Disseminated Intravascular Coagulation: Pathophysiological Mechanisms and Manifestations

Abstract

Current concepts of the many complex pathophysiological mechanisms and clinical and laboratory manifestations of disseminated intravascular coagulation (DIC) are presented. Considerable attention has been devoted to interrelationships within the hemostasis system. Only by clearly understanding these extraordinarily complex pathophysiological interrelationships can the clinician and laboratory scientist appreciate the divergent and wide spectrum of often confusing clinical and laboratory findings in patients with DIC. Many therapeutic decisions are controversial and will remain so until more is published about specific therapeutic modalities and survival patterns. The future holds promise for not only newer antithrombotic agents, but also agents which will block, blunt or modify cytokine activity and the activity of vasoactive substances. Also, therapy must be highly individualized depending on the nature of DIC, age, etiology of DIC, site and severity of hemorrhage or thrombosis and hemodynamic and other clinical parameters.

Mortality in virulent canine babesiosis is associated with a consumptive coagulopathy

“…Diagnosis of a consumptive coagulopathy was based on the criteria for the approach to DIC in people defined by ISTH, which has previously been validated in dogs; i.e. indications of pro-coagulant activation (prolonged PT, prolonged aPTT, decreased coagulation factor activity, low platelet count), inhibitor consumption (low AT, low PC) and increased fibrinolytic activity (high DDimer) (Bick et al, 1999;Taylor FB Jr. et al, 2001;Wiinberg et al, 2010). For this study, overt DIC was defined as the presence of hemostatic abnormalities together with overt hemorrhage.…”

“…Non-overt DIC was defined as the presence of hemostatic abnormalities in the absence of gross clinical signs of hemorrhage (Bick et al, 1999;Wiinberg et al, 2008).…”

“…If uncontrolled, the hypercoagulable state may lead to DIC, which has been identified as a major risk factor for poor outcome in both human and canine medicine (Laforcade et al, 2003;Weiss and Rashid, 1998). The criteria for the definition of DIC in people, established by the International Society of Thrombosis and Hemostasis (ISTH), include procoagulant activation, inhibitor consumption, and increased fibrinolytic activity (Bick et al, 1999;Wiinberg et al, 2008). Clinical signs associated with DIC vary considerably and can range from no signs (non-overt DIC) to signs of organ failure, secondary to microvascular thrombosis, and overt hemorrhage (overt DIC) (Bick et al, 1999;Wiinberg et al, 2008).…”

“…The criteria for the definition of DIC in people, established by the International Society of Thrombosis and Hemostasis (ISTH), include procoagulant activation, inhibitor consumption, and increased fibrinolytic activity (Bick et al, 1999;Wiinberg et al, 2008). Clinical signs associated with DIC vary considerably and can range from no signs (non-overt DIC) to signs of organ failure, secondary to microvascular thrombosis, and overt hemorrhage (overt DIC) (Bick et al, 1999;Wiinberg et al, 2008). A recent study in dogs has indicated that the same criteria can be used for diagnosing DIC in dogs and a significant difference in plasma based assays was observed between survivors and non-survivors (Wiinberg et al, 2010).…”

Computational Tasks in Medical Nanorobotics

“…Additional protocols are required to allow clottocytes to prevent accidental but potentially fatal catastrophic natural clotting cascades such as disseminated intravascular coagulation or DIC [57]. One solution is to equip clottocytes with sensors to detect decreased serum levels of fibrinogen, plasminogen, alpha 2 -antiplasmin, antithrombin III, factor VII, and protein C, and elevated levels of thrombin and various fibrin/fibrinogen-derived degradation products [2i].…”