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Etiopathophysiology of disseminated intravascular coagulation

S Bakhshi1, L S Arya

  • 1Department of Pediatrics, Division of Hematology Oncology, All India Institute of Medical Sciences, New Delhi 110 029.

The Journal of the Association of Physicians of India
|December 4, 2003
PubMed

Insights

Disseminated intravascular coagulation (DIC) is a serious condition involving clotting and bleeding, often caused by sepsis. Understanding its complex pathways is crucial for patient outcomes.

Area of Science:

  • Hematology
  • Critical Care Medicine
  • Pathophysiology

Background:

  • Disseminated intravascular coagulation (DIC) is a complex syndrome characterized by simultaneous activation of coagulation and fibrinolysis.
  • Thrombosis leads to end-organ damage, while consumption of clotting factors causes bleeding, complicating patient management.
  • Sepsis is the most frequent trigger for DIC, highlighting the critical link between infection and coagulation disorders.

Purpose of the Study:

  • To elucidate the intricate roles of various endogenous mediators in the pathogenesis of DIC.
  • To explore the contribution of coagulation inhibitors, cytokines, kinins, complement, and vasoactive peptides in DIC.
  • To provide a comprehensive overview of the molecular mechanisms underlying DIC, particularly in the context of sepsis.

Main Methods:

  • Review of existing literature on the pathophysiology of DIC.
  • Analysis of the roles of specific molecular pathways including coagulation, fibrinolysis, and inflammatory cascades.
  • Discussion of the impact of sepsis on these pathways and the resulting clinical manifestations.

Main Results:

  • Sepsis-induced DIC involves consumption of antithrombin, diminishing its anti-inflammatory effects and serving as a poor prognostic indicator.
  • Elevated plasminogen activator inhibitor-1 (PAI-1) in sepsis impairs fibrinolysis, exacerbating microvascular thrombosis.
  • Multiple endogenous systems, including coagulation inhibitors, cytokines, kinins, complement, and vasoactive peptides, significantly influence DIC development and severity.

Conclusions:

  • DIC is a multifaceted disorder driven by dysregulated coagulation and fibrinolysis, with sepsis as a primary initiator.
  • The interplay between coagulation factors, inflammatory mediators, and endogenous inhibitors dictates the clinical course and prognosis of DIC.
  • A deeper understanding of these pathways is essential for developing targeted therapeutic strategies for DIC.

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