Abstract
The therapy of brain oedema described is based on the haemodynamic effects of an increase in capillary permeability of the semipermeable blood-brain barrier (BBB). The transcapillary fluid fluxes are normally controlled by the crystalloid osmotic pressure differences. After a trauma when the BBB is more open for solutes these fluxes will instead be controlled by the colloid osmotic and hydrostatic capillary pressures and will tend towards a Starling fluid equilibrium causing an interstitial or vasogenic oedema. Therefore, an aim of a potential therapy of posttraumatic brain oedema should be to decrease hydrostatic capillary pressure and to preserve a normal colloid osmotic pressure. We present a clinical application of this hypothesis by reducing hydrostatic capillary pressure via precapillary vasoconstriction as obtained by infusion of dihydroergotamine and, if necessary, also by decreasing blood pressure by means of s1- blockade and α2-stimulation (clonidine). Colloid osmotic pressure is maintained with albumin infusions. Preliminary results indicate that this treatment of brain oedema after a head trauma is effective in decreasing ICP, increasing survival rate and improving outcome.
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