• Wendy L Wright.
• Neuroscience Intensive Care Unit, Emory University Hospital Midtown, Atlanta, GA, USA. wwrigh2@emory.edu
• Curr Neurol Neurosci Rep. 2012 Aug 1; 12 (4): 466-73.

AbstractSodium and fluid management in the brain injured patient directly impacts cerebral edema and cerebral perfusion pressure. Sodium is a major determinant of neuronal size and therefore hyponatremia is aggressively avoided, as hypoosmolar states result in cerebral edema. Negative fluid balance is often avoided because resultant drop in cerebral perfusion pressure can contribute to cerebral ischemia, further inducing secondary neuronal injury. Patients with brain injury are at risk for disorders of sodium and fluid balance (eg, syndrome of inappropriate antidiuresis, cerebral salt wasting, and diabetes insipidus). Knowledge of normal homeostatic and brain regulatory volume mechanisms is necessary to avoid inducing further neuronal or systemic injury while trying to correct sodium and fluid disorders in brain injured patients. Osmotherapy is a common part of managing cerebral edema in neurocritical care units, but more studies are needed to establish practice guidelines.

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