“…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 ]. With the contribution of platelets removed in terms of attachment to fibrin polymers, contraction, and release of factor XIII known to further enhance the speed of clot growth and strength [ 37 ], the coagulation kinetics observed involve only the various coagulation pathway proteins, with fibrinogen playing a critical role in final thrombus strength [ 38 ].…”