Mechanisms of hypercoagulability.

Following certain major operative procedures, large amounts of tissue factor may be released from damaged tissues to venous blood. Mechanical and chemical injury to the collecting veins exposes subendothelial procoagulant proteins. This initiates a marked local hypercoagulable process. Subsequently, venous bloodborne procoagulant debris induce a substantial thrombin generation as blood passes the lung capillaries. Thus, the lungs seem to have a central role in the mechanisms of hypercoagulability in high-risk patients. Hypercoagulable blood is squeezed out in the peripheral circulation and may favor thrombosis formation both in central and peripheral vessels. In addition, reduced venous blood flow for several days to weeks after the operation may put these patients at-risk for thromboembolic complications for a long time. Several predisposing genetic and acquired factors associated with thrombophilia have been proposed to contribute to this hypercoagulable process. However, few studies and conflicting results have been reported. The clinical penetrance of the described thrombophilic abnormalities and their contribution to the hypercoagulable process in "high-risk" patients are, at present, unclear. The post-traumatic hypercoagulability seems to be a systemic phenomenon, at least following major orthopedic surgery. Cardiorespiratory and vascular complications play a prominent role as a cause of death and morbidity during and after this kind of surgery.