The main and earliest symptom of hypernatremia is intense thirst; if this is not perceived or not satisfied, signs of central nervous system suffering appear:
accompanied by spasticity, hyper-reflexia, nausea and vomiting. The nervous symptoms are due to dehydration-induced shrinkage of the brain cells, which release water to the hyper-osmotic extracellular compartment. For this reason, vascular ruptures with cerebral hemorrhage or subarachnoid hemorrhage may also appear. The signs and symptoms of hypernatremia are more evident the higher the serum sodium concentration and the more rapidly the disorder has established. The rapid increase in plasma sodium concentration, without the brain having the opportunity to adapt, often leads to permanent neurological damage.
In children, hypernatremia may result in hyperpnea, muscle weakness, restlessness, insomnia, lethargy, and high-pitched crying. Further progression of hypernatremia, especially during hypernatremic dehydration, leads the young patient to lethargy, convulsions and coma.
The acute onset of hypernatremia increases mortality, as well as advanced age is another unfavorable prognostic element. The mortality rate is high for natremia values above 180 mEq/L in acute forms, particularly in adults; this rate is greater than 40% in children and approximately 75% in adults.
The chronic form of hypernatremia is somewhat less severe and has a lower mortality. Within 1-3 days from the onset of hypernatremia, the brain is in fact able to implement a series of compensatory mechanisms to increase the osmolarity of the intracellular environment: it increases the synthesis of osmotically active substances and reduces their excretion. In this way the osmotic gradient decreases and with it the loss of intracellular water is reduced.
These adaptations are of great importance from a therapeutic point of view.
- Hypovolemic hypernatremia: correction of the volume deficit by administration of hypotonic saline solutions (or isotonic in case of symptoms of severe hypovolemia) until the symptoms of hypovolemia improve; Removal of the cause. Then we proceed with the correction of the water deficit* with 0.45% hypotonic sodium-chloride solution or 5% glucose solution.
- Euvolemic hypernatremia: correction of water deficit* with hypotonic 0.45% sodium-chloride solution or 5% glucose solution, carefully controlling blood sodium levels to avoid water intoxication. In central or neurogenic diabetes insipidus, the administration of Vasopressin is necessary; in nephrogenic diabetes insipidus administer diuretics and limit sodium intake in the diet (see drugs for the treatment of diabetes insipidus)
- Hypervolemic hypernatremia: excess sodium must be removed using diuretics (furosemide) associated with replenishment with hypotonic fluids; if hypernatremia is refractory to treatment, dialysis is used
* Free Water Deficit = TBW x ((natremia/140)-1)
where TBW = total body water estimated by multiplying the patient’s weight in kg by 0.6 or his lean mass by 0.4
Approximately, half of the free water deficit should be covered over the first 24 hours and the second half over the next 24-48 hours. A more rapid and aggressive correction is recommended only in cases of acute hypernatremia
For clinical purposes, then, it is very important to decide whether the form is acute or chronic:
- acute hypernatremia: onset less than 24 hours ago, with or without neuropsychic manifestations. It must be corrected within 24 hours: reduce sodium levels by approximately 1-2 mEq/l per hour
- chronic hypernatremia: days have passed since the onset of hypernatremia; in this case the hyperosmotic adaptation phenomena of the brain cells have already been completed; this requires a slower correction of vascular volume and water deficit (over 48-72 hours instead of 24), in order to avoid the appearance of cerebral edema, with coma, convulsions and death. To avoid this eventuality it is necessary to lower the sodium concentration to no more than 0.5 mEq/l per hour