The Brain Response to Infusion Edema: Dynamics of Fluid Resolution

Abstract

It is now generally accepted that the release of fluid from damaged cerebral vessels into a space of limited compliance gives rise to the development of local tissue pressure gradients which act to propel the fluid through the brain tissue [12, 13]. The concomitant increase of tissue conductance due to widening of extracellular channels facilitates the spread of edema from the site of the lesion [10]. It is hypothesized that this local increase of tissue pressure is sufficient in magnitude to advance the edema front toward the ventricles where it is cleared by the cerebrospinal fluid (CSF) system, and this sink action of the CSF is thought to play a major role in the resolution process [14]. Our work has shown tissue pressure gradients develop following cold injury, however, they are of relatively small magnitude and dissipate within a few hours [9]. Further studies of tissue biomechanics have shown that with edema tissue resistance to passage of fluid is decreased and that this alteration of hydraulic property accounts for the rapid equilibration of pressure within the brain parenchyma [15]. In our view, the magnitude of pressures developed are more than sufficient to propel fluid through the white matter. However, these hydrostatic gradients can be sustained only with a continued seepage of fluid from the site of injury. Without a continued extravasation of fluid, equilibration of the tissue pressure to the level of the ICP occurs rapidly. For this reason, the role of hydrostatic gradients in the resolution process of edema fluid may be limited.

This work was supported by Grant No. 1131624225A2 from the National Institute of Health and the Departmnet of Neurosurgery of the Albert Einstein College of Medicine