Brain edema

The cellular mechanisms of secondary brain injury described above contribute to brain edema, and subsequently to increased intracranial pressure, decreased cerebral perfusion, and cerebral ischemia. Brain edema has classically been described as either vasogenic or cytotoxic. Vasogenic edema results from disruption of the blood-brain barrier which is maintained by tight junctions between the endothelial cells that line the vessels of the brain. Injury to these cells allows extravasation of fluid and proteins into the interstitial space of the brain parenchyma. Disruption of endothelial cells may be primary, resulting from the initial impact or subsequent hemorrhage, or secondary, resulting from free-radical generation, cytokines, and other secondary mechanisms of injury.

Cytotoxic or cellular edema is edema of the cells themselves, whereas vasogenic edema is edema of the interstitial space. Cytotoxic edema results from failure of cellular ion homeostasis and membrane function. Secondary injury at a cellular level results in loss of ion homeostasis and membrane dysfunction. The time course of brain edema is variable. However, it is believed that vasogenic edema occurs early after injury and cytotoxic edema occurs in a more delayed fashion. Brain edema is often maximal 24 to 48 h after traumatic brain injury.

Brain edema is significant as a marker for injury and also as a cause of secondary injury. This is because the brain is in a closed container—the skull. Intracranial pressure is determined by the volumes of three elements contained in the skull: the brain parenchyma, the blood, and the cerebrospinal fluid. An increase in the volume of any of these elements will result in increased intracranial pressure after compensatory mechanisms are exhausted. As intracranial pressure rises, there is an initial passive release of cerebrospinal fluid into the spinal canal. There is also an innate compliance of the craniospinal axis that allows for an increase in intracranial contents without an initial increase in intracranial pressure. However, once the compensatory reserve is exhausted, there is a precipitous rise in intracranial pressure.

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