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Updated: Aug 20, 2026

Leveraging Turbidity and Thromboelastography for Complementary Clot Characterization
Published on: June 4, 2020
The effect of dilution on plasma coagulation kinetics determined by thrombelastography is dependent on antithrombin
Vance G Nielsen1, Ralph T Lyerly, William Q Gurley
1Department of Anesthesiology, The University of Alabama at Birmingham, Birmingham, Alabama.
Hemodilution-associated hypercoagulability has been the focus of several investigations because significant morbidity and mortality have been associated with perioperative thrombophilia. Because most investigations implicate imbalances in procoagulant/anticoagulant activity as the etiology of hemodilution-associated hypercoagulability, we determined the effects of dilution on coagulation kinetics and clot strength with thrombelastography (TEG(R)). Control plasma (+/-celite activation) and antithrombin (AT)-deficient (<10% activity) plasma were diluted 0%, 10%, 20%, and 30% with saline. TEG(R) variables measured included time to clot initiation (reaction time, R), speed of clot propagation (angle, alpha), and clot strength (amplitude, A; or shear elastic modulus, G). Dilution of control plasma (10%-30%) resulted in a significant (P < 0.05) 16% decrease in R values, no change in alpha values, and decrease in A and G values. AT-deficient plasma had significantly smaller R values compared with control, and dilution did not change R values in AT-deficient plasma. Celite activation eliminated dilution-associated changes in R values in control plasma but resulted in linear decreases (R(2) = 0.88-0.96, P < 0.0001) in alpha, A, and G in response to dilution. Thus, our data indirectly support the concept that decreases in AT activity cause dilution-mediated hypercoagulability in plasma. Finally, celite activation permits quantification of dilution with TEG.
Hemodilution-associated hypercoagulability has been the focus of several investigations because significant morbidity and mortality have been associated with perioperative thrombophilia. Because most investigations implicate imbalances in procoagulant/anticoagulant activity as the etiology of hemodilution-associated hypercoagulability, we determined the effects of dilution on coagulation kinetics and clot strength with thrombelastography (TEG(R)). Control plasma (+/-celite activation) and antithrombin (AT)-deficient (<10% activity) plasma were diluted 0%, 10%, 20%, and 30% with saline. TEG(R) variables measured included time to clot initiation (reaction time, R), speed of clot propagation (angle, alpha), and clot strength (amplitude, A; or shear elastic modulus, G). Dilution of control plasma (10%-30%) resulted in a significant (P < 0.05) 16% decrease in R values, no change in alpha values, and decrease in A and G values. AT-deficient plasma had significantly smaller R values compared with control, and dilution did not change R values in AT-deficient plasma. Celite activation eliminated dilution-associated changes in R values in control plasma but resulted in linear decreases (R(2) = 0.88-0.96, P < 0.0001) in alpha, A, and G in response to dilution. Thus, our data indirectly support the concept that decreases in AT activity cause dilution-mediated hypercoagulability in plasma. Finally, celite activation permits quantification of dilution with TEG.
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