Microvascular thrombosis and multiple organ dysfunction syndrome

Crit Care Med. 2010 Feb;38(2 Suppl):S35-42. doi: 10.1097/CCM.0b013e3181c9e31d.

Abstract

This paper will review the involvement of disseminated intravascular coagulation-induced microvascular thrombosis in the pathogenesis of multiple organ dysfunction syndrome and the interaction between disseminated intravascular coagulation and systemic inflammatory response syndrome in critically ill patients. The published literature on clinical and experimental studies are the data sources of the study. Histologic evidence of microvascular thrombosis and tissue injury in disseminated intravascular coagulation has been reported in clinical, experimental, and autopsy findings. Proinflammatory cytokine-evoked neutrophil-endothelial activation and interplay between inflammation and coagulation through protease-activated receptors contribute to enhanced microvascular fibrin deposition in organs. In a clinical setting, systemic inflammatory response syndrome and disseminated intravascular coagulation synergistically play pivotal roles in the development of multiple organ dysfunction syndrome and in the poor prognosis of critical illness. Disseminated intravascular coagulation contributes to microvascular thrombosis and subsequent multiple organ dysfunction syndrome. Recent knowledge on the relationship between disseminated intravascular coagulation and systemic inflammatory response syndrome gives further insight into the pathogenic mechanisms of multiple organ dysfunction syndrome in critically ill patients.

Publication types

  • Review

MeSH terms

  • ADAM Proteins / physiology
  • ADAMTS13 Protein
  • Acute Kidney Injury / etiology
  • Acute Lung Injury / etiology
  • Animals
  • Cerebrovascular Disorders / etiology
  • Cytokines / physiology
  • Disseminated Intravascular Coagulation / complications
  • Endothelium, Vascular / physiology
  • HMGB1 Protein / physiology
  • Humans
  • Liver Diseases / etiology
  • Microvessels / physiopathology
  • Multiple Organ Failure / etiology*
  • Neutrophils / physiology
  • Receptors, Proteinase-Activated / physiology
  • Thrombosis / complications*
  • Thrombotic Microangiopathies / complications

Substances

  • Cytokines
  • HMGB1 Protein
  • Receptors, Proteinase-Activated
  • ADAM Proteins
  • ADAMTS13 Protein
  • ADAMTS13 protein, human