Platelet Function during Platelet-Rich Plasma Sequestration in Complex Cardiac Surgical Procedures - Prospective Controlled Study
Journal Title: Biomedical Journal of Scientific & Technical Research (BJSTR) - Year 2018, Vol 6, Issue 2
Abstract
Cardiopulmonary bypass (CPB) is associated with common activation of all four integral components of hemostasis, that is, the endothelium, plasma proteins, platelets and fibrinolysis. The causative factors include the presence of an artificial non-endothelial surface of the CPB system, non-pulsatile blood flow, hemodilution, hypothermia, surgical trauma and a systemic inflammatory response to CPB. Microthrombi formation, coagulation defects and hypercoagulability in the postoperative period may occur. The key pathway of activation is platelet binding to collagen via von Willebrand factor, platelet activation and aggregation and formation of an initial hemostatic plug. Thrombin generation (tF+fVIIa →fIXa →fXa →prothrombin →thrombin) activates platelets, fV, fVIII and fXI. Fibrinogen and fXIII stabilize the clot. Fibrinogen bound to the CPB circuit provides a strong binding site for platelets via the GP IIb/IIIa receptor. Bound platelets are activated, promoting further thrombin formation via the PAR-1 receptor. Shed blood, if reinfused, increases platelet activation. Plasmin erodes the clot and directly activates platelet consumption [1-15]. The use of antifibrinolytics preserves platelet activation and reduces platelet GPIb receptor cleavage [16]. Thrombocytopenia during and after CPB is common but an isolated platelet count below 50G/L is usually not associated with serious bleeding if no other hemostasis disorders are present [17]. Platelet function is slightly increased by mild hypothermia and decreased by severe hypothermia. Some commonly used drugs other than heparin; protamine and platelet inhibitors reduce platelet activation or aggregation (NO donors such as nitrates or phosphodiesterase inhibitors such as milrinone). In summary, platelets are one of the most fragile components of hemostasis during CPB. Current cell-salvage techniques are capable of preserving platelets by autologous platelet-rich plasma (PRP) sequestration. The present study tested platelet function during and after PRP sequestration in cardiac surgery procedures using CPB. We hypothesized that platelet count and aggregability would be preserved by the method. Methods Patients were enrolled after their written informed consent and local ethics committee approval were obtained. The study comprised patients scheduled for elective cardiac surgery with an estimated CPB time of more than two hours (complex procedures such as multiple valvular, combined, redo and thoracic aortic surgery). The inclusion criterion was initial hematocrit >0.35 as 800ml of whole blood had to be collected and processed before CPB. Excluded were patients with hematocrit <0.35, on active antiplatelet agents or known to have hematological disorders. The CPB method included the Capiox RX 25 membrane oxygenator with rheoparin coating, Stöckert S5 centrifugal pump, crystalloid/colloid priming (Plasmalyte1000mL, HAES 6% 500mL, Mannitol 20% 200mL) and St. Thomas cold blood cardioplegia. Anticoagulation was provided with unfractionated heparin (UFH) as follows: 3 mg/ kg i.v. bolus + 1mg/kg into the priming volume, a targeted activated coagulation time (ACT) (Hemochron, kaolinactivated) >400s, with possible additional bolus doses of UFH. Heparin reversal after CPB termination was accomplished with protamine sulphate at a 1:1 weight ratio to heparin. Prophylactic administration of tranexamic acid 30mg/kg i.v. bolus and 15mg/kg into CPB was mandatory. After induction of general anesthesia, 800mL of whole blood was collected from a large-bore (min. 8 Fr) central venous catheter and replaced with an adequate volume of a balanced crystalloid solution. Blood was processed in the Sorin Xtra cell saver (LivaNova, Italy). The manufacturer’s protocol was used (175ml Latham bowl, 2-port sequestration system, CPD-A bags for whole blood collection, Vacutainer EDTA tubes, prime flow 100ml/min with manual reduction to 70mL/min after complete filling, PRP spill flow 20 ml/ min). Red blood cell (RBC) and PRP sequestration was performed simultaneously. PRP was stored at room temperature in the operating theater under an anesthetist’s supervision and always retransfused immediately after CPB before the end of surgery. RBCs were retransfused in the theater if necessary or postoperatively in the ICU according to hematocrit and the clinical situation. The transfusion protocol was guided by the center’s experiences and thromboelastography (TEG 5000, Haemonetics, USA); kaolinactivated plain and heparinase cups were used for each test. Blood samples were collected from an arterial line and processed in the laboratory before surgery, from PRP, after PRP retransfusion and at the end of surgery.
Authors and Affiliations
Slavik L, Hajek R, Chaloupkova P, Ulehlova J, Lonsky V
Keywords
Related Articles
- EP ID EP592305
- DOI 10.26717/BJSTR.2018.06.001317
- Views 144
- Downloads 0
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