This work was done at the College of Veterinary Medicine, University of Georgia, Athens, GA. Findings were presented in part at the 9th International Colic Symposium, Liverpool, UK, June 2008.
Thrombelastography in Horses with Acute Gastrointestinal Disease
Article first published online: 11 FEB 2011
Copyright © 2011 by the American College of Veterinary Internal Medicine
Journal of Veterinary Internal Medicine
Volume 25, Issue 2, pages 307–314, March/April 2011
Total views since publication: 19
How to Cite
Epstein, K.L., Brainard, B.M., Gomez-Ibanez, S.E., Lopes, M.A.F., Barton, M.H. and Moore, J.N. (2011), Thrombelastography in Horses with Acute Gastrointestinal Disease. Journal of Veterinary Internal Medicine, 25: 307–314. doi: 10.1111/j.1939-1676.2010.0673.x
- Issue published online: 7 MAR 2011
- Article first published online: 11 FEB 2011
- Submitted August 13, 2010; Revised November 17, 2010; Accepted December 13, 2010.
- Point-of-care coagulation testing;
- Viscoelastic coagulation testing
Background: Coagulopathies in horses with gastrointestinal disease are frequently identified and associated with morbidity and fatality.
Objective: Determine if thrombelastography (TEG) identifies abnormalities associated with lesion type, presence of systemic inflammatory response syndrome (SIRS), morbidity, and fatality more consistently than traditional coagulation testing.
Animals: One-hundred and one horses examined for gastrointestinal disease and 20 healthy horses.
Methods: TEG, tissue factor (TF)-TEG, and traditional coagulation panels parameters and percentages of horses with coagulopathies were compared for lesion type, presence of SIRS, complications, and survival.
Results: Changes in individual parameters and increased incidence of coagulopathies were associated with fatality (R, P= .007; k-value [K], P= .004; clot lysis [CL]30, P= .037; CL60, P= .050; angle [Ang], P= .0003; maximum amplitude [MA], P= .006; lysis [Ly]30, P= .042; Ly60, P= .027; CI, P= .0004; ≥ 2 TEG coagulopathies, P= .013; ≥ 3 TEG coagulopathies, P= .038; TF-R, P= .037; TF-K, P= .004; TF-CL30, P < .0001; TF-CL60, P < .0001; TF-Ang, P= .005; TF-Ly30, P= .0002; TF-Ly60, P < .0001; TF-CI, P= .043; ≥ 1 TF-TEG coagulopathies, P= .003; ≥ 2 TF-TEG coagulopathies, P= .0004; prothrombin tme [PT], P < .0001; activated partial throboplastin time [aPTT], P= .021), inflammatory lesions (MA, P= .013; TF-CL30, P= .033; TF-CL60, P= .010; TF-Ly60, P= .011; ≥ 1 TF-TEG coagulopathy, P= .036; ≥ 2 TF-TEG coagulopathy, P= .0007; PT, P= .0005; fibrinogen, P= .019), SIRS (MA, P= .004; TF-CL30, P= .019; TF-CL60, P= .013; TF-Ly30, P= .020; TF-Ly60, P= .010; PT, P < .0001; aPTT, P= .032; disseminated intravascular coagulation, P= .005), and complications (ileus: aPTT, P= .020; diarrhea: TF-CL30, P= .040; TF-Ly30, P= .041; thrombophlebitis: ≥ 1 TF-TEG coagulopathy, P= .018; laminitis: MA, P= .004; CL60, P= .045; CI, P= .036; TF-MA, P= .019; TF-TEG CI, P= .019). Abnormalities in TEG and TF-TEG parameters were indicative of hypocoagulation and hypofibrinolysis.
Conclusions and Clinical Importance: TEG identifies changes in coagulation and fibrinolysis associated with lesion type, SIRS, morbidity, and fatality in horses with gastrointestinal disease.