HYPONATRAEMIA
DERIVED, NOT MEMORISED
One mechanism map. Ten steps. Start with what the sodium concentration actually means, then derive tonicity, ADH, urine osmolality, urine sodium, the classic volume states, the major causes and the treatment logic.
Built from mechanism-first teaching used by Ninja Nerd and Osmosis, aligned to the European diagnostic approach: confirm hypotonicity, then urine osmolality, then urine sodium and context.
relative to
H₂O
Why can sodium fall even when total body sodium has not?
Serum sodium is a concentration. Change the amount of water while effective body solute stays similar, and the concentration changes.
Try it
Measured sodium
mmol/L — simplified visual model
The amount of sodium in the second beaker has not changed. The concentration falls because the denominator — water — increases.
If total body sodium stays similar but water increases, serum sodium will…
Why does hyponatraemia make the brain swell?
Hypotonic ECF → water enters cells
Speed changes the physiology
Acute fall: little time to adapt → greater cerebral swelling and neurological symptoms.
Chronic fall: brain cells shed electrolytes and organic osmolytes → less swelling, but greater vulnerability to rapid correction.
Two patients both have Na 121. Which worries you more immediately?
Why must you check tonicity before calling it SIADH?
A low measured sodium can occur in three different osmotic contexts.
Relative water excess. This is the branch that enters the usual ADH/urine algorithm.
Classically marked hyperglycaemia. Sodium falls because extracellular effective osmolality is raised by another osmole.
Rare with modern direct ISE methods; can occur with very high lipids or proteins using some indirect methods.
Na 124, glucose 38 mmol/L. What must you avoid doing?
Why can ADH stay on even when plasma is already dilute?
The override
If plasma is dilute, osmoreceptors say: switch ADH off.
If circulation is threatened, baroreceptor pathways say: retain water.
Circulatory defence can override osmolality. That single principle explains why a dehydrated or underfilled patient can remain hyponatraemic with concentrated urine.
A child is hypotonic and clearly volume depleted. What do you expect ADH to do?
What does urine osmolality tell you about ADH?
Move the urine osmolality
≤100: ADH effectively off
The kidney is maximally diluting the urine. Think relative excess water intake or low solute intake rather than persistent ADH action.
What does urine sodium tell you about effective circulating volume?
Urine Na ≤30 mmol/L
The kidney is avidly conserving sodium. This supports low effective arterial volume.
Think GI losses, haemorrhage/third spacing, or an oedematous state such as heart failure or cirrhosis where the arterial circulation is still sensed as underfilled.
Urine Na >30 mmol/L
Consider SIADH, renal salt loss, diuretics, adrenal insufficiency, and other causes where the kidney is not avidly sodium-retaining.
Important: diuretics can make urine sodium misleading. Use the clinical context and paired blood/urine samples.
Hypotonic hyponatraemia, Uosm 420, urine Na 12. What is the most useful physiological interpretation?
Why is the body retaining water?
Tap each mechanism family.
1. True volume depletion
2. Low effective arterial volume with oedema
3. SIADH / non-osmotic ADH
4. Endocrine mimics
5. Water intake overwhelms excretion
6. Too little solute to excrete water
Why do hypovolaemic, euvolaemic and hypervolaemic hyponatraemia look different?
Hypovolaemic
Sodium and water both lost, with proportionally greater sodium loss. ADH stays on because circulation is threatened.
vomitingdiarrhoeadiureticsEuvolaemic
Modest retained water without obvious oedema. SIADH is the classic mechanism, but endocrine causes must be considered.
SIADHcortisol deficiencyHypervolaemic
Total body sodium may be increased, but water is increased even more. The concentration still falls.
heart failurecirrhosisrenal failureWhich category proves that hyponatraemia does not necessarily mean total body sodium is low?
Why does severe symptomatic hyponatraemia become a neurological emergency?
Severe neurological symptoms change the priority
In severe symptomatic hypotonic hyponatraemia, cerebral oedema is the immediate threat. Hypertonic saline is used for controlled initial correction while the cause is investigated in parallel.
After rescue, correction must be limited and monitored closely — especially in chronic hyponatraemia and in patients at higher risk of osmotic demyelination.
MeducateMe principle: teach the mechanism here; exact paediatric bolus volumes, targets and correction limits should follow the current local or national guideline at the point of care.