The sepsis-coagulant axis: a review

Area of Science:

• Biomedical Science
• Hematology
• Inflammation Research

Background:

• Coagulation activation is a normal part of the inflammatory response.
• Inflammatory cytokines shift endothelium to a prothrombotic state, activating coagulation and platelets.
• Initial fibrinolytic activation is followed by inhibition, creating a procoagulant state.

Purpose of the Study:

• To explain the mechanisms of coagulation activation during inflammation.
• To describe the pathophysiology of disseminated intravascular coagulation (DIC) in sepsis.
• To review current and emerging treatments for DIC.

Main Methods:

• Review of inflammatory and coagulation pathways.
• Analysis of the imbalance between coagulation and fibrinolysis.
• Discussion of the role of DIC in sepsis-induced organ failure.

Main Results:

• Inflammatory cytokines promote a procoagulant state by altering endothelial function and activating coagulation factors.
• A net procoagulant state results from the imbalance between coagulation and fibrinolysis.
• Disseminated intravascular coagulation (DIC) arises when coagulation and platelet activation overwhelm regulatory mechanisms.

Conclusions:

• DIC is a critical factor in sepsis-related multiple organ failure and mortality.
• Existing treatments like heparin and aspirin have limited efficacy in managing DIC.
• Novel, more potent therapeutic agents for DIC are anticipated for clinical use.