Platelet and Fibrin Alterations on Thromboelastography in Children Undergoing Congenital Cardiac Surgery with Cardiopulmonary Bypass

Background: Children who undergo congenital heart surgery with cardiopulmonary bypass are at risk for alterations in coagulation due to abnormal flow patterns as well as the stresses of cardiopulmonary bypass circuits, drugs and surgery. They are also at risk for thrombosis including arterial ischemic stroke, shunt obstructions and catheter-related thrombi. Therefore understanding their hemostatic parameters will likely help to manage their disease.

Aim: This study determined coagulation and platelet profiles using thromboelastography (TEG) prior to and following surgery in children undergoing congenital heart surgery. Such baseline data are critical to development of clinical trials to prevent thrombosis associated with congenital heart disease.

Methods: Children between the ages from birth to 18 years were eligible for this study. With consent and assent (as appropriate) 3 mL of whole blood were drawn prior to surgery and again 12-48 hours after surgery when children were recovering and tolerating oral intake. TEG with platelet mapping was performed using activation with kaolin for whole blood global TEG, an initiator of coagulation for fibrin contribution to TEG, and arachidonic acid (AA) for platelet contribution to TEG. Results were analyzed using means and standard deviations. Statistical differences pre and post operatively were calculated with ANOVA.

Results: To date, paired samples have been analyzed on 20 children, mean age 8.2 years, range 3 months to 15.5 years. Whole blood global TEG was normal in all 20 children both pre and post operatively, with the exception of a minimally prolonged reaction time in one child at each time point. No child exhibited clinical bleeding or clotting during the study. Fibrin contribution to TEG increased postoperatively on both maximal amplitude (MA) as well as angle of clot (Ang). In contrast, platelet mapping TEG via AA decreased significantly postoperatively on both MA and ang (figure 1). Overall, TEG platelet mapping showed a mean of 20% inhibition preoperatively (within the reference range) and 81% inhibition postoperatively (below the reference range). Of note, there were 3 children less than 6 months, and all 3 showed increased platelet MA postoperatively.

Conclusion: Children with congenital heart defects exhibit normal overall coagulation on TEG in a steady state preoperatively and 12 to 48 hours postoperatively. Postoperatively, platelet function in response to AA is significantly decreased by TEG platelet mapping, which may represent platelet exhaustion, while the fibrin contribution to TEG is significantly increased. Infants less than 6 months of age may show accelerated recovery of platelet function. Studies to better understand coagulation and platelet function in congenital heart disease as well as response to antithrombotic therapy are in process. TEG assays will be compared to more precise assays of coagulation and platelet function. Choices in antithrombotic therapy for clinical care or research trials in children undergoing congenital heart surgery should be data driven.

Figure 1.

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TEG MA and Ang Preop (black) and Postop (grey)

Figure 1.

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TEG MA and Ang Preop (black) and Postop (grey)

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