Management of Post-Bypass Hemostatic Disorders 1. Rule out a surgical cause.

Copious chest tube drainage usually results from a vessel in need of suture. A generalized ooze suggests a nonsurgical cause. Keep the blood pressure in the low normal range whilst the surgeons effect repair, and optimally for sometime thereafter to maximize the potential for clot formation. 2. Maintain normothermia. In the effort to restore intravascular volume rapidly, clinicians must infuse refrigerated blood products only with adequate warming, lest they cause or accentuate hypothermia, thereby decreasing platelet function and enzymatic activity of clotting proteins. 3. Determine the cause. While surgeons are checking anastomoses, assure complete heparin neutralization with an ACT and aPTT, the latter showing prolongation at smaller blood concentrations of heparin. Consider measuring fibrinogen concentration, D-dimer, and thrombin time, the last of which is prolonged only by residual heparin, inadequate amount or functionality of fibrinogen, and fibrin degradation products. 4. Give more protamine if the ACT exceeds its baseline (preheparin) value by greater than 10 seconds (or the aPTT is more than 1.3 times its control value). A dose of 25 to 50 mg usually suffices. Do so upon learning the ACT results and while awaiting other laboratory results. 5. In the absence of hypovolemia, consider application of 5 cm of PEEP to help tamponade bleeders in the chest. This maneuver may be most effective after the sternum is closed because of limitations in the ability of PEEP to effectively increase mediastinal end-expiratory pressure while the sternum remains open. 6. Platelet transfusion and/or DDAVP. If testing uncovers platelet dysfunction, or if it is highly suspected, give 1 unit of platelet concentrates per 10 kg body weight for an estimated effective platelet count below 100 K/L. While awaiting platelet concentrates from the blood bank, consider administration of DDAVP 0.3 ug/kg especially if there is laboratory evidence of platelet dysfunction (e.g., decreased MA on TEG). This may resolve the coagulopathy and avoid the need for platelet concentrates. 7. Fresh frozen plasma. Give 15 mL/kg for a prothrombin time or aPTT in excess of 1.5 times control, or an INR in excess of 2. 8. Give antifibrinolytic medication. Although these agents work best when administered prophylactically before and during CPB, about half of their benefit occurs if given (or continued) in the post-CPB period. An increased D-dimer value or teardrop-shaped TEG tracing suggest active fibrinolysis that would warrant antifibrinolytic agent administration or higher doses if antifibrinolytic agents are already being administered. Anecdotal reports suggest that the addition of a second antifibrinolytic agent (e.g., aprotinin in addition to aminocaproic acid) may increase the risk for intravascular clotting. 9. Give recombinant Factor VIIa (rVIIa) or cryoprecipitate. Recombinant Factor VIIa has been associated with miracle cures of post-CPB coagulopathy, but it is extremely expensive and probably has been overutilized as a result of unrealistic expectations, and has been associated with some hypercoagulable complications. rVIIa probably makes the most sense when given as a secondary intervention when two rounds of FFP 10 to 15 mL/kg and platelet concentrates 1 unit/10 kg have not resolved the coagulopathy. Overwhelming coagulopathy may at times call for earlier use of this potentially lifesaving agent. Cryoprecipitate 1 unit per 4 kg body weight (generally 15 to 20 units in adults), will correct fibrinogen deficiency (less than 100 mg/dL). Its use is best reserved for situations where hypofibrinogenemia has been documented.