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Published on: September 9, 2012
Disseminated Intravascular Coagulation
Benjamin M Boral1, Dennis J Williams2, Leonard I Boral2
1From the Departments of Medicine.
Insights
Disseminated intravascular coagulation (DIC) is a serious condition where widespread clotting depletes blood components, leading to both bleeding and organ damage. Treatment focuses on supportive care and blood component replacement.
Area of Science:
- Hematology
- Pathophysiology
- Critical Care Medicine
Background:
- Disseminated intravascular coagulation (DIC) is a complex syndrome, not a distinct disease.
- It involves the systemic activation of coagulation pathways.
Observation:
- DIC results from overwhelming coagulation activation, consuming platelets and factors.
- This leads to microvascular fibrin thrombi and potential tissue ischemia.
- Acute DIC is associated with conditions like septic shock, trauma, burns, and leukemia.
Findings:
- Massive tissue factor stimulus drives excess thrombin generation, overwhelming anticoagulant mechanisms.
- Consumption of coagulation factors and platelets contributes to a hemorrhagic phase.
- Multiorgan dysfunction syndrome can arise from tissue ischemia.
Implications:
- Understanding DIC's pathophysiology is crucial for accurate diagnosis and management.
- Supportive care and blood component therapy are key in treating bleeding DIC patients.
- Early recognition and management of underlying causes are vital for patient outcomes.
Objectives:
To provide a review of the definition, pathophysiology, differential diagnosis, and treatment of disseminated intravascular coagulation (DIC).
Methods:
A case scenario and a review of the literature related to the pertinent facts concerning DIC are provided.
Results:
DIC is a systemic pathophysiologic process and not a single disease entity, resulting from an overwhelming activation of coagulation that consumes platelets and coagulation factors and causes microvascular fibrin thrombi, which can result in multiorgan dysfunction syndrome from tissue ischemia. Some conditions associated with acute DIC include septic shock, exsanguinating trauma, burns, or acute promyelocytic leukemia.
Conclusions:
The massive tissue factor stimulus results in excess intravascular thrombin, which overcomes the anticoagulant systems and leads to thrombosis. Because of consumption of coagulation factors and platelets, DIC also has a hemorrhagic phase. Treatment of the bleeding patient with DIC is supportive with the use of blood components.
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