Hyponatremic Dehydration

Hyponatremia is defined as a serum sodium level of less than 130 meq/L. There are many causes of hyponatremia, which are usually categorized on the basis of whether total body water is increased, decreased, or normal. Hyponatremic dehydration most commonly occurs when a parent replaces acute fluid losses from vomiting and diarrhea with free water. Much less common causes of hyponatremic dehydration include adrenal insufficiency states, third-space losses from ascites or pancreatitis, and diuretic use.

In severe cases of hyponatremic dehydration, shock can result. However, the most common clinical manifestations of symptomatic hyponatremia involve the central nervous system. Although a gradual reduction in serum sodium is usually well tolerated, a sudden decrease can result in irritability, lethargy, and seizures. Seizures are most common with a serum sodium level of less than 120 meq/L, but are more dependent on the rate of fall than the absolute value of serum sodium.

The management of hyponatremic dehydration associated with cardiovascular instability consists of the infusion of normal saline in 20 mL/kg boluses until the patient is stable. Many patients with gastroenteritis who suffer hyponatremic-induced convulsions will stop seizing following the administration of a bolus of normal saline alone. Subsequent management is aimed at restoring both the volume and sodium deficits. The standard formula used in correcting serum sodium is

(Na desired- Na measured) x 0.6 * kg body wt in which 0.6 reflects the fractional distribution of sodium. To prevent overcorrection, the desired sodium is usually 125 meq/L, which corrects osmolarity sufficiently to prevent further seizures. In stable patients, the correction is carried out over several hours, as there is no physiologic advantage to raising the serum sodium rapidly. In patients with profound hyponatremia or persistent seizures, it may be necessary to infuse 3% NS at a dose up to 12 meq/kg; in clinical practice, this is rarely necessary. In patients with profound hyponatremia, rapid correction of serum sodium has resulted in central pontine demyelinolysis.

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