Laboratory Investigation

Kidney International (1989) 35, 69–75; doi:10.1038/ki.1989.9

Brain dehydration and neurologic deterioration after rapid correction of hyponatremia

Richard H Sterns1, Darbbie J Thomas1 and Robert M Herndon1

1Departments of Medicine and Neurology, University of Rochester School of Medicine, Rochester, New York, USA

Correspondence: Richard H Sterns MD, Rochester General Hospital, 1425 Portland Avenue, Rochester, New York 14621, USA.

Received 31 July 1987; Revised 15 August 1988.

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Abstract

Brain dehydration and neurologic deterioration after rapid correction of hyponatremia. We made rats severely hyponatremia varying the rate of onset and duration of the disturbance, and then compared rapid correction to slow correction. An acute fall in the plasma Na to 106 mEq/liter within seven hours caused seizures and coma, but these findings resolved and survival was 100%after either rapid or slow correction. A more gradual fall in plasma Na to 95 mEq/liter in three days caused neither seizures nor coma. Measurements of brain water and electrolytes showed that adaptive losses of brain Na and K (maximally depleted within seven hours) and slower losses of non-electrolyte solutes progressively reduced brain edema. After three days of hyponatremia, rapid correction to 119 mEq/liter with 1 m NaCl or to 129 mEq/liter by withdrawing DDAVP caused brain dehydration because lost brain K and non-electrolyte solutes were recovered slowly. This treatment was followed by a delayed onset of severe neurologic findings, demyelinating brain lesions and a mortality rate of over 40%. Slow correction (0.3 mEq/liter/hr) avoided these complications and permitted 100%survival. We conclude that the rat adapts quickly to hyponatremia and can survive with extremely low plasma sodium concentrations for prolonged periods. Although rapid correction is well tolerated when hyponatremia is of brief duration, it may cause brain damage in animals that have had time to more fully adapt to the disturbance.

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