Hyponatremia after traumatic brain injury [Neurosurgery Wiki]

This page is read only. You can view the source, but not change it. Ask your administrator if you think this is wrong.
====== Hyponatremia after traumatic brain injury ======

[[Hyponatremia]] is frequent in patients suffering from [[traumatic brain injury]], [[subarachnoid hemorrhage]], or following [[intracranial]] [[procedure]]s, with approximately 20% having a decreased serum [[sodium]] concentration to <125 mmol/L. The [[pathophysiology]] of hyponatremia in neurotrauma is not completely understood, but in large part is explained by the syndrome of inappropriate secretion of [[antidiuretic hormone]] ([[SIADH]]). The abnormal water and/or sodium handling creates an osmotic gradient promoting the shift of water into brain cells, thereby worsening [[cerebral edema]] and precipitating neurological deterioration. Unless hyponatremia is corrected promptly and effectively, [[morbidity]] and [[mortality]] increases through [[seizure]]s, elevations in [[intracranial pressure]], and/or [[herniation]]. The excess mortality in patients with severe [[hyponatremia]] (<125 mmol/L) extends beyond the time frame of hospital [[admission]], with a reported [[mortality]] of 20% in hospital and 45% within 6 months of follow-up. Current options for the management of [[hyponatremia]] include fluid restriction, [[hypertonic saline]], [[mineralocorticoid]]s, and osmotic diuretics. However, the recent development of [[vasopressin]] receptor antagonists provides a more physiological tool for the management of excess water retention and consequent hyponatremia, such as occurs in [[SIADH]]
((Kleindienst A, Hannon MJ, Buchfelder M, Verbalis JG. Hyponatremia in
Neurotrauma: The Role of Vasopressin. J Neurotrauma. 2016 Apr 1;33(7):615-24.
doi: 10.1089/neu.2015.3981. Epub 2015 Dec 23. Review. PubMed PMID: 26472056.
)).