Hyponatremia in Critically Ill Neurological Patients

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Abstract
Hyponatremia is the most common and important electrolyte disorder encountered in the neurologic intensive care unit (NICU). Advances in our knowledge of the pathophysiological mechanisms at play in patients with acute neurologic disease have improved our understanding of this derangement. Evaluation of hyponatremia requires a structured approach beginning with the measurement of serum and urine osmolalities. Most cases of hyponatremia in the NICU are associated with serum hypotonicity. Iatrogenic causes, most conspicuously inadequate tonicity of intravenous fluids, should be promptly identified and removed when possible. Two main mechanisms are responsible for most noniatrogenic cases of hyponatremia in patients with neurologic or neurosurgical disease: inappropriate secretion of antidiuretic hormone (SIADH) and cerebral salt wasting syndrome (CSW). Distinction between these two syndromes may be difficult and must be based on an accurate assessment of the patient’s volume status. SIADH is associated with normal or slightly expanded volume status and should be treated with fluid restriction. Patients with CSW are hypovolemic and require adequate fluid and sodium replacement. Correction of hyponatremia should not exceed 8 to 10 mmol/L over any 24-hour period to avoid the risk of osmotic demyelination. Hyponatremia may complicate the clinical course of many acute neurologic and neurosurgical disorders. It is most often iatrogenic causes, CSW, or SIADH. Physicians working with critically ill neurologic patients should be familiar with management strategies addressing these underlying pathophysiological mechanisms.