title: Thromboelastometry (TEM) findings in disseminated intravascular coagulation in a pig model of endotoxinemia.
abstract: Standard coagulation tests have a low specificity and sensitivity for diagnosing disseminated intravascular coagulation. The aim of this study was to determine whether whole blood thromboelastometry (TEM) detects lipopolysaccharide (LPS)-induced changes in coagulation. Blood samples from 10 pigs were drawn at baseline, before and at the end of LPS infusion and 2, 3, 4 and 5 h after the start of endotoxinemia. Simultaneous to TEM, standard coagulation tests and extended coagulation analysis including tissue plasminogen activator (t-PA) and plasminogen activator inhibitor 1 (PAI-1) were performed. Endotoxinemia resulted in a significant acceleration of the nonactivated TEM (NATEM) clotting time 2 h after the end of LPS infusion; in contrast, the changes in international normalized ratio and activated partial thromboplastin time suggested delayed initiation of coagulation. NATEM maximum clot firmness (MCF) and fibrin-based thromboelastometry test (FIBTEM)-MCF decreased significantly from baseline until the last time point (from 64.6 ± 7.8 and 35.1 ± 12.8 mm to 52.8 ± 4.6 and 21.4 ± 11.8 mm, respectively; P = 0.01 for both parameters). A sharp, transient increase of t-PA had no effect on maximum lysis in the NATEM test. PAI-1 increased significantly 3 h after the start of LPS infusion, paralleled by a decrease in maximum lysis. In conclusion, TEM was superior to standard coagulation tests in reflecting initial activation of coagulation during endotoxinemia. TEM further suggested consumption of coagulation substrate; at the same time, inhibition of plasminogen activation was accompanied by improved clot stability. Further investigations are necessary to establish the clinical relevance of these findings.
authors.affiliation: Ludwig Boltzmann Institute for Experimental and Clinical Traumatology, Vienna, Austria. herbert.schoechl@trauma.lbg.ac.at
authors.forename: Herbert
authors.initials: H
authors.lastname: Schöchl
authors.forename: Cristina
authors.initials: C
authors.lastname: Solomon
authors.forename: Arthur
authors.initials: A
authors.lastname: Schulz
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Voelckel
authors.forename: Alexander
authors.initials: A
authors.lastname: Hanke
authors.forename: Martijn
authors.initials: M
authors.lastname: Van Griensven
authors.forename: Heinz
authors.initials: H
authors.lastname: Redl
authors.forename: Soheyl
authors.initials: S
authors.lastname: Bahrami
mesh_terms: D000818:Animals; D001772:Blood Cell Count; D001777:Blood Coagulation / Q000187:drug effects; D004195:Disease Models, Animal; D004211:Disseminated Intravascular Coagulation / Q000097:blood* / Q000209:etiology; D019446:Endotoxemia / Q000139:chemically induced / Q000150:complications*; D005342:Fibrinolysis / Q000187:drug effects; D008070:Lipopolysaccharides / Q000008:administration & dosage / Q000633:toxicity; D008297:Male; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D013552:Swine; D013916:Thrombelastography / Q000379:methods*; D010959:Tissue Plasminogen Activator / Q000097:blood
chemical_list: D008070:Lipopolysaccharides; D017395:Plasminogen Activator Inhibitor 1; D010959:Tissue Plasminogen Activator