Hemostasis

The International Society of Thrombosis and Haemostasis (ISTH) defined a sepsis-induced coagulopathy (SIC) as “infection-induced organ dysfunction and coagulopathy” in 2019 (Iba et al 2019). Although sepsis is one of the main triggers of disseminated intravascular coagulation (DIC), there is recognition that sepsis can result in a coagulopathy that precedes overt DIC. Sepsis-induced coagulopathy is […]

Hypercoagulability is defined as excessive thrombin generation and is a prothrombotic state, in that the animal is predisposed to or may be suffering from thrombosis. Thrombosis is exceedingly difficult to detect clinically, particularly when it occurs within the internal microvasculature, however sudden onset of neurologic or pulmonary signs, progressive deterioration of organ function or unexpected

Disorders of fibrinolysis can result in thrombosis (if fibrinolysis is deficient or inhibited) or hemorrhage (accelerated fibrinolysis). Due to the difficulties with confirming fibrinolysis and the fact that fibrinolysis will be, in large part, dictated by the strength of the fibrin clot that forms initially (thin fibers formed under conditions of low thrombin are more

Pathologic thrombosis can occur through a variety of mechanisms, including excess clot formation, insufficient or inhibited fibrinolysis, or a combination of both. The three main triggers for thrombosis are described by Virchow’s triangle, which lists abnormal blood flow (usually stasis versus turbulence), endothelial dysfunction or injury, and hypercoagulability, although these mechanisms clearly overlap and may

In the past, coagulation defects associated with trauma were attributed to triggering of DIC or resuscitative therapy, such as hemodilution. Although DIC and hemodilution still exist in trauma and contribute to hemostastic defects, it is now recognized that trauma incites its unique coagulopathy, which we are just beginning to understand (see review by Chang et

Protein C is a serine protease that is produced in the liver and consists of light and heavy chain, linked by a disulfide bond. The protein has a half-life of 8 hours, although intravenously administered activated protein has a half-life <20 minutes (Okijama et al 1990). Protein C has similar structure to other vitamin K-dependent

Antithrombin (AT) is produced in the liver and is an important endogenous anticoagulant, inhibiting the activity of most activated coagulation factors, although its greatest inhibitory effect is against thrombin and FXa. Its activity is enhanced by heparin (hence its use as an anticoagulant), which is provided in vivo by heparin-like glycosaminoglycans on the surface of

The tables below provide a general summary of interpretation of platelet count results (degree of thrombocytopenia can provide information on mechanism, and thus cause, of thrombocytopenia) and screening coagulation panel results. Note, only common diseases are listed (not all possibilities are covered. See also the algorithm for an approach to diagnostic testing for an animal with a suspected

The table below provides expected test abnormalities with certain hemostatic disorders. Note, that these are generalizations of the most common scenario and do not cover the range of possibilities or all diseases seen in animals. This table can be used as a guide to help interpretation of laboratory testing results. Disorder ACT* APTT PT TCT**

  The results of hemostasis screening tests dictate the need for further or more specific diagnostic testing or may prompt additional assays. The choice of assays (screening or otherwise) should  be guided by knowledge of the patient (age, breed, sex, access to anticoagulant rodenticides, parasite exposure, type of bleeding symptoms, presence of underlying disease etc).