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Central pontine myelinolysis and pontine lesions after rapid correction of hyponatremia: A prospective magnetic resonance imaging study
Author(s) -
Brunner John E.,
Redmond Janice M.,
Haggar Allan M.,
Kruger Davida F.,
Elias Stanton B.
Publication year - 1990
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410270110
Subject(s) - hyponatremia , central pontine myelinolysis , hypernatremia , magnetic resonance imaging , medicine , lesion , sodium , anesthesia , pathology , radiology , chemistry , organic chemistry
The rate at which profound hyponatremia should be corrected is the focus of a recent clinical debate. We prospectively studied neurological outcomes with serial magnetic resonanace imaging in 13 hyponatremic subjects with serum sodium concentrations of less than 115 mmol/L (mean initial serum sodium concentration, 103.7; range, 93–113 mmol/L). All subjects were corrected to mildly hyponatremic levels at 24 hours and ultimately underwent an increase in serum sodium concentration of 25 mmol/L without development of hypernatremia. Magnetic resonance imaging revealed the development of pontine lesions in 3 patients. The correction rate of hyponatremia over the first 24 hours was significantly faster in patients with pontine lesions (mean ± SD, 1.25 ± 0.4 mmol/(L ± hr) versus 0.74 ± 0.3 mmol/(L ± hr); ±<0.05). Initial sodium concentration was also significantly lower in the pontine lesion group (97.3 ± 6.7 vs 105.6 ± 5.2 mmol/L, p ± <0.05). We conclude that the correction rate of hyponatremia plays a significant role in the pathogenesis of pontine lesions in individuals with profound hyponatremia who undergo large increases in sodium concentration as a result of severe initial hyponatremia.