Decreased Platelet Number and Function and Increased Fibrinolysis Contribute to Postoperative Bleeding in Cardiopulmonary Bypass Patients

Abstract

SummaryWe simultaneously evaluated platelet and fibrinolytic parameters to assess their individual and combined contributions to postoperative blood loss in cardiopulmonary (CP) bypass patients. Platelet count, platelet aggregability, hematocrit, plasminogen (PLG) concentration, alpha2-antiplasmin (AP) concentration, free protease activity (fPA), and antithrombin-III (AT-III) were measured in nine patients undergoing surgery using cardiopulmonary bypass. Chest tube drainage was used as the measure of postoperative blood loss. Hematocrit, platelet count, PT .G , AP and AT-TTT all decreased during CP bypass, with PLG and AT-III decreasing much more than dilution. During CP bypass, platelet aggregability to A DP did not change significantly from pre-bypass, but aggregability to arachidonic acid (AA) decreased significantly. Following protamine administration there was a large increase (83%) in fPA, the platelet count showed a further drop (from 61 % to 50% of pre-bypass levels) . and platelet aggregability decreased significantly (from 95% to 34% of prebypass levels for ADP, and from 55% to 11.9% for A A). Chest tube drainage during the first four postoperative hours correlated positively (p <0.05) with the combination of increase in free protease activity and decrease in platelet count. The total chest tube drainage correlated significantly with the combination of decrease in platelet count and the decrease in platelet aggregability. These combinations of changes correlated significantly with postoperative blood loss whereas the individual changes did not. These data indicate that during the early postoperative period the increased fibrinolytic activity and the decreased platelet count together contribute toward postoperative blood loss in CP bypass patients, and that during the entire first 24 hour period postoperatively the decreased platelet number and decreased platelet function are important contributors to blood loss.

Effect of Clopidogrel Premedication in Off-Pump Cardiac Surgery

“…15,16,19 Bleeding after CABG can be a combination of inadequate surgical hemostasis, coagulation, and platelet abnormalities. 20 Exposure to cardiopulmonary bypass (CPB) causes dilutional thrombocytopenia, 21,22 coagulopathy, 23 sheer-induced platelet dysfunction, 22,24 a systemic inflammatory response, and activation of plasminogen. 25,26 The safety and efficacy of off-pump CABG (OPCAB) have been confirmed through numerous reports.…”

Effects of Continuous Administration of Clopidogrel Before Off-Pump Coronary Artery Bypass Grafting in Patients With Acute Coronary Syndrome A Propensity Score Analysis

“…5 Exposure to cardiopulmonary bypass (CPB) causes dilutional thrombocytopenia, coagulopathy, shear-induced platelet dysfunction, a systemic inflammatory response and activation of plasminogen, and the safety and efficacy of offpump CABG (OPCAB) have been confirmed. [6][7][8][9][10][11][12][13][14][15] By eliminating the deleterious effects of CPB, OPCAB surgery has been found to result in a 2-fold reduction in postoperative bleeding, lower surgical reexploration rates and a 25% decrease in transfusion requirements. 16,17 Clopidogrel, however, may reduce these advantages of OPCAB surgery by increasing perioperative hemorrhagic complications.…”

Intraoperative Autotransfusion of RBC and PRP

“…During CPB, platelets are damaged by contact with the surfaces of the extracorporeal circuit, subsequently circulating as mostly nonfunctional cells. After CPB, reduced platelet counts and impaired function result in a notably impaired procoagulatory blood moiety 54,56 . Aggregation ability and adhesiveness of platelets are inhibited, and a decrease in ß-thromboglobulin, a-granules and membrane binding sites can be observed 52,54,56 .…”

“…After CPB, reduced platelet counts and impaired function result in a notably impaired procoagulatory blood moiety 54,56 . Aggregation ability and adhesiveness of platelets are inhibited, and a decrease in ß-thromboglobulin, a-granules and membrane binding sites can be observed 52,54,56 . Administration of heparin does not sufficiently prevent this CPB-induced activation of the clotting system, the extrinsic fibrinolysis and the protein C-thrombomodulin system 53,57 .…”