Intraoperative Monitoring of Platelet Activity for Patients with Reactive Thrombocytemia and the Mechanism of Adenosine-5'-Diphosphate-Induced Blood Coagulation

Intraoperative Monitoring of Platelet Activity for Patients with Reactive Thrombocytemia and the Mechanism of Adenosine-5’-Diphosphate-Induced Blood Coagulation

Shinji Kohro, M.D., Ph.D., Michiaki Yamakage, M.D., Ph.D., Kaori Satoh, M.D., Akiyoshi Namiki, M.D., Ph.D. Anesthesiology, Sapporo Medical Univ. Sch. of Med., Sapporo, Hokkaido, Japan.

INTRODUCTION: Patients with thrombocytemia are at the risk for development of thromboembolism, especially in the perioperative period. We intraoperatively monitored adenosine-5’-diphosphate (ADP)-induced whole blood coagulation in patients with thrombocytemia using a platelet aggregation monitor (WBA analyzer™; SSR Engineering Co., Kanagawa, Japan). To determine the mechanism of ADP-induced platelet activation, we also investigated ADP-induced blood coagulation using a standard blood viscometer (Sonoclot™; Scienco Co., Wheat Ridge, CO). METHODS: We monitored platelet function in two patients with reactive thrombocytemia using a WBA analyzer, which can measure ADP-induced whole blood coagulability. A WBA analyzer does not require separation of platelet-rich plasma by centrifugation and is thought to be useful for intraoperative platelet function monitoring. The blood sample is divided in four cuvettes and incubated with different concentrations of ADP (final concentrations: 5, 10, 20 and 40 µM) for 5 min. After incubation, aspiration resistances through a mesh filter are measured as an index of aggregation. In another series of experiment, 6 adult volunteers were enrolled in the study. Venous blood samples were collected from the cephalic vein of each volunteer, and whole blood coagulability was measured using two sets of Sonoclot. As a control, 20 µl of normal saline was added to one cuvette, and the same volume of ADP (diluted with normal saline, final concentration of 40 µM) was added to another cuvette. The following variables were recorded: 1) sonACT, i.e., Sonoclot-measured activated clotting time (liquid phase or onset of clot formation); 2) clot rate, i.e., slope of the Sonoclot signature (fibrin gel formation stage); 3) time-to-peak, i.e., duration from the start of measurement to the peak of Sonoclot signature; 4) clot retraction rate, i.e., ratio of the signature 5 min after peak to the signature at a peak; and 5) maximum signature. Data are expressed as means ± SD. All data were analyzed using paired t-test. P < 0.05 was considered significant. RESULTS: Both patients with reactive thrombocytemia showed dose-independent hypercoagulability during the operation (Figure 1). We administrated heparin to both patients, and the coagulability showed dose-dependent patterns. In healthy volunteers, ADP reduced clot rate by > 74%, clot retraction rate by > 1%, peak signature by > 80%, and increased time-to-peak by > 470%. CONCLUSION: It is not clear why coagulability in the patients with thrombocytemia showed an ADP dose-independent pattern. Results of experiments showed that the mechanism of ADP-induced whole blood coagulation would involve an inhibition of clot retraction but not clot formation. The relationship between ADP-independent hypercoagulability in thrombocytemia and ADP-induced clot retraction inhibition is still unknown. Anesthesiology 2003; 99: A543

 

Figure 1

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