Venous Thromboembolism Management in Oncology

Venous thromboembolism (VTE) represents a leading non‐cancer cause of death in patients with malignancy and arises from a complex interplay of tumour‐related procoagulant activity, patient characteristics and anticancer therapies. Tumour cells can activate the coagulation cascade directly or via release of tissue factor‐bearing microparticles, while factors such as chemotherapy, surgery, central venous catheters and prolonged immobility further elevate risk. Certain malignancies—particularly pancreatic, brain and lung cancers—carry the highest incidence of VTE. Management encompasses risk assessment, primary thromboprophylaxis in high‐risk ambulatory and postoperative patients, acute anticoagulant treatment and decisions on long‐term anticoagulation. Low molecular weight heparin has long been standard, but more recent studies support use of direct oral anticoagulants in selected patients with careful consideration of bleeding risk. Biomarkers such as D-dimer and clinical prediction scores guide individualised prophylaxis, and multidisciplinary collaboration is essential to balance thrombosis prevention against haemorrhagic complications. Emerging approaches, including genetic risk models and real-time biomarker monitoring, promise to refine patient selection and optimise duration of therapy, thereby improving outcomes worldwide.

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Venous Thromboembolism Management in Oncology publication trend

The graph below shows the total number of articles in venous thromboembolism management in oncology across all publications each year (not limited to Nature Index journals).

Technical terms

Venous thromboembolism (VTE): A spectrum of conditions comprising deep vein thrombosis and pulmonary embolism resulting from clot formation within the venous system.

Deep vein thrombosis (DVT): The formation of a blood clot in a deep vein, typically in the lower limbs, which may embolise to the lungs.

Pulmonary embolism (PE): Obstruction of the pulmonary artery or its branches by a clot, often originating from a deep vein thrombosis, causing impaired gas exchange and haemodynamic instability.

Thromboprophylaxis: The use of anticoagulant agents or mechanical measures to prevent the formation of thrombosis in at‐risk patients.

D-dimer: A fibrin degradation product present in the blood after clot formation and breakdown, used as a biomarker to assess thrombotic activity.

Khorana score: A clinical risk assessment tool that stratifies ambulatory cancer patients by site of tumour, blood counts and body mass index to predict VTE risk.

Low molecular weight heparin (LMWH): A class of anticoagulants derived from standard heparin, administered subcutaneously, commonly used for VTE prevention and treatment in cancer patients.

Direct oral anticoagulants (DOACs): A group of orally administered agents that inhibit specific clotting factors (such as factor Xa) and are increasingly used as alternatives to heparin in selected cancer populations.

References

1. Risk of Venous Thromboembolism in Patients with Cancer: A Systematic Review and Meta-Analysis. PLOS Medicine (2012).
2. Cancer-Associated Thrombosis: An Overview of Mechanisms, Risk Factors, and Treatment. Cancers (2018).
3. A clinical prediction model for cancer-associated venous thromboembolism: a development and validation study in two independent prospective cohorts. The Lancet Haematology (2018).
4. Guidance for the prevention and treatment of cancer-associated venous thromboembolism. Journal of Thrombosis and Thrombolysis (2016).
5. Multivariable clinical-genetic risk model for predicting venous thromboembolic events in patients with cancer. British Journal of Cancer (2018).