A drop in blood flow can cause venous congestion in the lower extremities, which may occur in reduced mobility, for example due to bed confinement, or external compression from enlarged lymph nodes, tumours or previous thromboses (1).
Blood vessel injury
The vessel endothelium (lining) provides a naturally smooth barrier between circulating blood and the thrombogenic tissues beneath. When vessel damage disrupts this barrier, platelet, aggregation and adhesion occurs, which initiates the blood clot formation process. Endothelial damage may be caused by prior Deep Vein Thrombosis (DVT), venous distension, trauma or surgery.
Changes in blood chemistry, which increases the tendency to clot, can occur due to a number of factors, such as dehydration, malignancy, surgery or trauma, oestrogen therapy or systemic inflammatory diseases.
Recognising and addressing the risk
It is likely that at least 50% of hospital inpatients will have one or more risk factors (2) and, without any form of prophylaxis, between 20% and 80% will develop Venous Thromboembolism (VTE) (3) . As VTE, is potentially avoidable, affecting millions of patients worldwide (2,4) and is the biggest cause of inpatient mortality (3), it is clear that effective prevention is critical.
- Turpie AG, Chin BS, Lip GY. Venous thromboembolism: pathophysiology, clinical features and prevention. BMJ. 2002; 325: 887-890.
- Cohen AT, Tapson VF, Bergman J-F et al. Venous thromboembolism and prophylaxis in the acute hospital setting (ENDORSE study): a multinational cross-sectional study. Lancet. 2008; 371: 387-394.
- GeertsWH, BergqvistD, PineoGF, et al. Prevention of venous thromboembolism: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th edition). Chest. 2008;133 (6 Suppl): 381S–453S.
- Heit J, Cohen A, Anderson FJ. Estimated annual number of incident and recurrent, non-fatal and fatal venous thromboembolism (VTE) events in the US. Blood. 2005; 106: 267A.