Journal
NEUROCRITICAL CARE
Volume 19, Issue 2, Pages 222-231Publisher
HUMANA PRESS INC
DOI: 10.1007/s12028-013-9824-3
Keywords
Hypernatremia; Brain injuries; Brain edema; Intracranial pressure; Stroke; Renal insufficiency
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Funding
- Department of Veterans Affairs (Baltimore)
- National Institute of Neurological Disorders and Stroke (NINDS) [NS060801, NS061808]
- National Heart, Lung and Blood Institute [HL082517]
- Department of the Army [W81XWH 1010898]
- Christopher and Dana Reeve Foundation
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Cerebral 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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