensus Treatment |
| Hypovolaemic |
Vomiting, diarrhoea, excessive sweating, Thiazide diuretics, Addison's disease. |
0.9% Sodium Chloride. Restore volume to stop the ADH "thirst" drive. |
| Euvolaemic |
SIADH (Lung CA, SSRIs, Carbamazepine, Pneumonia), Hypothyroidism. |
Fluid Restriction (1st line). 800mL–1L. Tolvaptan (V2 receptor antagonist) as 2nd line. |
| Hypervolaemic |
Congestive Heart Failure, Liver Cirrhosis, Nephrotic Syndrome. |
Fluid & Salt Restriction + Loop Diuretics. Treat the underlying organ failure. |
💡 Clinical Pearls & Advanced Tips
- The "Corrected Sodium" in Hyperglycaemia: Glucose is osmotically active.
Formula: Corrected Na⁺ = Measured Na⁺ + 2.4 × ([Glucose - 5.5] / 5.5).
- The Danger of "Beer Potomania": Heavy beer drinkers have very low protein intake. They cannot excrete water because they lack the "solute" (urea) to take the water with it. They are at extreme risk of ODS.
- Thiazides vs. Loops: Thiazides block sodium reabsorption in the distal tubule but leave the "concentrating power" of the kidney intact, leading to profound hyponatraemia. Loop diuretics (Furosemide) actually help treat hyponatraemia by "washing out" the medullary gradient.
- Potassium Correction: Replacing K⁺ will actually raise your serum Na⁺. If you are correcting both, you must monitor sodium even more frequently to avoid over-correction.
📚 References