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Related Experiment Videos

Disseminated intravascular coagulation (DIC).

E F Mammen1

  • 1Wayne State University, Detroit, MI, USA.

Clinical Laboratory Science : Journal of the American Society for Medical Technology
|October 6, 2001
PubMed
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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:

Related Experiment Videos

  • 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.