Acute infections, venous thrombosis, and recommended thromboprophylaxis

One of the most serious complications of acute infection is venous thromboembolism (VTE). The mechanism of host procoagulant responses in bacterial and viral infections is complex, and various factors are known to trigger the proinflammatory responses and activate systemic coagulation. Host defense mechanisms include proinflammatory cytokines such as interleukins, tumor necrosis factor-α, and complement system proteins, all of which can induce coagulopathy. Tissue factor (TF) expression on monocytes/macrophages, neutrophil and platelet activation, produce activation of thrombosis. This thromboinflammatory response, together with extracellular vesicles, causes endothelial damage that further increase thrombin generation. A key role in the development of thrombosis has TF. Penetration of the infection into the body leads to the formation of the TF-f.VIIa complex on cell surfaces and in the bloodstream, which launches the initial phase of coagulation by activating factors IX and X. Bacterial lipopolysaccharides stimulate the synthesis and expression of TF on endothelial cells and monocytes. Acute infections diagnosed in hospital or treated in the community were associated with a markedly increased risk of VTE. The association was strongest within the first 2-4 weeks (sometimes up to 12 weeks) after infection onset and gradually declined thereafter. but remained approximately twofold higher for almost all types of infection for up to 1 year of follow-up. The highest risk increases associated with respiratory tract infections. According to 9th ACCP Guidelines 2012 updated by CHEST Guideline and Expert Panel Report 2020 for hospitalized patients with acute infection and acutely ill hospitalized medical patients with hospital-diagnosed infection, who are at increased risk of thrombosis, thromboprophylaxis with LMWH, low-dose unfractioned heparin (bid or tid), or fondaparinux is recommended. The panel cautions against the use of DOAC and antiplatelet agents.