Clotting Disorders and Hemostatic Mechanisms in Sepsis
Summary
Sepsis induces a complex interplay between inflammation and coagulation, leading to haemostatic dysregulation. Pathogen-triggered cytokine release activates endothelial cells and platelets, promoting tissue factor expression and thrombin generation. This shift towards a procoagulant state is compounded by impaired anticoagulant pathways—most notably reduced protein C activity—and suppressed fibrinolysis. Microvascular thrombosis ensues, contributing to organ hypoperfusion and failure. In severe cases, disseminated intravascular coagulation (DIC) develops, characterised by widespread clot formation alongside consumption of clotting factors and platelets, raising the risk of both thrombosis and bleeding. Endothelial dysfunction further exaggerates vascular leakage and leukocyte recruitment, while alterations in complement cascades and neutrophil extracellular traps amplify thrombo-inflammatory feedback loops. Understanding these mechanisms is crucial for targeted interventions that restore balance between coagulation and anticoagulation without increasing haemorrhagic risk.
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Clotting Disorders and Hemostatic Mechanisms in Sepsis publication trend
The graph below shows the total number of articles in clotting disorders and hemostatic mechanisms in sepsis across all publications each year (not limited to Nature Index journals).
Technical terms
Disseminated intravascular coagulation (DIC): A pathological state of systemic clot formation and consumption of clotting factors leading to simultaneous thrombosis and bleeding risks.
Protein C: A vitamin-K-dependent anticoagulant enzyme that, when activated, degrades coagulation factors Va and VIIIa, modulating thrombin generation.
Purpura fulminans: An acute, life-threatening condition characterised by DIC, skin necrosis and gangrene, often complicating severe infection.
Microthrombi: Tiny clots that form in the microcirculation, obstructing capillary flow and contributing to organ dysfunction.
Endothelial dysfunction: Impairment of the vascular lining leading to altered barrier function, procoagulant surface expression and leukocyte adhesion.
References
- Symmetrical peripheral gangrene caused by urosepsis: Case reports and literature review. Medicine (2024).
- Relationship Between Symmetrical Peripheral Gangrene Patients and Using Vasopressors in the Intensive Care Unit. Cureus (2024).
- Human protein C concentrate in the treatment of purpura fulminans: a retrospective analysis of safety and outcome in 94 pediatric patients. Critical Care (2010).
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