Hyponatraemia is a common electrolyte disturbance that is often difficult to diagnose and to manage. In all cases there is retention of water relative to sodium. It is usually mediated by ADH which is released appropriately (most cases) or inappropriately (SIADH).

Easily reversible causes include drugs, endocrine and psychogenic polydipsia. Thiazides are probably the commonest cause of hyponatraemia and are more likely than loop diuretics to cause hyponatraemia because they impair free water clearance to a greater extent. Other drug induced causes are carbamazepine, antidepressants and desmopressin. Endocrine causes include hypothyroidism, hypoadrenalism and hypopituitarism. Once these have been excluded it is conventional to classify patients by their extracellular fluid (ECF) volume status. Causes range from vomiting and diarrhoea (ECF reduced), nephrotic syndrome, cirrhosis and heart failure (ECF expanded) to the Syndrome of Inappropriate ADH secretion (SIADH) (euvolaemic).

Hyponatraemia may be mild, moderate or severe biochemically. Mild hyponatraemia is generally considered to mean serum sodium 130–135 mmol/L. Hyponatraemia is moderate with serum sodium 125–129 mmol/L and severe when serum sodium is less than 125 mmol/L.

Most cases will be asymptomatic. The clinical features, when present, are those of cerebral oedema as water enters the brain. Initially there may be nausea, confusion and headache. Later there may be vomiting and cardiorespiratory distress leading ultimately to abnormal and deep somnolence, seizures and coma (GCS ≤8).

Those at risk of cerebral oedema have acute hyponatraemia that develops within 48 h i.e. the brain swells because water moves across blood brain barrier before the brain has had time to adapt. Hyponatraemia is chronic if documented to exist for at least 48 h and considered to be chronic if the timing of onset is not known, unless there is clinical evidence of the contrary.

In many situations the cause of the hyponatraemia is evident from the history (e.g. recently commenced thiazide for hypertension) or the clinical examination (e.g. stigmata of chronic liver disease). In all cases the patient should have an accurate assessment of ECF volume status. The following five tests are will guide you to the aetiology of hyponatraemia, though all may not be necessary in every case (e.g. mild hyponatraemia following initiation of a thiazide):