Background: Clinical diagnosis of platelet dysfunction is complex and technically challenging. The wide repertoire of platelet responses requires a test panel to assess different parameters of platelet reactivity. While “global” hemostasis analyzers and whole blood assays have potential for testing platelet function, their ability to evaluate platelet procoagulant activity is ill-defined.
Objectives: The aim of this study was to determine whether platelet procoagulant deficiency, the pathophysiologic defect of Scott syndrome, could be detected in point-of-care and whole blood assays.
Methods: Study subjects were 4 Scott syndrome-affected German Shepherds and 8 control dogs. We evaluated 2 point-of-care instruments: the platelet function analyzer (PFA-100) and thromboelastograph (TEG). TEG analysis was performed on recalcified citrated whole blood with and without tissue-factor activation. A whole blood flow cytometric assay was configured to detect thrombin-induced platelet P-selectin expression and platelet-derived microparticle release. Cytometric samples were analyzed after 1 hour and 1 day of storage.
Results: We found no significant differences between Scott and control dogs in PFA-100 COL/ADP closure times or in any TEG parameter in tissue-factor–activated samples. In nonactivated samples, mean clotting time (K) and time to maximal rate of thrombus generation were significantly prolonged in Scott dogs; however, values overlapped with those of control dogs. Cytometric analysis of samples from Scott dogs showed significantly diminished platelet-derived microparticle release. Samples from all dogs reanalyzed after 1 day of storage had nonspecific increases in basal P-selectin expression and vesiculation.
Conclusion: A whole blood cytometric assay to detect stimulated platelet microparticle release can be used to screen for Scott syndrome. However, platelet activation artifacts preclude overnight storage for next-day analysis.