• P O Grände, C H Nordström, and B Asgeirsson.
• Anestesi- och intensivvårdskliniken, Universitetssjukhuset, Lund.
• Nord Med. 1994 Jan 1; 109 (5): 157-9.

AbstractMortality is high among patients developing post-traumatic brain oedema and increased intracranial pressure following severe head injury. Although routine treatment varies from one centre to another it often includes one or more of such measures as hyperventilation, high-dose barbiturate therapy, osmotherapy or the drainage of cerebrospinal fluid. The preservation of high cerebral perfusion pressure is fundamental to traditional treatment, often combined with inotropic support, as ischemia is considered to be a crucial factor with regard to the development of secondary injuries and oedema in the brain. In the article is described a new treatment of posttraumatic brain oedema, based on the hypothesis that the development of oedema is instead largely due to disturbance of brain volume control mechanisms resulting from increased permeability of the semi-permeable blood-brain barrier. If this hypothesis is true, oedema therapy should include measures to decrease hydrostatic capillary pressure and preserve normal colloid osmotic pressure. Our new therapy therefore includes hypotensive treatment in the form of beta 1-blockade and alpha 2-stimulation and precapillary vasoconstriction by dihydroergotamine (DHE) infusion, all of which reduce capillary pressure. The DHE may also constrict venous vessels, resulting in reduced blood volume. Colloid osmotic pressure is preserved with albumin infusion. Normovolemia is attained despite manifest fluid balance. With this therapy both mortality and morbidity have been reduced significantly, as compared to retrospective figures for a comparable control group.

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