The complex physiopathology of the post-thrombotic syndrome following deep venous thrombophlebitis involves a sequence of hemodynamic and biochemical events; development of the clinical picture, which remains susceptible to change, is a late occurrence following a long free interval. Despite re-establishment of venous patency, residual valvular lesions can cause orthostatic reflux. While residual occlusion generally has few long term repercussions, failure of the calf muscle venous pump is a serious potential consequence of such reflux. The clinical picture is less severe when the popliteal vein valves are not destroyed. The responsibility of wall compliance alterations has been proved as well. The initial thrombosis and/or the reflux may lead to associated incompetency of the perforating veins, then of the superficial venous network, thus aggravating the hemodynamic disturbances. The increased venous pressure results in alterations in upstream circulation, especially in the venous capillaries; the resultant increase in intraluminal pressure reduces fluid reabsorption. Edema remains intermittent so long as the lymphatic network withstands the excess workload. Thereafter, post-thrombotic lymphedema develops; the accompanying tissue fibrosis, a classical feature of the clinical picture, is attributed to the elevated concentration of macromolecules. This stage corresponds to lipo-dermato-sclerosis. The increase in the fibrinogen concentration, the reduction in tissue fibrinolytic activity, and the formation of pericapillary fibrin cuffs have all been considered as possible causes of leg ulceration. In fact, the assumed phenomenon of secondary hypoxia has not been demonstrated, and the fibrin cuffs do not appear to constitute a true barrier.(ABSTRACT TRUNCATED AT 250 WORDS)

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   |clé=     pubmed:8027676
   |texte=   [Physiopathology of post-thrombotic syndrome. Update 1994].
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