Seminars in thrombosis and hemostasis
-
Semin. Thromb. Hemost. · Jun 2010
ReviewLaboratory testing in disseminated intravascular coagulation.
The diagnosis of disseminated intravascular coagulation (DIC) relies on clinical signs and symptoms, identification of the underlying disease, the results of laboratory testing, and differentiation from other pathologies. The clinical features mainly depend on the underlying cause of the DIC. The laboratory diagnosis of DIC uses a combination of tests because no single test result alone can firmly establish or rule out the diagnosis. ⋯ New tests are being explored for utility in DIC, and some additional tests may be useful on a case-by-case basis, depending on the proposed cause of the DIC or their local availability. For example, clot waveform analysis is useful but currently limited to a single instrument. Also, procalcitonin is an inflammatory biomarker that may be useful within the context of septic DIC, and activated factor X clotting time is an emerging test of procoagulant phospholipids that also seems to hold promise in DIC.
-
Semin. Thromb. Hemost. · Jun 2010
ReviewDisseminated intravascular coagulation in obstetric and gynecologic disorders.
Disseminated intravascular coagulation (DIC) is a syndrome characterized by a massive, widespread, and ongoing activation of the coagulation system, secondary to a variety of clinical conditions. Many obstetric complications, such as abruptio placentae, amniotic fluid embolism, endotoxin sepsis, retained dead fetus, post-hemorrhagic shock, hydatidiform mole, and gynecologic malignancies, might trigger DIC. ⋯ At present, the therapeutical approach to pregnancy- and gynecologic-related DIC comprises the specific and aggressive treatment of the underlying disease, eventually followed by a supportive blood product replacement therapy and restoration of physiological anticoagulant pathways. This article reviews the etiopathogenesis, clinical manifestations, laboratory diagnosis, and therapy of pregnancy- and gynecologic-related DIC.
-
Semin. Thromb. Hemost. · Jun 2010
ReviewSnakebite doesn't cause disseminated intravascular coagulation: coagulopathy and thrombotic microangiopathy in snake envenoming.
The most common coagulopathy associated with snake envenoming worldwide is venom-induced consumption coagulopathy (VICC), which results from activation of the coagulation pathway by snake toxins including thrombin-like enzymes, prothrombin activators, and factor X activators. VICC has often been likened to disseminated intravascular coagulation (DIC) because of the elevated D-dimer, prolonged prothrombin time, and low fibrinogen. However, VICC is not characterized by other important features of DIC, such as evidence of systemic microthrombi and end-organ failure. ⋯ This thrombotic microangiopathy appears to only occur in conjunction with VICC but in several different snakes worldwide including vipers and elapids. Consistent with thrombotic microangiopathy, it progresses despite the resolution of the coagulopathy, suggesting a distinct but related process. The existence of the overlapping clinical syndromes of VICC and thrombotic microangiopathy in snake envenoming is the likely reason for the mistaken idea that snakebite causes DIC.
-
Physical injuries, especially road traffic injuries, are a leading cause of death and morbidity worldwide, ranking fifth among the leading causes of death in the United States. Immediate and early trauma deaths are mainly determined by primary brain injuries and/or hemorrhages, whereas late mortality is caused by secondary brain injuries, host defense failure, and superimposed complications including also disseminated intravascular coagulation (DIC). Trauma patients are particularly susceptible to the early development of coagulopathy, and the most severely injured patients are coagulopathic on hospital admission. ⋯ As such, the multifaceted derangement of hemostasis occurring after massive traumatic injuries, especially those involving the brain, is mainly sustained by release of procoagulants (fats, phospholipids) and constitutive tissue factor from the injured tissue into the circulation, associated with a systemic inflammatory response that also promotes tissue factor hyperexpression on monocytes and the other cells. The excessive, non-wound-related thrombin generation is insufficiently antagonized by physiological anticoagulant pathways and amplified by impaired endogenous fibrinolysis. The resulting burst of systemic thrombin generation, coupled with platelet hyperaggregability, shock, hypothermia, and tissue hypoperfusion, further contribute to the development of DIC and microvascular bleeding.
-
Semin. Thromb. Hemost. · Jun 2010
ReviewDisseminated intravascular coagulation in infectious disease.
Severe infection and inflammation almost invariably lead to hemostatic abnormalities, ranging from insignificant laboratory changes to severe disseminated intravascular coagulation. Systemic inflammation as a result of severe infection leads to activation of coagulation, due to tissue factor-mediated thrombin generation, downregulation of physiological anticoagulant mechanisms, and inhibition of fibrinolysis. ⋯ Apart from the general coagulation response to inflammation associated with severe infection, specific infections may cause distinct features, such as hemorrhagic fever or thrombotic microangiopathy. The relevance of the cross-talk between inflammation and coagulation is underlined by the results of the treatment of severe systemic infection with modulators of coagulation and inflammation.