Hospitalization with acute infection increases the risk of venous thromboembolism

By Gro Grimnes
PhD-student at TREC

In a recently published study, we found that acute infection in hospitalized patients is a strong trigger for venous thromboembolism. The risk of venous thromboembolism increases even more if infection and immobilization co-exist.

After 17 years of follow-up, 707 out of 27 158 persons attending the fourth Tromsø Study in 1994/95 were diagnosed with venous thromboembolism (VTE). VTE is a multi-causal disease, and more than one risk factor may contribute to the thrombosis in each patient. In the present study, we aimed to investigate triggering factors for VTE. The hospital medical records for the 707 VTE-cases were searched for risk factors during all hospital contacts registered in the 18 months prior to the diagnosis of the VTE. We compared the occurrence of transient risk factors in the 3-month period prior to the VTE with four preceding 3-month control periods (i.e. within 18-6 months before the VTE). In a case-crossover design like this, stable factors such as chronic illnesses and genetic factors are in the case-period and in the control-periods, as each case serves as his or her own control. This design is therefore well suited to investigate transient risk factors such as acute infection.

We found that acute infection was a prevalent and strong trigger for VTE. More than 1/3 of the study participants were diagnosed with an infection in the 3-month period before the VTE. This corresponded to an 11-fold increased VTE-risk after controlling for other risk factors such as cancer, surgery and immobilization. The risk of VTE was particularly high in those with acute infection and immobilization occurring at the same time.

Pulmonary embolism has traditionally been regarded a complication to deep vein thrombosis in the lower extremities. However, in about 50% of cases with pulmonary embolism, no deep vein thrombosis is found. Where the thrombosis origins from in these remaining cases is not completely understood,but local thrombus formation in the lung is among the possible explanations. We therefore aimed to investigate whether the site of the infection influenced the VTE presentation. We found that respiratory tract infection was a strong trigger for pulmonary embolism, and that the risk of pulmonary embolism was much higher after a than after a urinary tract infection. This supports the concept that infections in the lungs might trigger local thrombosis. However, since pulmonary embolism and respiratory tract infections can present with similar symptoms, early signs of pulmonary embolism can be misdiagnosed as respiratory tract infection, and more studies are needed to investigate this hypothesis further.

We conclude that acute infection is a prevalent and strong trigger for VTE in hospitalized patients, especially when combined with immobilization. As venous thromboembolism by administrating anticoagulant treatment, our results emphasize that VTE-prevention should be considered in hospitalized patients with infection.

Reference: Grimnes G et al. Acute infection as a trigger for incident venous thromboembolism: Results from a population-based case-crossover study. Research and Practice in Thrombosis and Haemostasis (2017).

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