• Andreas Straub, Daniela Schiebold, Hans Peter Wendel, Carole Hamilton, Thomas Wagner, Eckhard Schmid, Klaus Dietz, and Gerhard Ziemer.
• Department of Thoracic, Cardiac and Vascular Surgery, University of Tübingen, Germany.
• Eur J Cardiothorac Surg. 2008 Sep 1;34(3):641-7.

ObjectiveCardiac surgery employing cardiopulmonary bypass (CPB) and deep hypothermic circulatory arrest (DHCA) can induce coagulation disturbances and bleeding complications that may be especially severe in infants. A better understanding of the coagulopathy and a quick method for its evaluation would be helpful in the management of patients exposed to CPB and DHCA. This study aimed to monitor coagulation defects in congenital heart surgery using rotational thromboelastometry (ROTEM), standard coagulation tests and platelet flow cytometry.MethodsThe study comprised 10 infants undergoing surgery for congenital heart disease on CPB and DHCA. Blood was sampled at skin incision, after heparinisation during CPB (directly pre- and directly post-DHCA) and after protamine administration post-CPB. ROTEM using different reagents including a heparinase-containing assay to evaluate coagulation during heparinisation, APTT and INR, and flow cytometry to evaluate platelet activation were performed.ResultsDuring CPB, the ROTEM indicated CPB-induced clotting factor depletion and platelet dysfunction that persisted after CPB and heparin neutralisation. ROTEM results were available within 15 min and therefore much faster than standard tests. ROTEM-guided specific blood product treatment resulted in satisfactory coagulatory function. The highest degree of platelet activation was found directly after DHCA.ConclusionsA major benefit of ROTEM is the quick detection of a developing coagulopathy already during CPB. ROTEM guides quick and specific blood product treatment after CPB, which may decrease bleeding complications in cardiac surgery. The finding of maximal platelet activation directly after DHCA suggests that not only CPB but also hypothermia activates platelets in vivo, thereby contributing to platelet dysfunction.

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