Intraoperative autologous transfusion during major reconstructive spine surgery decreased allogeneic red blood cell transfusions, but patients were exposed to significant numbers of allogeneic blood products.
This study reports a prospective study of 160 randomized patients undergoing major reconstructive spine surgery.
Without delaying start of surgery, 80 patients underwent hemapheresis with coincidental normovolemic hemodilution in the operating room to sequester autologous blood components.
A therapeutic dose plateletpheresis product and an average of 2 U each of freshly collected autologous red cells and fresh plasma were prepared prior to surgical incision.
The same supplies and equipment were used subsequently to carry out intraoperative autologous transfusion (IAT).
Autologous plasma and platelets were transfused to Sequestration patients, contributing to a significant decrease of total allogeneic donor exposures.
One or more autologous red blood cell unit equivalents were cost effectively salvaged and retransfused to 78% of the Sequestration patients.
Altogether, autologous red cells comprised 87% of the total red cells transfused.
During the same time period, 80 age-sex-and weight-matched controls, who received IAT only, were accrued for comparison with Sequestration patients.
Of all red cells transfused to control patients, autologous units comprised 47%. Both patient groups received the same total perioperative red blood cell support. (...)
Mots-clés Pascal : Transfusion, Système autologue, Chirurgie, Peropératoire, Colonne vertébrale, Reconstruction anatomique, Analyse coût, Stratégie, Evaluation, Homme, Economie santé, Soin intensif, Système ostéoarticulaire
Mots-clés Pascal anglais : Transfusion, Autologous system, Surgery, Intraoperative, Vertebral column, Anatomical reconstruction, Cost analysis, Strategy, Evaluation, Human, Health economy, Intensive care, Osteoarticular system
Notice produite par :
Inist-CNRS - Institut de l'Information Scientifique et Technique
Cote : 98-0381841
Code Inist : 002B27D01. Création : 25/01/1999.