Autotransfusion in coronary artery bypass grafting: disparity in laboratory tests and clinical performance.
OBJECTIVE
Autotransfusion during and after cardiac surgery is widely performed, but its effects on coagulation, fibrinolysis, and inflammatory response have not been known in detail.


METHODS
Hemostatic and inflammatory markers were extensively studied in 40 coronary artery bypass patients undergoing a consistent intraoperative and postoperative autotransfusion protocol. An identical autotransfusion protocol was applied to 4916 consecutive coronary patients and the overall clinical results were evaluated in this large patient population.


RESULTS
The autologous blood pooled before bypass remained nearly inactivated after storage. A slight elevation of thrombin-antithrombin complex and prothrombin fragment 1.2, as well as plasmin/alpha(2)-antiplasmin complex was found in the content of the extracorporeal circuit after surgery, indicating thrombin formation and fibrinolytic activity. Also some increase of beta-thromboglobulin was present. In the mediastinal shed blood, complete coagulation, as evidenced by the absence of fibrinogen, had taken place and all parameters described above were extremely elevated. However, no thrombin activity was detected. As for the inflammatory response, moderately increased levels of complement activation products, terminal complement complex, and interleukin-6 traced in the extracorporeal circuit reached very high levels in mediastinal shed blood. Autotransfusion of the residual extracorporeal circuit blood and the mediastinal drainage was followed by elevation of most of these markers in circulating plasma. On the other hand, no correlating harmful effects were recorded in the study patients or in the consecutive 4916 patients. Coagulation disturbances were rare and allogeneic transfusions were required in fewer than 4% of all patients.


CONCLUSIONS
The hemostatic and immunologic systems were moderately activated in the autologous blood remaining in the extracorporeal circuit, whereas the mediastinal shed blood was highly activated in all aspects. However, autotransfusion had no correlating clinical side-effects and the subsequent exposure to allogeneic blood products was minimal.
Flom-Halvorsen
H I
HI
Department of Cardiac Surgery, Oslo Heart Center, University of Oslo, Rikshospitalet, Oslo, Norway.
Ovrum
E
E
Tangen
G
G
Brosstad
F
F
Ringdal
M A
MA
Oystese
R
R
D000368:Aged; D000933:Antifibrinolytic Agents; D000990:Antithrombin III / Q000032:analysis; D015415:Biomarkers / Q000097:blood; D001777:Blood Coagulation / Q000502:physiology; D001804:Blood Transfusion, Autologous; D002315:Cardiopulmonary Bypass; D003167:Complement Activation; D015938:Complement Membrane Attack Complex / Q000032:analysis; D001026:Coronary Artery Bypass; D004322:Drainage; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D005341:Fibrinolysin / Q000032:analysis; D005342:Fibrinolysis / Q000502:physiology; D006487:Hemostasis / Q000502:physiology; D006801:Humans; D015850:Interleukin-6 / Q000097:blood; D007430:Intraoperative Care; D016014:Linear Models; D008297:Male; D008482:Mediastinum; D008875:Middle Aged; D010446:Peptide Fragments / Q000032:analysis; D010447:Peptide Hydrolases / Q000032:analysis; D011182:Postoperative Care; D011516:Prothrombin / Q000032:analysis; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology; D013917:Thrombin / Q000096:biosynthesis; D000979:alpha-2-Antiplasmin / Q000032:analysis; D001620:beta-Thromboglobulin / Q000032:analysis
D000933:Antifibrinolytic Agents; D015415:Biomarkers; D015938:Complement Membrane Attack Complex; D015850:Interleukin-6; D010446:Peptide Fragments; D000979:alpha-2-Antiplasmin; C046193:antithrombin III-protease complex; D001620:beta-Thromboglobulin; C037742:plasmin-plasmin inhibitor complex; C045879:prothrombin fragment 1.2; D000990:Antithrombin III; D011516:Prothrombin; D005340:Fibrinogen; D010447:Peptide Hydrolases; D013917:Thrombin; D005341:Fibrinolysin