• Richard H Sterns, John K Hix, and Stephen M Silver.
• Chest. 2013 Aug 1;144(2):672-9.

AbstractHyponatremia is common in critical care units. Avoidance of neurologic injury requires a clear understanding of why the serum sodium (Na) concentration falls and why it rises, how the brain responds to a changing serum Na concentration, and what the goals of therapy should be. A 4 to 6 mEq/L increase in serum Na concentration is sufficient to treat life-threatening cerebral edema caused by acute hyponatremia. In chronic (> 48 h), severe (< 120 mEq/L) hyponatremia, correction by > 8 to 10 mEq/L/d risks iatrogenic osmotic demyelination syndrome (ODS); therefore, a 4 to 6 mEq/L daily increase in serum Na concentration should be the goal in most patients. With the possible exception of hyponatremia caused by heart failure or hepatic cirrhosis, a rapid initial increase in serum Na for severe symptoms and avoidance of overcorrection are best achieved with 3% saline given in either a peripheral or central vein. Inadvertent overcorrection can be avoided in high-risk patients with chronic hyponatremia by administration of desmopressin to prevent excessive urinary water losses. In patients with hyponatremia with oliguric kidney failure, controlled correction can be achieved with modified hemodialysis or continuous renal replacement therapies. ODS is potentially reversible, even in severely affected patients who are quadriplegic, unresponsive, and ventilator dependent. Supportive care should be offered several weeks before concluding that the condition is hopeless.

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