Causes of Hypo-Osmolar Hyponatraemia
| Category | Cause | Mechanism | |
|---|---|---|---|
| Hypovolaemic | Gastrointestinal losses | Vomiting | Sodium loss outstrips water loss, non-osmotic (baroreceptor) stimulation of ADH secretion |
| Diarrhoea | |||
| Third space disease, for example ileus | |||
| Renal losses | Diuretics | Sodium loss outstrips water loss, non-osmotic (baroreceptor) secretion of ADH secretion | |
| Salt-losing nephropathy | |||
| Mineralocorticoid insufficiency/adrenal insufficiency | |||
| Cerebral salt-wasting | |||
| Euvolaemic | Glucocorticoid insufficiency | ACTH stimulation and non-osmotic (baroreceptor) stimulation of ADH secretion, | |
| Severe hypothyroidism | Non-osmotic (baroreceptor) stimulation of ADH secretion | ||
| Psychogenic polydipsia/water intoxication | Water intake exceeds renal capacity for excretion (typical threshold >15 L daily if renal function and solute intake normal) | ||
Very low solute intake (e.g. ‘beer potomania’) Excess hypotonic fluid, for example 5% dextrose post-operatively | Maximally dilute urine is 50 mOsmol/Kg. Reduced daily solute limits water excretion capacity, e.g. if 50 mOsmol/day, maximal urine volume is 1 L Oncotic pressure overcomes impermeability of collecting duct to water which is retained in excess of sodium | ||
| Hypervolaemic | Cardiac failure | Non-osmotic (baroreceptor) stimulation of ADH secretion | |
| Renal failure | Reduced water excreting capacity | ||
| Liver failure, cirrhosis/ascites | Splanchnic vasodilatation, isotonic third space fluid loss (ascites), non-osmotic (baroreceptor) stimulation of ADH secretion | ||
| Hypoalbuminaemia, for example nephrotic syndrome | Isotonic loss of fluid to interstitial space, non-osmotic (baroreceptor) stimulation of ADH secretion | ||