• P O Grände, B Asgeirsson, and C H Nordström.
• Department of Anaesthesia and Intensive Care, University Hospital and University of Lund, Sweden.
• J Trauma. 1997 May 1;42(5 Suppl):S23-31.

BackgroundPreservation 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.Results And ConclusionsWe contend that in the long run, the interstitial volume in such a tissue can be reduced only through reduction in arterial inflow pressure providing an otherwise optimal therapy to improve microcirculation. Therefore we argue, in contrast to the conventional view, that antihypertensive and antistress therapy may be of value by reducing the interstitial tissue volume during treatment of brain edema, and that the problem with ischemia during such therapy can be handled when considering an otherwise optimal intensive care. These physiologic principles of interstitial tissue volume regulation form the basic concept for the "Lund therapy" of severe head injuries, which is a new and controversial therapy of posttraumatic brain edema.

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