Plasma and plasma components in the management of disseminated intravascular coagulation.

Abstract

A variety of clinical conditions can cause systemic activation of coagulation that ranges from insignificant laboratory changes to severe disseminated intravascular coagulation (DIC). DIC consists of a widespread systemic activation of coagulation, resulting in diffuse fibrin deposition in small and midsize vessels. There is compelling evidence from clinical and experimental studies that DIC is involved in the pathogenesis of microvascular dysfunction and contributes to organ failure. In addition, the massive and ongoing activation of coagulation can result in depletion of platelets and coagulation factors, which might cause bleeding. Recent insight into important pathogenetic mechanisms that might lead to DIC has resulted in novel preventive and therapeutic approaches to patients with sepsis and derangement of coagulation. Supportive strategies aimed at inhibition of coagulation activation might theoretically be justified and have been found beneficial in experimental and initial clinical studies. These strategies comprise inhibition of tissue factor-mediated activation of coagulation or restoration of physiological anticoagulant pathways.

• Authors: Marcel Levi, Evert de Jonge, Tom van der Poll
• Journal: Best practice & research. Clinical haematology (Best Pract Res Clin Haematol) Vol. 19 Issue 1 Pg. 127-42 ( 2006) ISSN: 1521-6926 [Print] Netherlands
• PMID: 16377546 (Publication Type: Journal Article, Review)

Chemical References

• Anticoagulants

Topics

• Anticoagulants (therapeutic use)
• Blood Component Transfusion
• Disseminated Intravascular Coagulation (drug therapy, physiopathology, therapy)
• Humans
• Plasma