You are the anesthesia provider for a 71-year-old man with multivessel coronary artery disease and normal preoperative labs who is undergoing a whopper of a coronary artery bypass graft (six vessels!) on cardiopulmonary bypass (CPB). Anticoagulation was managed with appropriate heparinization and protamine reversal as dictated by the HEPCON Heparin Management System. Amicar (Medtronic, Inc., Minneapolis, MN) was given pre-CPB in anticipation of a long CPB run (187 minutes). Following heparin neutralization, the floodgates appear to burst open and profuse bleeding from the surgical field is apparent; the hemoglobin measured just before CPB separation is 10 mg/dL. The surgeon notes that there is no apparent “surgical bleeding,” only diffuse oozing from all tissues and anastomoses. He requests immediate administration of fresh frozen plasma (FFP), cryoprecipitate, banked red blood cells (RBCs), and “rescue aprotinin therapy.” Central laboratory coagulation studies are sent off STAT. FFP, platelets, and banked RBCs are immediately available in the operating room. What is the best course of treatment for the patient at this time?

Start a thromboelastograph (TEG) right away if available; it will help diagnose the nature of the coagulopathy within 15 minutes. Do not administer “rescue aprotinin” to patients already treated with an antifibrinolytic. In the absence of preoperative antiplatelet or antithrombotic therapy, the bleeding is most likely due to the platelets getting knocked around in the CPB circuit (mechanical shear stress activation) during the prolonged pump run. Administer 6 U of platelets pronto! Platelets should not be given too quickly to avoid hypotension associated with bradykinin release. Give crystalloid to maintain intravascular volume. Do not inject concentrated calcium solutions in the same intravenous line as the platelets because it will activate them in the tubing! Following administration of the platelets, the field becomes considerably less oozy, and the central laboratory reports a platelet count (drawn pretransfusion) of 140 th/mm3; the activated partial thromboplastin time (aPTT) is normal, and the prothrombin time (PT) is prolonged. No additional blood products are given. The platelet count was not helpful in diagnosing the nature of this coagulopathy because many of the counted platelets were dysfunctional or “spent platelets.” The PT was
also misleading. Pretransfusion TEG confirms poor platelet function and normal coagulation protein function.

If anyone is going to experience a clinically significant perioperative coagulopathy, it will probably be a cardiac surgical patient. The complexity of cardiac surgical procedures distinguishes the coagulopathy seen in these patients. Remember that cardiac surgery patients are routinely exposed to variable time periods of CPB. Whether the Silastic CPB circuit is uncoated, bonded with heparin, or bonded with a uniquely charged coating (Smart tubing, SMART; Cobe Cardiovascular, Arvarda, CO), the coagulopathy observed has been shown to correlate with the length of time spent on CPB (i.e., there is an increasing incidence of coagulopathy as CPB time increases). In general, CPB times exceeding 3 hours should alert the clinician to the potential for development of a clinically significant coagulopathy. Blood-synthetic tubing/filter interfaces and blood-air interfaces within the CPB circuitry initiate activation of systemic inflammatory pathways. Systemic inflammation is tied to the coagulation system and can provoke imbalance toward hypocoagulability. CPB-associated mechanical trauma to the blood elements (e.g., CPB induces shear stress injury, which activates platelets) causes anemia, thrombocytopenia, and a functional platelet defect that contributes to the development of coagulopathy. In addition, the same processes associated with the conduct of cardiac surgery reproducibly manifest an antifibrinolytic state that is only partially overcome through the pre-CPB initiation of antifibrinolytic agents. Furthermore, because many cardiac surgery patients have undergone previous percutaneous coronary interventions (e.g., coronary stenting and/or angioplasty) or present with a low cardiac output syndrome, they are routinely treated with antiplatelet and/or antithrombotic agents. The cardiologists love to give these drugs that cause cardiac surgery patients to bleed! These treatments are associated with increased postoperative hemorrhage and the increased need for transfusion of allogeneic blood products. Several antithrombotic (e.g., low-molecular-weight heparin) and antiplatelet (e.g., clopidogrel) agents cannot be neutralized pharmacologically and will require the administration of allogeneic blood products to overcome their effects.