Management of hyponatraemia

Depends on
1 rate of development
2 severity
3 underlying cause

In RAPID development (over hours to days)
There is high morbidity due to cerebral oedema…
SO we should correct the plasma Na rapidly!
Eg. Infusion of hypertonic (3%) NaCl solutions, espescially when patient is obtunded/convulsing

HOWEVER, rapid correction in SLOW development (weeks to months) can be hazardous to the brain (cerebral cells adapted to hypo-osmolality by reducing intracellular osmolality to maintain cell vol). sudden extracellular osmolality can lead to water shifting out of cerebral neurons, abruptly reducing their volume & risking detachment from their myelin sheath. Resulting ‘myelinolysis’ can produce permanent structural/functional damage – fatal!

In SLOW development
Rate of correction should be < 10mmol/day

For underlying cause
Control source of Na loss
Eg. IV saline if warranted
Dilutional hyponatraemia – fluid restriction 600-1000ml/day
Plus withdrawal of precipitating stimulus (eg. a drug causing SIADH)

Where inadequate rise in plasma Na results, treat with demeclocycline 600-900mg/day – enhance water excretion by interfering with collecting duct responsiveness to ADH

Persistent hyponatraemia due to prolonged SIADH – oral urea therapy 30-45g/day – provides solute load to promote water excretion.

Hypovolaemic patients – diuretics with strict fluid restriction (catiously!)

With significant hyperaldosteronism – K+ sparing diuretics