Synopsis
Treat cerebral symptoms immediately, classify hypotonic hyponatraemia physiologically and prevent osmotic injury from uncontrolled sodium correction.
- Base emergency treatment on neurological symptoms and their likely relation to hyponatraemia, not on the sodium concentration alone; profound chronic hyponatraemia may be asymptomatic while a rapid moderate fall can cause cerebral oedema.
- Confirm tonicity: hyperglycaemia causes translocational hyponatraemia, and very high lipid or protein can create measurement artefact with some laboratory methods.
- For severe or moderately severe symptoms, the Society for Endocrinology recommends 150 mL of 3% sodium chloride over 20 minutes, repeated according to the measured response in a suitable monitored environment.
- Target a 5 mmol/L rise during the first hour, then limit total increase to no more than 10 mmol/L in the first 24 hours and 8 mmol/L per 24 hours thereafter.
- Obtain paired serum osmolality, urine osmolality and urine sodium early, but do not delay emergency hypertonic treatment to complete aetiological classification.
- Exclude adrenal insufficiency and clinically important hypothyroidism before calling euvolaemic hypotonic hyponatraemia syndrome of inappropriate antidiuresis.
- A sudden water diuresis after volume or cortisol restoration can make sodium rise much faster than predicted; urine output is an early warning signal for overcorrection.
- Vaptans are not recommended for severe or moderately severely symptomatic presentations; cause-specific longer-term treatment requires endocrine, renal and local formulary governance.
Key red flags
Seizure, cardiorespiratory arrest, persistent vomiting, coma or Glasgow Coma Scale at or below eight defines the highest emergency category in Society guidance.
Confusion, headache or nausea without vomiting may still reflect cerebral oedema and warrants immediate experienced assessment and the symptomatic pathway.
Hypotension, weight loss, hyperkalaemia, hypoglycaemia or steroid exposure raises adrenal insufficiency; pituitary disease can lack hyperkalaemia and still cause dangerous cortisol deficiency.
A brisk new dilute urine output, rapidly improving cause or unexpectedly large sodium increment predicts aquaresis and demands immediate intensified monitoring and senior action.
Investigation priorities
Confirm the value and measure correction without inter-method variation obscuring small but important changes.
Management branches
Hyponatraemia accompanies severe or moderately severe neurological symptoms without a more convincing immediate explanation.
- Use ABCDE, bedside glucose and seizure care, call an experienced senior clinician and transfer to an environment able to deliver hypertonic saline with rapid sodium measurement.
- Give 150 mL 3% sodium chloride or locally equivalent hypertonic solution over 20 minutes, remeasure sodium using the same platform and repeat as the Society algorithm directs towards a 5 mmol/L first-hour rise.
- Once symptoms improve or the initial target is reached, stop hypertonic treatment, begin cause-specific care and enforce the subsequent 24-hour correction limits.