Increased risk of venous thromboembolism within the first year after Staphylococcus aureus bacteraemia: a nationwide observational matched cohort study

Abstract

Objectives. Recent evidence suggests that there is an association between infection and venous thromboembolism (VTE). Here, we examined the risk of VTE after Staphylococcus aureus bacteraemia (SAB) compared to the risk in control subjects.Design and setting. Register-based nationwide observational cohort study of hospitalized patients and matched control subjects from the general population in Denmark between 1995 and 2008.Results. Amongst 15 669 SAB cases and 156 690 controls, 182 and 511, respectively, experienced VTE within 1 year. The overall incidence rate (IR) of VTE amongst cases was highest within the first 30 days [IR of deep vein thrombosis (DVT), 39.3 (95% confidence interval (CI) 28.9-53.4)/1000 person-years (PYs); IR of pulmonary embolism (PE), 16.3 (95% CI 10.1-26.2)/1000 PYs]. IRs of DVT were particularly increased amongst cases with a previous diagnosis of VTE, communityacquired infection, a history of injection drug use and in younger age groups. The overall hazard ratio of VTE for cases compared to controls declined from 15.6 (95% CI 10.3-23.5) in the first 30 days after SAB to 4.5 (95% CI 3.2-6.2) from 181 to 365 days after infection. The increased risk of VTE amongst SAB patients persisted after excluding cases with identified VTE risk factors.Conclusions. There was a particularly high risk of VTE during the first month following an episode of SAB. The risk declined over time, but remained at a threefold increased level compared to control subjects, suggesting that there are shared risk factors for SAB and VTE. Patients with SAB and welldocumented risk factors for VTE may benefit from thromboprophylaxis.

Antibiotic use associated with VTE and its implications: a new trigger for thromboprophylaxis and for reclassification of some unprovoked to provoked VTE's?

“…At first sight, the observation seems obvious and quite plausible, that an infection severe enough to be treated by prescription antibiotics could be a marker or indicator of VTE. Others have made similar observations (Schmidt et al ; Mejer et al ; Dalager‐Pedersen et al ). It appears a likely surrogate for bed rest, immobilisation, fever, bacteraemia, potential exsiccosis etc.…”

“…; the infection trigger is further made plausible by well established procoagulant effects of bacterial and viral infection, the acute phase reaction comprising of increased fibrinogen and von Willebrand factor concentrations, direct and indirect procoagulant platelet and endothelial effects that have been consistently reported. In fact bacteriaemia of various pathogens is associated with thrombotic events (and mortality in general; Mejer et al ; Dalager‐Pedersen et al ; Nielsen ; Nielsen et al ; Wiese et al ). Local effects of infections have been recognized as triggers leading to thrombosis of adjacent vessels, such as in pancreatitis, septic jugular vein thrombosis, ovarian vein thrombosis, etc.…”

Infection as cause of immobility and occurrence of venous thromboembolism: analysis of 1635 medical cases from the RIETE registry

“…In the literature, information on thrombogenic effects of various types of infection are limited [28,29], and some Authors suggested that the effect on risk of VTE might be generic and not linked to specific types of infection [1,6]. According to our data, patients with respiratory tract infections more likely presented with PE (as compared with isolated DVT) than patients with other types of infection (namely urinary, and sepsis).…”

Interaction between inherited thrombophilia and HIV infection: fact or fancy?

“…For example, acute Cytomegalovirus infection, which is far more common than HIV infection, doubles the risk of VTE. 5 Other well established risk factors for VTE are Staphylococcus aureus infection 6 and active tuberculosis. 7 More broadly, in a large population based study, respiratory tract, urinary tract, skin, gastro intestinal, and bacteraemic infec tions diagnosed in the community or in hospital were associated with a 2.6 fold to 3.3 fold increased risk of VTE after adjustment for other factors.…”