ENDOTHELIAL injury and circulatory stasis occurring in association with operation and the postoperative state are obvious causes of postoperative venous thrombosis. Hewson,1 however, in 1771 showed that stasis per se will not necessarily cause thrombosis. Furthermore endothelial injury involving any but the smaller veins is rare during a surgical procedure. Many have therefore turned their attention to searching for postoperative alterations in the blood itself which might cause it to be more readily coagulable. The modern wide use of anticoagulants to prevent the occurrence or the extension of venous thrombosis gives added meaning to an attempt to define any hyper-coagulability which may exist. Presented in this report are the results of certain studies relative to such an attempt.
Figure 1 presents a graphic summary of the coagulation mechanism in the light of our present knowledge. Any diagram of this complex and controversial mechanism leads to oversimplification and, perhaps, to
WARREN R, AMDUR MO, BELKO J, BAKER DV. POSTOPERATIVE ALTERATIONS IN THE COAGULATION MECHANISM OF THE BLOOD: Observations on Circulating Thromboplastin. Arch Surg. 1950;61(3):419–432. doi:10.1001/archsurg.1950.01250020424002
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