Deep Vein Thrombosis — Blood Clots in Cancer Care

Deep vein thrombosis describes the pathological formation of a coagulated blood mass inside deep venous structures. Unlike superficial thrombophlebitis, which affects veins near the skin surface, DVT involves major vessels that return deoxygenated blood to the heart. If left untreated, fragments of the clot can detach, travel through the right heart chambers, and occlude pulmonary arteries, resulting in a potentially life-threatening pulmonary embolism (PE).

In oncology, DVT forms part of cancer-associated thrombosis (CAT). Malignant tumours actively release pro-coagulant factors, inflammatory cytokines, and extracellular vesicles that stimulate platelet aggregation and fibrin deposition. Concurrently, extrinsic compression of blood vessels by physical tumour masses, prolonged bed rest after surgical procedures, and the presence of indwelling central venous catheters all impede venous return, fulfilling the classic elements of Virchow's triad.

Recognising DVT is critical because venous thromboembolism is one of the leading causes of preventable mortality among people receiving cancer treatment. Developing a clot can interrupt active cancer therapies, delay surgical procedures, and cause prolonged leg pain or swelling known as post-thrombotic syndrome. Clinicians regularly evaluate individual risk factors to prescribe preventive blood-thinning medicines, ensuring that both the cancer and associated vascular risks are managed safely without provoking excessive bleeding complications.

The primary diagnostic test for lower-extremity DVT is compression duplex ultrasonography, which evaluates venous blood flow and vessel compressibility non-invasively. Blood tests measuring D-dimer levels reflect fibrin degradation; however, D-dimer is frequently elevated in cancer patients regardless of thrombosis, limiting its specificity. For suspected pelvic, abdominal, or central catheter-related clots, computed tomography (CT) venography or magnetic resonance venography provides detailed anatomical visualisation.

Cancer-associated thrombosis occurs across all malignancies, but the incidence is particularly high in pancreatic, gastric, brain, ovarian, and lung cancers, as well as haematological malignancies like multiple myeloma. Advanced stage, metastatic dissemination, and hospitalisation significantly heighten this risk. Pelvic tumours that mechanically compress the iliac veins or inferior vena cava also markedly raise local rates of lower-extremity thrombosis.

Once diagnosed, DVT is treated promptly with therapeutic anticoagulation to arrest clot expansion and minimise pulmonary embolism risks. Direct oral anticoagulants (DOACs) such as apixaban and rivaroxaban, alongside low-molecular-weight heparins (LMWH) like dalteparin, represent the standard of care in oncology. Anticoagulation is typically maintained for at least three to six months, or indefinitely while active malignancy and systemic cancer therapies persist.