Managing the coagulopathy associated with cardiopulmonary bypass

Abstract

Cardiopulmonary bypass (CPB) has allowed for significant surgical advancements, but accompanying risks can be significant and must be expertly managed. One of the foremost risks is coagulopathic bleeding. Increasing levels of bleeding in cardiac surgical patients at the time of separation from CPB are associated with poor outcomes and mortality. CPB‐associated coagulopathy is typically multifactorial and rarely due to inadequate reversal of systemic heparin alone. The components of the bypass circuit induce systemic inflammation and multiple disturbances of the coagulation and fibrinolytic systems. Anticipating coagulopathy is the first step in managing it, and specific patient and procedural risk factors have been identified as predictors of excessive bleeding. Medication management pre‐procedure is critical, as patients undergoing cardiac surgery are commonly on anticoagulants or antiplatelet agents. Important adjuncts to avoid transfusion include antifibrinolytics, and perfusion practices such as red cell salvage, sequestration, and retrograde autologous priming of the bypass circuit have varying degrees of evidence supporting their use. Understanding the patient's coagulation status helps target product replacement and avoid larger volume transfusion. There is increasing recognition of the role of point‐of‐care viscoelastic and functional platelet testing. Common pitfalls in the management of post‐CPB coagulopathy include overdosing protamine for heparin reversal, imperfect laboratory measures of thrombin generation that result in normal or near‐normal laboratory results in the presence of continued bleeding, and delayed recognition of surgical bleeding. While challenging, the effective management of CPB‐associated coagulopathy can significantly improve patient outcomes.

The association of prothrombin complex concentrates with postoperative outcomes in cardiac surgery: an observational substudy of the FIBRES randomized controlled trial

“…2 The causes of coagulopathy are multifactorial and include thrombocytopenia and platelet dysfunction, decreased fibrinogen concentration, impaired thrombin generation, and depletion of coagulation factors. 3,4 Regarding the latter, the average patient undergoing cardiac surgery with cardiopulmonary bypass (CPB) has a 40-50% drop in coagulation factor levels and a [ 50% drop in thrombin generation capacity, suggesting that it is an important cause of coagulopathy. [5][6][7] Frozen plasma (FP) is the treatment of choice in bleeding patients with coagulation factor deficiency and is administered to approximately 15% of all patients undergoing cardiac surgery in the United States.…”

Imaging the dynamics and microstructure of fibrin clot polymerization in cardiac surgical patients using spectrally encoded confocal microscopy

“…Despite heparin anticoagulation, residual fibrin formation may yet occur that may be exacerbated over the duration of CPB. Thrombin bound to fibrin may be deposited within the CPB circuit that may influence a number of ensuing processes including thrombin‐induced fibrinolysis, consumption of clotting factors or activation of platelets that may all influence fibrin clot properties 23 . Increased C‐reactive protein levels following the activation of inflammatory cells may further impair hemostasis 23 .…”

“…Thrombin bound to fibrin may be deposited within the CPB circuit that may influence a number of ensuing processes including thrombin‐induced fibrinolysis, consumption of clotting factors or activation of platelets that may all influence fibrin clot properties 23 . Increased C‐reactive protein levels following the activation of inflammatory cells may further impair hemostasis 23 . Additional factors include hypothermia that may slow down coagulation kinetics, delay the reversal of heparin and may affect impair platelet function and fibrin clotting.…”

Manejo intraoperatório do sangramento em cirurgias de grande porte com métodos viscoelástico

“…O "efeito rebote" da heparina consiste na recorrência da sua atividade anticoagulante mesmo após sua neutralização pela protamina, e tem potencial de inibir a coagulação e a função Manejo intraoperatório do sangramento em cirurgias de grande porte com métodos viscoelástico Queiroz DV, et al plaquetária. Entretanto, o excesso de protamina pode ter efeito adverso semelhante, além de potencializar a fibrinólise e causar trombocitopenia 12,13,15 .…”