2014
DOI: 10.1007/s10157-014-1021-y
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Correction of hyponatremia and osmotic demyelinating syndrome: have we neglected to think intracellularly?

Abstract: Glial cell minimizes volume changes and injury in response to hyperosmolar stress via mobilization and/or utilization of various electrolytes and metabolic factors. The prevention of ODS likely requires both minimization of correction rate and optimization of intracellular response during the correction phase when a sufficient supply of various factors is necessary.

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Cited by 19 publications
(19 citation statements)
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“…The substance exchange through vascular wall increased and damaged nerve myelin sheath cell. At the same time, the elevation of serum sodium concentration associated with serum osmotic changes by a large fluctuation, may be break up the steady state of cell volume [10]. It then developed central nervous myelinolysis diseases.…”
Section: Discussionmentioning
confidence: 99%
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“…The substance exchange through vascular wall increased and damaged nerve myelin sheath cell. At the same time, the elevation of serum sodium concentration associated with serum osmotic changes by a large fluctuation, may be break up the steady state of cell volume [10]. It then developed central nervous myelinolysis diseases.…”
Section: Discussionmentioning
confidence: 99%
“…It then developed central nervous myelinolysis diseases. And hypertonic stress leads to cell death in variety of cell types, particulaly oligodendrocytes [10]. Associated with the coexsiting factors, such as malnutrition, alcoholism, and so on, contribute to this process.…”
Section: Discussionmentioning
confidence: 99%
“…Potassium is an osmotically active solute like sodium and the repletion of low potassium levels will increase the serum osmolality and result in the shifting of sodium from intracellular to extracellular space [ 16 ]. Monitoring and provision of other osmotically active substrates such as serum phosphate and magnesium are also necessary in the correction of hyponatremia by reducing osmolality differences between compartments [ 17 ]. Our patient was managed with the guiding principle that the serum sodium concentration should be corrected at a rate of no more than 10 meq/L in the first 24 hours, 18 meq/L in the first 48 hours, and 20 meq/L in the first 72 hours to prevent iatrogenic brain injury and central pontine myelinolysis [ 18 , 19 ].…”
Section: Discussionmentioning
confidence: 99%
“…Hypophosphatemia may be a risk factor for ODS [ 3 ]. Our routine hyponatremia treatment protocol requested a STAT level, which was likely life-saving.…”
Section: Discussionmentioning
confidence: 99%