VTE in Oncology

Malignant disease is a well-known risk factor for VTE. Patients with confirmed malignancy are considered to have a 2- to 6-fold increase in risk of VTE, and malignancy-associated surgery increases this risk still further.1 In addition to being the most common complication of cancer, VTE is the second leading cause of death in cancer patients.2

The VITAE study assessing VTE rates in Europe estimates that each year 150,000 VTE-related deaths are linked with a cancer diagnosis.3

The risk of VTE varies with cancer type, exceeding 10% for cancers of the pancreas and brain. It has also been noted that VTE occurs frequently in perceived low-risk subgroups such as patients with haematologic malignancies and in those with non-metastatic disease.4

Cancer patients are predisposed to VTE risk because of multiple, compounding risk factors such as

  • changes in coagulability linked with malignancy and use of cancer therapies (chemotherapy, hormone therapy, and radiation)
  • surgical intervention and use of central venous catheters
  • basal risk factors such as immobility5

Both UFH and LMWH have been validated in terms of their efficacy and safety in the prevention of VTE in cancer patients undergoing surgical intervention, as well as for the primary treatment and secondary prevention of recurrent VTE.6,7

Prolonged thromboprophylaxis after cancer surgery appears to further reduce risks of VTE. In a study in which the LMWH enoxaparin was given for 4 weeks after surgery for abdominal or pelvic cancer rather than for 1 week, the rate of VTE was reduced from 12% to 4.8%.6  A post-hoc analysis of the FAMOUS study raised the possibility of the benefit of extended prophylaxis using dalteparin LMWH therapy, it showed an improvement in survival in those patients with a better prognosis given LMWH.8

Studies suggesting that LMWHs may prolong survival in patients with solid tumour malignancy have excited interest in basic research into possible antineoplastic mechanisms of action for these drugs.5

Guidelines on prevention of VTE highlight the need for cancer patients to receive optimal prophylaxis. The current ACCP guidelines make a Grade 1A recommendation that patients undergoing surgery for cancer should receive LMWH or low-dose UFH. Grade 2A recommendations are that patients with a central venous catheter should receive LMWH or fixed-dose warfarin and that after cancer surgery, post-discharge LMWH prophylaxis should be considered.9


  1. Samama MM, Dahl OE, et al. Quantification of risk factors for venous thromboembolism: a preliminary study for the development of a risk assessment tool. Haematologica. 2003;88:1410-21.
  2. Cohen AT, et al. Assessment of venous thromboembolism risk and the benefits of
    thromboprophylaxis in medical patients. Thromb Haemost. 2005;94:750-9.
  3. Cohen AT, et al. Venous thromboembolic disease in cancer patients in Europe: an opportunity for improved prevention. The VITAE Thrombosis Study. ECCO 13–The European Cancer Conference; October-November 2005; Paris, France [Poster].
  4. Khorana AA, Francis CW, et al. Thromboembolism in hospitalized neutropenic cancer patients. J Clin Oncol. 2006;24:484-90.
  5. Kakkar AK, Levine MN. Thrombosis and cancer: implications beyond Trousseau. J Thromb Haemost. 2004;2:1261-2.
  6. Bergqvist D, Agnelli G, et al. Duration of prophylaxis against venous thromboembolism with enoxaparin after surgery for cancer. N Engl J Med. 2002;346:975-80.
  7. ENOXACAN Study Group. Efficacy and safety of enoxaparin versus unfractionated heparin for prevention of deep vein thrombosis in elective cancer surgery: a double-blind randomized multicentre trial with venographic assessment. ENOXACAN Study Group. Br J Surg. 1997;84:1099-103.
  8. Kakkar AK, et al. Low molecular weight heparin, therapy with dalteparin, and survival in advanced cancer: the fragmin advanced malignancy outcome study (FAMOUS). J Clin Oncol. 2004;22:1944-8.
  9. Geerts WH, Pineo GF, et al. Prevention of venous thromboembolism: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. 2004;126 Suppl 3:338S-400S.
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