Neurological and neuropathological sequelae of correction of chronic hyponatremia

Abstract

The effect of correction of chronic hyponatremia at different rates was studied in 91 rats maintained at a plasma [Na+] of 112 +/- 1 mmol/liter for 19 +/- 1 days. Hyponatremia was corrected into normal ranges (140 to 145 mmol/liter) using three different methods. Rats corrected by water restriction achieved normal plasma [Na+] by 2.1 +/- 0.2 day and had a maximal (4 hr) correction rate of 1.0 +/- 0.1 mmol/liter.hr; rats corrected by water diuresis achieved normal plasma [Na+] by 1.6 +/- 0.1 day and had a maximal correction rate of 2.8 +/- 0.2 mmol/liter.hr; rats corrected by hypertonic saline infusion achieved normal plasma [Na+] by 5.4 +/- 0.3 hr and had a maximal correction rate of 5.7 +/- 0.4 mmol/liter.hr. A fourth control group was not corrected. No demyelinative lesions were found in the brains from the uncorrected rats, whereas the occurrence of such lesions in the brains of the corrected rats was highly correlated with the maximal rate of increase in plasma [Na+] (r = 0.68, P less than 0.001), and to a lesser degree with the magnitude of the increase in plasma [Na+] over the first 24 hours of correction (r = 0.41, P less than 0.001). Brain myelinolysis was first observed in animals whose maximal (4 hr) rate of correction exceeded 1.75 mmol/liter.hr, and the incidence of demyelination increased progressively in rats with more rapid rates of correction. Similarly, myelinolysis was first observed in rats whose magnitude of correction at 24 hours exceeded 16 mmol/liter and also increased in rats with larger 24 hour magnitudes of correction.(ABSTRACT TRUNCATED AT 250 WORDS)

Rapid Correction Rate of Hyponatremia as an Independent Risk Factor for Neurological Complication Following Liver Transplantation

“…*P < 0.05 compared to slow correction rate development of neurological complications after liver transplantation is more closely associated with the correction rate of hyponatremia rather than hyponatremia. The risks of rapid correction of hyponatremia itself and its associations with osmotic demyelination syndrome have been demonstrated in animal models (Kleinschmidt-DeMasters and Norenberg 1981;Laureno 1983;Verbalis and Martinez 1991), and the risk of rapid correction is currently emphasized in clinical practice. Rapid correction rate was associated with neurological sequelae in patients with severe hyponatremia (Sterns et al 1994).…”

Astrocytes Are an Early Target in Osmotic Demyelination Syndrome

“…1 Aggressive correction of chronic hyponatremia in patients can induce fatal CNS demyelination. 4,5,43 During chronic hyponatremia, organic osmolyte stores are depleted, and the reaccumulation of these osmolytes is impaired upon rapid hyponatremia correction. 6 -8 Recent evidence suggests that insufficient organic osmolytes during correction of chronic hyponatremia is involved in astrocyte death in ODS.…”

“…Sweden) through osmotic minipump (Alzet) and a liquid diet (AIN 76; Technilab BMI Sommeren Netherlands). 43 Hyponatremia was maintained for 4 days and was rapidly corrected by a single intraperitoneal injection of 1 M NaCl. To obtain a wide range of SNa levels for S100B analysis, rats were administered Figure 7.…”

Disorders of water balance

“…The rate of change of plasma sodium should be less than 12 mmol over 24 hours 22,24 and should not exceed 25 mmol over 48 hours. 25 Regular measurement of plasma electrolytes at two-hourly intervals is important so that the infusion can be stopped or the rate adjusted, where appropriate.…”