title: A new therapy of post-trauma brain oedema based on haemodynamic principles for brain volume regulation.
abstract: OBJECTIVE
  To evaluate a new therapy of posttraumatic brain oedema, with the main concept that opening of the blood-brain barrier upsets the normal brain volume regulation, inducing oedema formation. This means that transcapillary fluid fluxes will be controlled by hydrostatic capillary and colloid osmotic pressures, rather than by crystalloid osmotic pressure. If so, brain oedema therapy should include reduction of hydrostatic capillary pressure and preservation of normal colloid osmotic pressure.
  
  
  METHODS
  11 severely head injured comatose patients with brain swelling, raised intracranial pressure (ICP), and impaired cerebrovascular response to hyperventilation.
  
  
  METHODS
  To reduce capillary hydrostatic pressure the patients were given hypotensive therapy (beta 1-antagonist, metoprolol and alpha 2-agonist, clonidine) and a potential precapillary vasoconstrictor (dihydroergotamine). The latter may also decrease cerebral blood volume through venous capacitance constriction. Colloid osmotic pressure was maintained by albumin infusions. The concept implies the need of a negative fluid balance with preserved normovolaemia.
  
  
  RESULTS
  ICP decreased significantly within a few hours of treatment with unaltered perfusion pressure in spite of lowered blood pressure. Of 11 patients 9 survived with good recovery/moderate disability, 2 died. This was compared to outcome in a historical control group with identical entry criteria, given conventional brain oedema therapy, where mortality/vegetativity/severe disability was 100%.
  
  
  CONCLUSIONS
  The results indicate that the therapy should focus on extracellular rather than intracellular oedema and that ischemia is not the main triggering mechanism behind oedema formation. We suggest that our therapy is superior to conventional therapy by preventing herniation during the healing period of the blood-brain barrier.
authors.affiliation: Department of Anaesthesia and Intensive Care, University Hospital of Lund, Sweden.
authors.forename: B
authors.initials: B
authors.lastname: Asgeirsson
authors.forename: P O
authors.initials: PO
authors.lastname: Grände
authors.forename: C H
authors.initials: CH
authors.lastname: Nordström
mesh_terms: D000293:Adolescent; D000328:Adult; D001812:Blood-Brain Barrier; D001929:Brain Edema / Q000209:etiology / Q000503:physiopathology / Q000628:therapy*; D001930:Brain Injuries / Q000150:complications / Q000503:physiopathology / Q000628:therapy*; D002675:Child, Preschool; D003128:Coma / Q000209:etiology / Q000503:physiopathology / Q000628:therapy; D003131:Combined Modality Therapy / Q000379:methods; D005260:Female; D006439:Hemodynamics; D006801:Humans; D007427:Intracranial Pressure; D008297:Male; D008875:Middle Aged; D013997:Time Factors; D016896:Treatment Outcome