
08-15-2007, 10:50 PM
|
|
Registered User
|
|
Join Date: Jan 2003
Posts: 1,422
Thanks: 0
Thanked 80 Times in 52 Posts
|
|
|
The pathogenesis of transfusion-related acute lung injury (TRALI).
1: Br J Haematol. 2007 Mar;136(6):788-99.
The pathogenesis of transfusion-related acute lung injury (TRALI).
Bux J, Sachs UJ.
DRK-Blood Service West of the German Red Cross, Hagen, Germany. j.bux@bsdwest.de
In recent years, transfusion-related acute lung injury (TRALI) has developed from an almost unknown transfusion reaction to the most common cause of transfusion-related major morbidities and fatalities. A clinical definition of TRALI was established in 2004, based on acute respiratory distress, non-cardiogenic lung oedema temporal association with transfusion and hypoxaemia. Histological findings reveal lung oedema, capillary leucostasis and neutrophil extravasation. However, the pathogenesis of TRALI remains controversial. Leucocyte antibodies, present in fresh frozen plasma and platelet concentrates from multiparous donors, and neutrophil priming agents released in stored cellular blood components have been considered to be causative. As neutrophils and endothelial cells are pivotal in the pathogenesis of TRALI, a threshold model was established to try to unify the various reported findings on pathogenesis. This model comprises the priming of neutrophils and/or endothelium by the patient's co-morbidity, neutrophil and/or endothelial cell activation by the transfused blood component, and the severity of the TRALI reaction.
PMID: 17341264 [PubMed - indexed for MEDLINE]
Abstract on PubMed
__________________
Mr. Jan B. Wade
Blood Management Consultant
Enhance Outcomes - Control Cost
For Information Call - 360 296-1807
Email
|