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  <controlfield tag="008">180411e20131001xx      s     000 0 eng  </controlfield>
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   <subfield code="a">10.1007/s12028-013-9824-3</subfield>
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   <subfield code="a">(NATIONALLICENCE)springer-10.1007/s12028-013-9824-3</subfield>
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   <subfield code="a">Induced and Sustained Hypernatremia for the Prevention and Treatment of Cerebral Edema Following Brain Injury</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Justine Ryu, Brian Walcott, Kristopher Kahle, Sameer Sheth, Randall Peterson, Brian Nahed, Jean-Valery Coumans, J. Simard]</subfield>
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   <subfield code="a">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.</subfield>
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   <subfield code="a">Springer Science+Business Media New York, 2013</subfield>
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   <subfield code="a">Hypernatremia</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Brain injuries</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Brain edema</subfield>
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   <subfield code="a">Intracranial pressure</subfield>
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   <subfield code="a">Stroke</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Renal insufficiency</subfield>
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   <subfield code="a">Ryu</subfield>
   <subfield code="D">Justine</subfield>
   <subfield code="u">Department of Neurosurgery, Massachusetts General Hospital and Harvard Medical School, 55 Fruit Street, White Building Room 502, 02114, Boston, MA, USA</subfield>
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   <subfield code="a">Walcott</subfield>
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   <subfield code="u">Department of Neurosurgery, Massachusetts General Hospital and Harvard Medical School, 55 Fruit Street, White Building Room 502, 02114, Boston, MA, USA</subfield>
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   <subfield code="a">Kahle</subfield>
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   <subfield code="u">Department of Neurosurgery, Massachusetts General Hospital and Harvard Medical School, 55 Fruit Street, White Building Room 502, 02114, Boston, MA, USA</subfield>
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   <subfield code="a">Sheth</subfield>
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   <subfield code="u">Department of Neurosurgery, Massachusetts General Hospital and Harvard Medical School, 55 Fruit Street, White Building Room 502, 02114, Boston, MA, USA</subfield>
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   <subfield code="a">Peterson</subfield>
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   <subfield code="u">Department of Neurosurgery, Massachusetts General Hospital and Harvard Medical School, 55 Fruit Street, White Building Room 502, 02114, Boston, MA, USA</subfield>
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   <subfield code="u">Department of Neurosurgery, Massachusetts General Hospital and Harvard Medical School, 55 Fruit Street, White Building Room 502, 02114, Boston, MA, USA</subfield>
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   <subfield code="a">Simard</subfield>
   <subfield code="D">J.</subfield>
   <subfield code="u">Department of Neurosurgery, University of Maryland, Baltimore, MD, USA</subfield>
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   <subfield code="t">Neurocritical Care</subfield>
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   <subfield code="z">Onlinezugriff via DOI</subfield>
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   <subfield code="D">1</subfield>
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   <subfield code="B">NATIONALLICENCE</subfield>
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   <subfield code="a">Metadata rights reserved</subfield>
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