Critical care clinics
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Coagulation problems are very common in intensive care patients. It is important to recognize potential problems, perform a rapid assessment, and start therapy. ⋯ This review outlines a set of often catastrophic coagulation problems, which may present both thrombotic and bleeding challenges. These include heparin induced thrombocytopenia, thrombotic thrombocytopenic purpura, and disseminated intravascular coagulation.
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Critical care clinics · Jul 2005
ReviewEmerging off-label uses for recombinant activated factor VII: grading the evidence.
Recombinant activated factor VII (rFVIIa) is currently licensed in the United States for treatment of bleeding episodes in patients with deficiencies of factor VIII (FVIII) or IX (FIX) who are refractory to factor replacement because of circulating inhibitors. A 1999 report of its successful use to stop what was deemed to be lethal hemorrhage after an abdominal gunshot wound in a young soldier without pre-existing coagulopathy has prompted exploration of other uses for rFVIIa. The virtual explosion of proposed uses of rFVIIa raises issues not only regarding our understanding of the coagulation system, but also regarding its efficacy, cost-effectiveness, and safety.
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Critical care clinics · Jul 2005
ReviewDoes disseminated intravascular coagulation lead to multiple organ failure?
Microvascular dysfunction with its associated impaired regional oxygen transport and use is believed to be the final common pathway in the development of multiple organ failure. The precise mechanisms underlying this dysfunction, however, are uncertain. Activation of the coagulation system is a key feature in the pathogenesis of sepsis, but whether it is also the cause of multiple organ failure is unclear. This article discusses the evidence for and against a key role for disseminated intravascular coagulation in the pathogenesis of multiple organ failure.
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End stage liver disease results in a complex and variably severe failure of hemostasis that predisposes to abnormal bleeding. The diverse spectrum of hemostatic defects includes impaired synthesis of clotting factors, excessive fibrinolysis, disseminated intravascular coagulation, thrombocytopenia, and platelet dysfunction. ⋯ Correction of hemostatic defects is required in patients who are actively bleeding or require invasive procedures. Fresh frozen plasma, cryoprecipitate, and platelet transfusion remain the mainstays of therapy until larger trials confirm the safety and efficacy of recombinant factor VIIa in this population.
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Disseminated intravascular coagulation (DIC) is a syndrome characterized by a systemic activation of coagulation leading to the intravascular deposition of fibrin in the (micro) vasculature and the simultaneous consumption of coagulation factors and platelets. The occurrence of microvascular thrombosis as a consequence of DIC is underscored by pathological, experimental and clinical findings, demonstrating a link between DIC and organ dysfunction. Pathogenetic pathways that play a role in the development of DIC include tissue factor-dependent activation of coagulation, defective physiological anticoagulant pathways (such as the antithrombin system and the protein C system), and impaired fibrinolysis, caused by elevated levels of plasminogen activator inhibitor type 1. Novel therapeutic strategies are based on current insights into the pathogenesis of DIC, and include anticoagulant strategies (eg, directed at tissue factor) and strategies to restore physiological anticoagulant pathways (such as activated protein C concentrate).