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==Overview==  
==Overview==  
'''Disseminated intravascular coagulation''', is a [[pathology|pathological]] process in the body where the [[blood]] starts to [[coagulation|coagulate]] throughout the whole body. This depletes the body of its [[platelet]]s and coagulation factors, and there is a paradoxically increased risk of [[hemorrhage]]. It occurs in critically ill patients, especially those with [[Gram-negative]] [[sepsis]] (particularly [[meningococcus|meningococcal]] sepsis) and [[acute promyelocytic leukemia]].<ref>Baglin, T., Disseminated intravascular coagulation: diagnosis and treatment, BMJ 1996; 312: 683-686.</ref> <ref>Bick, R.L., Disseminated intravascular coagulation: pathophysiological mechanisms and manifestations, Sem Thromb Hemostasis 1998; 24: 3-18.</ref> <ref>Penner, J.A., Disseminated intravascular coagulation in patients with multiple organ failure of non-septic origin, Sem Thromb Hemostasis 1998, 24: 45-52.</ref> <ref>Riewald, M., Riess, H., Treatment options for clinically recognized disseminated intravascular coagulation, Sem Thromb Hemostasis 1998; 24: 53-59.</ref>
'''Disseminated intravascular coagulation''', is a [[pathology|pathological]] process in the body where the [[blood]] starts to [[coagulation|coagulate]] throughout the whole body. This depletes the body of its [[platelet]]s and coagulation factors, and there is a paradoxically increased risk of [[hemorrhage]]. It occurs in critically ill patients, especially those with [[Gram-negative]] [[sepsis]] (particularly [[meningococcus|meningococcal]] sepsis) and [[acute promyelocytic leukemia]].<ref>Baglin, T., Disseminated intravascular coagulation: diagnosis and treatment, BMJ 1996; 312: 683-686.</ref> <ref>Bick, R.L., Disseminated intravascular coagulation: pathophysiological mechanisms and manifestations, Sem Thromb Hemostasis 1998; 24: 3-18.</ref> <ref>Penner, J.A., Disseminated intravascular coagulation in patients with multiple organ failure of non-septic origin, Sem Thromb Hemostasis 1998, 24: 45-52.</ref> <ref>Riewald, M., Riess, H., Treatment options for clinically recognized disseminated intravascular coagulation, Sem Thromb Hemostasis 1998; 24: 53-59.</ref>
DIC is a complex and highly variable disorder, whose manifestations depend upon the inciting event, the host response and underlying comorbid disease. Additionally, the morbidity and mortality in patients with DIC often depends more on the underlying disease and he specific pathophysiology. As such, well-designed studies are obviously difficult to design, and there is therefore little consensus regarding management. The term DIC has evolved from the terms ‘consumptive coagulopathy’ and later, ‘defibrination syndrome’. Although most physicians are aware of the hemorrhage that is seen in patients with DIC, the ‘coagulation’ in DIC actually refers to both hemorrhage and thrombosis. In actuality, the thrombosis, both micro and macro-vascular, with resulting ischemia, contributes more to morbidity and mortality than the hemorrhage.
Bick defines DIC as ‘a systemic thrombohemorrhagic disorder seen in association with well-defined clinical situations AND laboratory evidence for procoagulant activation, fibrinolytic activation, inhibitor consumption, and evidence of end-organ damage’.
==References==
==References==



Revision as of 16:24, 28 August 2012

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Disseminated intravascular coagulation, is a pathological process in the body where the blood starts to coagulate throughout the whole body. This depletes the body of its platelets and coagulation factors, and there is a paradoxically increased risk of hemorrhage. It occurs in critically ill patients, especially those with Gram-negative sepsis (particularly meningococcal sepsis) and acute promyelocytic leukemia.[1] [2] [3] [4]

DIC is a complex and highly variable disorder, whose manifestations depend upon the inciting event, the host response and underlying comorbid disease. Additionally, the morbidity and mortality in patients with DIC often depends more on the underlying disease and he specific pathophysiology. As such, well-designed studies are obviously difficult to design, and there is therefore little consensus regarding management. The term DIC has evolved from the terms ‘consumptive coagulopathy’ and later, ‘defibrination syndrome’. Although most physicians are aware of the hemorrhage that is seen in patients with DIC, the ‘coagulation’ in DIC actually refers to both hemorrhage and thrombosis. In actuality, the thrombosis, both micro and macro-vascular, with resulting ischemia, contributes more to morbidity and mortality than the hemorrhage.

Bick defines DIC as ‘a systemic thrombohemorrhagic disorder seen in association with well-defined clinical situations AND laboratory evidence for procoagulant activation, fibrinolytic activation, inhibitor consumption, and evidence of end-organ damage’.

References

  1. Baglin, T., Disseminated intravascular coagulation: diagnosis and treatment, BMJ 1996; 312: 683-686.
  2. Bick, R.L., Disseminated intravascular coagulation: pathophysiological mechanisms and manifestations, Sem Thromb Hemostasis 1998; 24: 3-18.
  3. Penner, J.A., Disseminated intravascular coagulation in patients with multiple organ failure of non-septic origin, Sem Thromb Hemostasis 1998, 24: 45-52.
  4. Riewald, M., Riess, H., Treatment options for clinically recognized disseminated intravascular coagulation, Sem Thromb Hemostasis 1998; 24: 53-59.

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