Venous Response to Surgical Trauma

Abstract

Since the days of VIRCHOW (1860) it has been common to assume that thrombosis is a consequence of the interaction of blood cells and plasma proteins with a vessel wall lesion. There has been no problem in accounting for vessel wall lesions in the arteries. However, venous lesions have not been demonstrated even in persons with extensive arterial disease. HUME et al. (1970) reviewed the literature and concluded that there was no evidence for a venous wall lesion prior to thrombosis. Furthermmore, in the natural history of deep venous thrombosis there is usually no trauma to the veins, or even the leg that thromboses. Since there was no evidence of a venous lesion, various investigators including HUME et al. (1970) have proposed that valve pockets serve as nidi for thrombus growth. If the information from postmortem examination of leg veins is considered alone, this proposal finds support. However, if information obtained by NICOLAIDES et al. (1971) by the use of venography and leg scans with labelled fibrinogen is also considered, this proposal cannot be entirely adequate, since more than half of the clinically significant thrombi started in the soleal veins which have no valves.