Investigation of Hyponatraemia (Low Sodium)
Patients with severe hyponatraemia may present with nausea, headache, lethargy, confusion, coma or respiratory arrest. If hyponatraemia develops rapidly, muscular twitches, irritability and convulsions can occur. The only manifestations of chronic hyponatreaemia may be lethargy, confusion and malaise.
The first step in investigating hyponatraemia is to exclude drug-related causes, especially diuretics, and then proceed to investigate pathological causes.
Is the patient taking:
- diuretics, particularly frusemide (lasix) and indapamide or alternative medicines such as Chinese herbs?
- opiates?
- carbamazepine (tegretol)?
Hyponatraemia is more commonly due to over-hydration than to sodium depletion.
Is the patient oedematous or overloaded? Consider liver failure or cardiac disease.
Is the patient dry? Consider fluid and sodium loss.
To differentiate true sodium depletion do spot urine and serum sodium and osmolality as indicated in the chart below.

To establish the cause:
- Assess volume status
If oedema is present think cardiac failure liver disease or renal disease as these are common causes of hyponatraemia. Alternatively if the patient is dry, sodium loss may have exceeded water loss. - Assess medication
Diuretics, in particular, loop diuretics and indapamide are commonly responsible. The incidence remains high especialy as they are not infreqently combined with ACE inhibitors or angiotensin receptor antagonists. Many medications, including psychiatric medication, may lead to inappropriate ADH secretion. - Check renal function
- Perform serum and urine osmolality (OSM) and sodium measurements.
If urine OSM>serum OSM and urine sodium is low consider sodium depletion (e.g. diuretics).
If urine OSM>serum OSM and urine sodium is high consider inappropriate ADH.
If urine OSM<serum OSM and urine sodium is low consider inappropriate water intake.
