Abstract
Surgery is associated with an increased risk of venous thromboembolic events (VTE)
including deep vein thrombosis and pulmonary embolism. Although the current treatment
regiments such as mechanical manipulation and administration of pharmacological prophylaxis
significantly reduced the incidence of postsurgical VTE, they remain a major cause
of postoperative morbidity and mortality worldwide. The pathophysiology of venous
thrombosis traditionally emphasizes the series of factors that constitute Virchow
triad of factors. However, inflammation can also be a part of this by giving rise
to a hypercoagulable state and endothelial damage. The inflammatory response after
surgery, which is initiated by a cytokine “storm” and occurs within hours of surgery,
creates a prothrombotic environment that is further accentuated by several cellular
processes including neutrophil extracellular traps formation, platelet activation,
and the generation of tissue factor–bearing microparticles. Although such inflammatory
markers are elevated in undergoing surgery, the precise mechanism by which they give
rise to venous thrombosis is poorly understood. Here, we discuss the potential mechanisms
linking inflammation to thrombosis, and highlight strategies that may minimize surgical
inflammation and reduce the incidence of postoperative VTE.
Keywords
surgery - inflammation - thromboembolism
