Sonoclot compared with Routine Coagulation Tests


Recent advances in the understanding of coagulation mechanisms have allowed for a reappraisal and a questioning of the value of the previous standards of the PT and APTT while giving credence to the value of the whole-blood monitoring technique of the Sonoclot  analyzer. The older view of a separate intrinsic and extrinsic coagulation system has been abandoned along with the waterfall descriptions of coagulation mechanisms with one enzyme working after another and with some mechanisms of feedback amplification and inhibition derived in a plasma milieu. None of this theory was actually applicable in moving blood. These concepts have been replaced by a concept of enzyme complexes existing on the surface of cells, passing one another their substances until the final product, fibrin, is formed. The cell surfaces of importance are those of the platelets, which are activated and adhere to the site of the injury. They localize the clotting process, enhance their activities, and protect the enzyme complexes from inhibitors that circulate to protect against propagation of the clotting activation downstream.


The surface concept provides an explanation of how some individuals with only a few percent of plasma coagulation factors can maintain hemostasis, while these same individuals will hemorrhage if their platelet function is compromised. Since PT and APTT are plasma tests designed with substitutes for platelet surfaces, it can readily be understood why these tests would not agree with the whole-blood Sonoclot analysis, which uses the actual cellular surfaces to monitor coagulation.  Once the importance of the platelet surfaces and of other cellular surfaces and their interactions with the coagulation process are understood, the value of the PT or APTT in clinical management should be questioned.  Since the Sonoclot analyzer is sensitive to platelet function, plasma factors, activators and inhibitors of coagulation, it represents an ideal monitor for hemostasis.


The Clinical Hemostasis Handbook, by Laposata et al, defines normal hemostasis as "the controlled activation of clot formation and clot lysis that stops hemorrhage without permitting inappropriate thrombosis." This means that hemostasis is the net result of two systems working in tandem, the coagulation system -- the system that produces the clot -- and the fibrinolytic system -- the system that dissolves the clot. When the balance between the two systems shifts toward procoagulation, the result is thrombosis; when the balance shifts toward fibrinolysis, the result is hemorrhage. Therefore a coagulation test that does not measure the net product of both the coagulation and the fibrinolytic systems, as does the Sonoclot test, will fail to properly analyze patient hemostasis. For example, in the case of fibrinolysis secondary to hypercoagulability, D-dimer, FDP, and FSP tests would show high fibrinolytic activity, while PT and PTT results would be normal due to their inherent lack of sensitivity to the hypercoagulable state. Based on these results, antifibrinolytic drugs might be prescribed, shutting off the fibrinolytic system, producing an imbalance toward procoagulability, and could result in AMI, stroke, etc.


The Sonoclot analyzer allows acquisition of continuous quantitative information on the developing clot; the time it takes for the first fibrin to develop, the kinetics of clot development, the strength and stability of the clot, taking into consideration all the components that make blood clot or lyse. Ignoring the interactive nature of hemostasis, analyzing separated blood components such as plasma, RBC, WBC, platelets, fibrinogen level, or factor assays, can result in artifacts that do not match the clinical condition. This should serve as a caution against basing therapy on these analyses, especially since there are significant risks associated with blood transfusions.


Also, measuring single factors quantitatively can be misleading because the quantity, as measured by an assay, does not reflect the actual functional activity. Functional activity of a factor also depends on the presence and activity of activators, inhibitors, and cellular elements.