Treatment of Symptomatic Hyponatremia and Its Relation to Brain Damage

Abstract

We studied the effects of replacement therapy in two groups of patients with symptomatic hyponatremia. Thirty-three patients, who were studied prospectively, had no evidence of cerebral demyelinating lesions. Their hyponatremia (mean serum sodium concentration [+/- SE], 108 +/- 1 mmol per liter) was increased to 126 +/- 1 mmol per liter with hypertonic saline (856 mM) delivered at a rate of 1.3 +/- 0.2 mmol per liter per hour. The serum sodium concentration did not rise to normal or hypernatremic levels in the first 48 hours of therapy, and none of these patients had a respiratory arrest or other hypoxic episode. Twelve patients, evaluated retrospectively, had evidence of cerebral demyelinating lesions at autopsy or on computerized axial tomography. The rate of correction of hyponatremia (1 +/- 0.2 mmol per liter per hour) was similar to the rate in the patients in Group I. However, at least one of four characteristics was present: an increase in serum sodium to normal or hypernatremic levels in the first 48 hours, a change in the serum sodium concentration of more than 25 mmol per liter in the first 48 hours, a hypoxic-anoxic episode, and an elevation of serum sodium to hypernatremic levels in patients with hepatic encephalopathy. Although these four features were associated with demyelination, our observations suggest that this complication does not depend on the rate of correction of hyponatremia.

Hypertonic Saline for Hyponatremia

“…Although there were significant differences in the time taken by the physicians to respond to low sodium levels-likely a result of the inherent differences between these settings with regard to the rapidity of phlebotomy, laboratory processing times, and medication dispensing as well as nurse staffing-the clinical setting did not seem to have an impact on either the rates of overcorrection or the neurologic outcomes. We were successful in maintaining a rate of rise in sodium concentration Յ12 mEq/L per d and 18 mEq/L in 48 h in 84% of patients, and in all patients correction remained well below 25 mEq/L in 48 h, a rate that is associated with a high incidence of severe posttherapeutic neurologic complications (14). Fortunately, there were no complications in patients who were overcorrected.…”

“…We do not dispute the recommendation that patients with active seizures or impending herniation be given 100-ml bolus infusions of hypertonic saline (12); however, we did not encounter any patients with such a presentation in this series. Similarly, case series (14,20) reporting a favorable outcome with more aggressive therapy did not include such patients.…”

Hyponatremia Treatment Guidelines 2007: Expert Panel Recommendations

“…76 Although many patients tolerate increases in serum [Na ϩ ] of this magnitude, such therapy cannot be justified unless there is proof that it is beneficial. There is some evidence that correction by Ͻ3 to 4 mmol/L in 24 hours may be associated with excess mortality in patients with acute 77 or postoperative hyponatremia.…”

Effects of Sugar, Salt and Distilled Water on White Blood Cells and Platelet Cells

“…High intake of salt effects Adrenaline (hormone produced by adrenal glands) which acts on membranes of platelet cells and results the platelet aggregation. Hence, intake salt concentration affects not only other systems but also changes reactivity of platelet cells [41][42] .…”