Hypernatremia for the Prevention and Treatment of Cerebral Edema in Traumatic Brain Injury
Status:
Withdrawn
Trial end date:
2013-08-01
Target enrollment:
Participant gender:
Summary
Cerebral edema is seen heterogenous group of neurological disease states that mainly fall
under the categories of metabolic, infectious, neoplasia, cerebrovascular, and traumatic
brain injury disease states. Regardless of the driving force, cerebral edema is defined as
the accumulation of fluid in the brain's intracellular and extracellular spaces. This occurs
secondary to alterations in the complex interplay between four distinct fluid compartments
within the cranium. In any human cranium; fluid is contained in the blood, the cerebrospinal
fluid, interstitial fluid of the brain parenchyma, and the intracellular fluid of the neurons
and glia. Fluid movement occurs normally between these compartments and depends on specific
concentrations of solutes (such as sodium) and water. In brain-injured states, the normal
regulation of this process is disturbed and cerebral edema can develop. Cerebral edema leads
to increased intracranial pressure and mortality secondary to brain tissue compression, given
the confines of the fixed-volume cranium. Additionally, secondary neuronal dysfunction or
death can occur at the cellular level secondary to the disruption of ion gradients that
control metabolism and function.
While studies utilizing bolus dosing of hyperosmolar therapy to target signs or symptoms of
increased intracranial pressure secondary to cerebral edema are numerous, there is a paucity
of studies relating to continuous infusion of hyperosmolar therapy for targeted sustained
hypernatremia for the prevention and treatment of cerebral edema. The investigators
hypothesize that induced, sustained hypernatremia following traumatic brain injury will
decrease the rate of cerebral edema formation and improve patient outcomes.