Management of Severe Hyponatremia and SIADH
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Severe or acute hyponatremia carries high risk for cerebral edema, seizure and brain death, and requires intensive care unit (ICU) admission and urgent correction. A small immediate correction is sufficient for preventing neurologic sequelae of hyponatremia. Severe chronic hyponatremia should be evaluated with attention to volume status and treated accordingly. The volume status of an ICU patient can be difficult to assess, and hyponatremia may be multifactorial. A small volume trial of isotonic fluids can be informative in these cases. In all cases of hyponatremia, correction should progress slowly with frequent monitoring of serum sodium. Osmotic demyelination syndrome (ODS) results from overly rapid correction of serum sodium. It can cause devastating paralysis, but meaningful recovery is possible. Vasopressin type 2 (V2) receptor antagonists are promising for management of the syndrome of inappropriate antidiuretic hormone activity (SIADH), but the potential for hypovolemia and overly rapid correction of serum sodium in critically ill patients is concerning, and there are no trials specific to ICU settings to guide use. Based on case reports and animal models, urea is an intriguing therapeutic option for correcting serum sodium with reduced risk of ODS, and for preventing ODS in high-risk patients.
KeywordsSevere hyponatremia Intensive care unit SIADH Vasopressin V2 receptor antagonist (vaptan) Osmotic demyelination syndrome Myelinolysis Cerebral edema Hypertonic saline Cerebral salt wasting Urea
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