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Disseminated intravascular coagulation (DIC)
1Wayne State University, Detroit, MI, USA.
Insights
Disseminated intravascular coagulation (DIC) involves systemic hemostasis activation, leading to bleeding or organ damage. Early diagnosis and treatment, including addressing the underlying cause and using anticoagulants or factor replacement, are crucial for better patient prognosis.
Area of Science:
- Hematology
- Pathophysiology
- Critical Care Medicine
Background:
- Disseminated intravascular coagulation (DIC) is a severe complication characterized by systemic activation of hemostasis.
- This activation, often triggered by tissue factor (TF) release, can lead to compensated DIC, where inhibitors manage the process, or decompensated DIC, marked by factor consumption and bleeding.
- Uncontrolled fibrin deposition due to insufficient fibrinolysis can result in multiple organ dysfunction syndrome (MODS).
Purpose of the Study:
- To elucidate the pathophysiology of DIC, including its compensated and decompensated states.
- To highlight diagnostic laboratory markers for DIC, differentiating between acute and compensated forms.
- To review current and potential therapeutic strategies for managing DIC and its complications.
Main Methods:
- Review of the hemostasis and fibrinolytic systems in the context of DIC.
- Analysis of diagnostic laboratory tests, including D-dimer, fibrin(ogen) split products (FSP), soluble fibrin monomer (FM), and molecular markers like TAT, F 1+2, and PAP complexes.
- Evaluation of treatment modalities, including supportive care, anticoagulation with heparin, and administration of natural anticoagulant concentrates.
Main Results:
- Compensated DIC can be diagnosed using molecular markers of in vivo hemostasis activation.
- Decompensated DIC diagnosis is supported by decreasing fibrinogen and platelet counts, and elevated D-dimer, FSP, and FM.
- Treatment involves addressing the underlying disease, correcting factor consumption, and potentially using anticoagulants or natural anticoagulant concentrates.
Conclusions:
- Effective management of DIC requires prompt identification of the underlying cause and appropriate therapeutic interventions.
- Laboratory tests are essential for diagnosing DIC, with specific markers aiding in distinguishing between compensated and decompensated states.
- While heparin use is limited to compensated DIC, natural anticoagulant concentrates show promise, and early treatment initiation improves patient outcomes.
Abstract:
DIC is a life-threatening complication of several disease states. It is characterized by systemic activation of the hemostasis system. In many instances the release of tissue factor (TF) from endothelial cells or other circulating cells triggers the system. Initially, the increased activation can be compensated for by the natural inhibitor systems, a state referred to as compensated DIC. As the trigger persists, inhibitors will be consumed leading to more coagulation. In this process many clotting factors, most notably fibrinogen and platelets are consumed, resulting eventually in a complete breakdown of the hemostasis system. This results in a profuse and diffuse bleeding tendency or decompensated DIC. The term consumptive coagulopathy denotes this process. Of crucial importance is the fate of fibrin that is formed from fibrinogen by thrombin. If the fibrinolytic system is insufficiently activated, fibrin will be deposited in the microcirculation leading to MODS. This will not occur if the fibrinolytic system is fully activated. The clinical suspicion of DIC must be confirmed by laboratory tests and decreasing fibrinogen levels and platelet counts support the diagnosis. The determination of D-dimer, fibrin(ogen) split products (FSP) and soluble fibrin monomer (FM) further support the diagnosis. FM suggest the presence of thrombin, FSP the generation of plasmin, and D-dimer, both thrombin and plasmin. While the tests are not specific for DIC, they can be helpful, in the proper clinical setting, to diagnose decompensated or acute DIC. The tests are not useful for the diagnosis of compensated DIC, except for D-dimer, FSP, and FM if elevated. Compensated DIC can be diagnosed by molecular markers of in vivo hemostasis activation, such as thrombin-antithrombin (TAT) complexes, prothrombin fragment 1 + 2 (F 1 + 2), or plasmin-antiplasmin (PAP) complexes. For the treatment of DIC it is imperative to remove the triggering underlying disease. The consumption of coagulation constituents can be corrected by cryoprecipitate, platelet concentrates, and fresh frozen plasma, if needed. This may reduce the bleeding tendency. Arrest of the activated hemostasis system by heparins, either subcutaneous in low doses or intravenous in therapeutic doses, is only recommended in patients with compensated DIC. If the patient bleeds, heparins should not be given. The administration of concentrates of natural anticoagulants, i.e., antithrombin, protein C, or tissue factor pathway inhibitor are safer than heparins since they do not exacerbate the bleeding tendency. These concentrates were found to be very effective in animal models of DIC; human experience is still limited. Generally, the earlier treatment is initiated, the better the patient's prognosis.