Remember, sodium and fluids are regulated by different processes, so they can go wonky in different ways.

Hypernatraemia is much rarer than hyponatraemia, and nearly always results from a lack of fluids in the body (dehydration), which can occur via several mechanisms in addition to simple lack of oral fluids.

Hyponatraemia as a finding alone doesn’t tell you anything because if could be caused by excess water or a sodium deficiency. A history (and a urine sample, if available) is required to interpret this finding. There are three basic types, which may be defined according to the extracellular volume status - hypovolaemic, euvolaemic and hypervolaemic - in which they usually occur or produce (although no classification is perfect).


  • ADH deficiency
    • Central (pituitary) diabetes insipidus
  • Iatrogenic
    • Administration of hypertonic sodium solutions
    • Administration of drugs with high sodium content (e.g. piperacillin)
    • Use of 8.4% sodium bicarbonate after cardiac arrest
  • Renal ADH insensitivity (peripheral AKA nephrogenic) diabetes insipidus
    • Lithium
    • Tetracyclines
    • Amphotericin B
    • Acute tubular necrosis
  • Osmotic diuresis
    • Total parenteral nutrition
    • Hyperosmolar hyperglycaemia
  • Also consider:
    • Impaired fluid intake/thirst/consciousness
    • High insensible fluid loss through skin or lungs


1. Hypovolaemic


This generally involves salt loss in excess of water loss, usually because homeostatic mechanisms are acting to improve volume (thirst, ADH release) at the expense of reduced plasma osmolality. Osmotic diuresis is considered separately in some classifications since it overpowers normal homeostatic mechanisms. However, it does lead to hypovolaemia (due to fluid loss) and hyponatreamia (due to dilution of plasma by fluid from intracellular compartments).

  • Extra-renal (urinary sodium <20 mmol/L)
    • Vomiting
    • Diarrhoea
    • Haemorrhage
    • Burns
    • Pancreatitis
  • Renal (Urinary sodium >20 mmol/L)
    • Osmotic diuresis (e.g. hyperglycaemia)
    • Diuretics (loop diuretics or thiazides)
    • Adrenocortical insufficiency
    • Tubulo-interstitial renal disease
    • Unilateral renal artery stenosis
    • Recovery phase of acute tubular necrosis (when ability to concentrate urine is still impaired)

2. Euvolaemic


Total body sodium unchanged (or slightly elevated) with volume expansion but with no obvious signs of oedema. Generally caused by water intake being in excess of what the kidneys can excrete.

  • Abnormal ADH release
  • Syndrome of inappropriate anti-diuretic hormone (SIADH)
  • Psychogenic polydipsia
  • Increased sensitivity to ADH
    • Chlorpropamine
    • Tolbutamide
  • ADH-like substances (e.g. desmopressin)

3. Hypervolaemic


Total body sodium elevated (or unchanged), but with greater increase in fluid volume.

4. “Pseudo-hyponatraemia” (Rare)

Pseudohyponatreamia is a laboratory anomaly, not a diagnosis. Proteins and lipoproteins usually make up <5% of plasma volume, and the space they take up excludes solutes like Na+ (proteins, because they are big; lipoproteins, because they are not in the aqueous phase). When either is in excess they make up more volume of plasma, but they take the place of where Na+ and other solutes might be. This appears to dilute Na+ and other solutes down per volume of plasma. Plasma osmolality is actually normal and no treatment is required.

  • Hyperlipaemia
  • Hyperproteinaemia

Adapted from Kumar and Clark’s Clinical medicine, 8th Edition.

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