Overview
Hyponatraemia describes a low sodium ion concentration in the blood. The serum sodium concentration is maintained via homeostasis through the use of:
- Antidiuretic hormone (ADH, also known as vasopressin):
- Reduces the amount of water lost in the urine, stimulates thirst, and increases water intake
- ADH lowers serum sodium
- The renin-angiotensin-aldosterone system (RAAS):
- Aldosterone retains sodium ions and increases the excretion of potassium ions. Where sodium goes, water follows. This increases the water content in the body and blood pressure.
- Aldosterone increases serum sodium
Epidemiology
- Hyponatraemia is the most common electrolyte abnormality seen in clinical practice
- Infants and the elderly are at an increased risk due to a reduced ability to express their thirst and control their fluid intake
Causes
Hypovolaemic hyponatraemia
Where the total body water and sodium ion concentration are decreased. It is associated with fluid losses or third-spacing (loss of fluid into interstitial spaces). Causes may be:
- Gastrointestinal losses – vomiting or diarrhoea
- Third-spacing – pancreatitis, hypoalbuminaemia
- Renal failure
- Addison’s disease
- Diuretic use – thiazides, loop diuretics
Euvolaemic hyponatraemia
Where the total body water increases but the total sodium ion concentration remains unchanged. It is not associated with hypo- or hypervolaemia. Causes may be:
- Medications:
- Vasopressin
- Antidepressants
- Thiazide diuretics
- Syndrome of inappropriate ADH secretion (SIADH) and its causes
- Hypothyroidism
Hypervolaemic hyponatraemia
Where the total body water and sodium ion concentration increase, but the water increases more. The baroreceptors detect a low intravascular volume, leading to inappropriate ADH release despite the water and sodium ion concentration increases. Causes may be:
- Heart failure
- Liver cirrhosis
- Nephrotic syndrome
- Psychogenic polydipsia
Presentation
Hyponatraemia may be asymptomatic depending on how quickly the sodium falls. A sudden fall in sodium can have severe symptoms, whereas a slow and chronic fall can be asymptomatic, even if the level is extremely low due to cerebral adaptation. Features may be:
- Headaches
- Nausea
- Vomiting
- Lethargy
- Muscle cramps
- Weakness
- Confusion
- Ataxia
- Altered consciousness (e.g. drowsiness)
- Cognitive impairment
- Seizures – focal or generalised
Features of volume status changes may be present:
- Hypovolaemia:
- Dry mucous membranes
- Reduced skin turgor
- Tachycardia
- Hypervolaemia:
- Lung crackles
- S3 heart sound
- Elevated jugular venous pressure
- Peripheral oedema
Differential Diagnoses
Pseudohyponatraemia
- High lipid and/or protein content in the plasma can lead to an incorrectly low serum sodium ion concentration
- High protein levels are often seen in multiple myeloma
Investigations
- U&Es:
- Sodium: reduced
- Other electrolyte imbalances may be seen (e.g. reduced potassium in Addison’s disease)
- Kidney function may be deranged
- Serum osmolality – differentiates between hypo- and hypervolaemic hyponatraemia:
- <275 mmol/kg – hypervolaemic hyponatraemia
- >295 mmol/kg – hypovolaemic hypernatraemia
- Normal – likely pseudohyponatraemia
- Urine sodium – confirms hypovolaemia or euvolaemia:
- If hypovolaemic:
- >20 mmol/L – suggests renal sodium loss (e.g. diuretic use/renal failure)
- ≤20 mmol/L – suggests non-renal losses (e.g. vomiting/diarrhoea)
- If hypervolaemic:
- >20 mmol/L – suggests renal failure or diuretic use
- ≤20 mmol/L – suggests heart failure, cirrhosis, or nephrotic syndrome
- If hypovolaemic:
- Urine osmolality – if the patient has euvolaemic hyponatraemia:
- ≥300 mmol/kg (high) – suggests SIADH or medication
- <100-150 mmol/kg (low) – suggests primary polydipsia
Management
Overview
Untreated hyponatraemia can lead to cerebral oedema and brain herniation in severe cases. Overly-quick correction can lead to central pontine myelinolysis. Therefore, the management of hyponatraemia varies depending on the duration, severity, symptoms, and suspected aetiology.
The severity of hyponatraemia is as follows:
- Mild: 130 – 134 mmol/L
- Moderate: 120- 129 mmol/L
- Severe: < 120 mmol/L
Acute, severe, symptomatic hyponatraemia
Defined as a sodium ion concentration of <120 mmol/L developing within the last 48 hours. The brain does not have time to adapt to the sudden hyponatraemia leading to cerebral oedema which can lead to brain herniation, requiring urgent treatment:
- 1st-line: hypertonic (3% NaCl) saline + HDU monitoring
Chronic hyponatraemia without severe symptoms
Defined as hyponatraemia developing >48 hours:
- If hypovolaemic cause is suspected: trial normal (0.9% NaCl) saline
- If the sodium ion concentration rises, this confirms hypovolaemic hyponatraemia
- If it falls, SIADH or another cause is likely
- If euvolaemic cause is suspected: fluid restriction
- Consider ADH receptor antagonists (-vaptans)
- If hypervolaemic cause is suspected: fluid restriction
- Consider loop diuretics or ADH receptor antagonists