Physiologic principles for volume regulation of a tissue enclosed in a rigid shell with application to the injured brain.

Abstract

Preservation of a high cerebral perfusion (mean arterial) pressure to prevent ischemia has become the primary focus during treatment of severe head trauma because ischemia is favored as a triggering mechanism behind intracellular brain edema development and poor outcome. A high cerebral perfusion pressure, however, simultaneously may increase the hydrostatic vasogenic edema. The present paper evaluates the mechanisms behind the vasogenic edema by analyzing the physiologic hemodynamic mechanisms controlling the volume of a tissue that is enclosed in a rigid shell, possesses capillaries permeable for solutes, and has depressed autoregulation.