Sodium II Disorders: Hypernatremia

Mechanism

Physiopathological Etiology

• Net loss of free water with preserved sodium: It occurs secondary to insensible decompensated cutaneous or pulmonary losses (prolonged febrile states) or through the kidneys due to the inability to concentrate urine. The classic example is Diabetes Insipidus, which can be of Central origin (congenital or acquired absence of pituitary synthesis or release of ADH) or of Nephrogenic origin (resistance of the main cell of the collecting duct to the stimulation of ADH, commonly induced by lithium toxicity or chronic hypercalcemia).
• Exogenous Sodium Overload (Saline Gain): Typically occurs iatrogenically through excessive infusion of vials of 8.4% hypertonic sodium bicarbonate during cardiopulmonary resuscitation or from incorrect preparation of milk formulas or hydration solutions.

Calculation of Free Water Deficit

To quantitatively guide the volume of fluid replacement in a hypernatremic dehydrated patient, the net free water deficit should be estimated using the following equation:

Free Water Deficit (Liters) = ACT · ( [Na⁺]_measured140 - 1 )

This calculated volume estimates only the amount of free water required to return plasma sodium to a physiological value of 140 mEq/L. It does not incorporate the patient's active concomitant continuous losses, so the total volume prescribed per day must take into account the calculated deficit plus the daily expenditure of insensible losses and ongoing diuresis.

Security

Safety Alert: Acute Cerebral Edema due to Rapid Correction

Just as the rapid correction of chronic hyponatremia destroys myelin sheaths, the ultra-rapid correction of chronic hypernatremia induces the formation of severe cerebral edema that can cause seizures, coma and intracranial hypertension.

When the cells of the nervous system chronically adapt to a hypertonic extracellular environment, they actively increase their intracellular osmolarity through the intracytoplasmic synthesis of organic compounds called idiogenic osmoles (taurine, choline, sorbitol). If the ECF becomes rapidly hypotonic by aggressive infusion of free water, an osmotic water gradient is generated that promotes massive entry of free water into the neuron, inducing generalized cellular edema.

Safe correction limit: Reduce plasma sodium at a maximum rate of 10 mEq/L in a 24-hour period, performing serum electrolyte determinations every 4 to 6 hours during the active phase of treatment.

Clinical

Clinical Management and Speed of Correction

The infusion of free water should preferably be carried out enterally or by slow intravenous administration of 5% glucose serum.