A common cause of hyponatraemia is hypotonic dehydration and iatrogenic water overload (eg overestimation of the degree of dehydration, inappropriate use of hypotonic solutions for rehydration and/or too rapid administration of maintenance fluids).
Hyponatremia is the result of “water intoxication”. It is the opposite of dehydration. Hyponatremia is the most common electrolyte disorder which can result in *brainstem malfunction due to cerebral edema.
Hyponatremic encephalopathy, the clinical manifestation of cerebral edema secondary to hyponatremia, can have a wide range of presentations. The early signs are usually nonspecific: nausea, vomiting, and headaches. Worsening of brain swelling then leads to decreased mental status and seizures. If the situation is not corrected, the final manifestations are coma, respiratory arrest and death.
Hyponatremia also results from a “surplus of water” due to Na negligence. Other evidence of fluid overload as indicated by “ascites” due to fluid build-up in the abdomen.
It is never appropriate to use hypertonic saline (3% saline) as “initial” fluid resuscitation in the dehydrated patient.
* The combination of 3.3% dextrose and 0.3% sodium
chloride (known as 2/3 and 1/3) contains only 51 mmol/L of
sodium. Outside of the body, the osmolarity of the solution
is 269 mOsmol/L (sodium and dextrose combined). Once the
solution is infused, however, the dextrose is rapidly
metabolized, which leaves two-thirds of the solution (667
mL) as electrolyte-free water and renders the solution
The basic fluid problem in SIADH is water overload and not salt depletion. This leads to excess water elimination as dilute urine.
Irreparable harm can befall the patient when abnormal serum sodium levels are corrected too quickly or too slowly. Rapid correction of hyponatremia, even mild hyponatremia, risks neurologic complications.