Coagulopathy induced by viperid snake venoms in a murine model: Comparison of standard coagulation tests and rotational thromboelastometry

Bothrops venom-induced hemostasis disorders in the rat: Between Scylla and Charybdis

“…Later, no prolongation of CT was recorded, suggesting no or only transient coagulation factor consumption undetectable at our sampling times. A previous work has reported a prolonged Extem CT at H1 after intravenous B. asper venom injection in mice which recovered at H3 [55]. A fast recovery of the clotting factors may correspond to the rapid elimination of venom procoagulant enzymes from the blood, consistent with reports on human snakebite envenomation in French Guiana in which prothrombin time and activated partial thromboplastin time were corrected faster than fibrinogen, even without antivenom administration [12,13].…”

“…Although not altered at H3 and H6, Extem MCF was significantly reduced at H24 after B. atrox venom injection, supporting the onset of venom-induced delayed hypocoagulability. This observation contrasted with Rucavado's study reporting no clot at H1 after intravenous B. PLOS NEGLECTED TROPICAL DISEASES asper venom injection in mice but a steady increase in clot amplitude with decreased strength at H24 [55]. Noteworthy, here we used the subcutaneous route to mimic snakebite condition, which may account for the observed differences in fibrinogen kinetics.…”

“…Crude venoms exhibit strong dosedependent procoagulant effects in vitro [49][50][51], while in vivo consumption of clotting factors result in blood hypocoagulability. To observe the time-dependent toxicity of the various enzymes present in Viperidae venoms, it is necessary to investigate the time-course of hemostasis disorders in vivo [52][53][54][55]. Recent global hemostasis assays, which have revolutionized the approach of hemorrhagic and thrombotic diseases, may improve understanding hemostasis disorders in Bothrops envenomation.…”

Ruthenium Antivenom Inhibits the Defibrinogenating Activity of Crotalus adamanteus Venom in Rabbits

“…While the utility of thrombelastographic methods in assessing the effects of hemotoxic venom was presented in the Introduction [ 5 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 ], the present study serves as an example wherein thrombelastography provides a depth of information not afforded by standard hematological methods. Rather than just documented decreases in fibrinogen concentration with either clotting-based or antigen-based methods following envenomation, the use of thrombelastography without and with platelet inhibition allowed the quantification of the impact of the loss of fibrinogen on all aspects of coagulation ( Figure 3 , Figure 4 , Figure 5 and Figure 6 ).…”

“…A methodology capable of documenting the effects of loss of fibrinogen in whole blood or plasma is thrombelastography, which has been utilized in clinical [ 5 ] and laboratory investigations [ 13 ] involving C. adamanteus venom. While one of the first utilizations of thrombelastography/thromboelastometry to assess coagulopathy after envenomation was reported thirty-four years ago [ 14 ], the vast majority of clinical and laboratory reports in human and veterinary settings have been published in the last decade, with a few examples cited for the interested reader [ 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 ]. Facile modifications of thrombelastographic methodologies that allow the assessment of changes in fibrinogen include using either antibodies to block platelet receptor glycoprotein IIb/IIIa to prevent attachment that forms fibrin polymers in whole blood [ 35 ], inhibiting the degranulation and formation of the glycoprotein IIb/IIIa by inhibiting microtubular activity with cytochalasin D [ 34 , 35 , 36 ], or by separating plasma in sodium citrate-anticoagulated whole blood [ 33 ].…”