• J Marc Simard, Brian P Walcott, Brian V Nahed, Sameer A Sheth, Kristopher T Kahle, Randall T Peterson, and Jean-Valery C E Coumans.
• Department of Neurosurgery, Massachusetts General Hospital and Harvard Medical School, 55 Fruit Street, White Building Room 502, Boston, MA, 02114, USA.
• Neurocrit Care. 2013 Oct 1;19(2):222-31.

AbstractCerebral edema develops in response to and as a result of a variety of neurologic insults such as ischemic stroke, traumatic brain injury, and tumor. It deforms brain tissue, resulting in localized mass effect and increase in intracranial pressure (ICP) that are associated with a high rate of morbidity and mortality. When administered in bolus form, hyperosmolar agents such as mannitol and hypertonic saline have been shown to reduce total brain water content and decrease ICP, and are currently the mainstays of pharmacological treatment. However, surprisingly, little is known about the increasingly common clinical practice of inducing a state of sustained hypernatremia. Herein, we review the available studies employing sustained hyperosmolar therapy to induce hypernatremia for the prevention and/or treatment of cerebral edema. Insufficient evidence exists to recommend pharmacologic induction of hypernatremia as a treatment for cerebral edema. The strategy of vigilant avoidance of hyponatremia is currently a safer, potentially more efficacious paradigm.

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