Sepsis and thrombosis

Semin Thromb Hemost. 2013 Jul;39(5):559-66. doi: 10.1055/s-0033-1343894. Epub 2013 Apr 27.


Activation of coagulation frequently occurs in severe infection and sepsis and may contribute to the development of thrombosis. Coagulation abnormalities in sepsis range from a small decrease in platelet count and subclinical prolongation of global clotting times to fulminant disseminated intravascular coagulation (DIC), characterized by simultaneous widespread microvascular thrombosis and profuse bleeding from various sites. Septic patients with severe forms of DIC may present with manifest thromboembolic disease or clinically less apparent microvascular fibrin deposition, which predominantly presents as multiple organ dysfunction. Thrombophilia is associated with a prohemostatic state and consequently with an increased tendency to develop thrombosis. Hypothetically, patients with thrombophilia may suffer from more severe coagulopathy in case of severe infection or sepsis, which may result in a more serious clinical course and an unfavorable outcome. On the basis of the knowledge of the pathogenesis of thrombosis in severe inflammation and sepsis, strategies aimed at the inhibition of coagulation activation have been developed and have been found favorable in experimental and clinical studies.

Publication types

  • Review

MeSH terms

  • Anticoagulants / therapeutic use
  • Blood Coagulation / drug effects
  • Disseminated Intravascular Coagulation / diagnosis
  • Disseminated Intravascular Coagulation / etiology
  • Disseminated Intravascular Coagulation / prevention & control
  • Humans
  • Multiple Organ Failure / diagnosis
  • Multiple Organ Failure / etiology
  • Multiple Organ Failure / prevention & control
  • Sepsis / blood
  • Sepsis / complications*
  • Thrombophilia / diagnosis
  • Thrombophilia / etiology
  • Thrombophilia / prevention & control
  • Thrombosis / diagnosis*
  • Thrombosis / etiology
  • Thrombosis / prevention & control*
  • Treatment Outcome


  • Anticoagulants