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  • Title: [Evaluation and management of post-thrombotic syndrome].
    Author: Hach W.
    Journal: Herz; 1989 Oct; 14(5):287-97. PubMed ID: 2680852.
    Abstract:
    The number of patients with postthrombotic syndrome subsequent to venous thrombosis is continuously increasing. The risk of venous thrombosis is increased by the increasing age of the population, through increasingly-extensive surgical intervention, through hormonal contraception and through prolonged airline flights and the risk appears diminished by modern thrombosis prophylaxis. The course of the disease can be divided into an acute phase of thrombosis with a duration of about one week, the subacute phase lasting from the second to the fourth week and the phase of the postthrombotic syndrome. Pathophysiology Thrombotic occlusion can be compensated for by recanalization and collateralization. Concomitant with the generation of the blood clot, fibrinolytic factors are activated which can serve to lyse the thrombus. After organization of the remaining clot, blood flow can be re-established. The extent of recanalization can be quantified radiologically. In 35.5% of the patients there is complete recanalization, in 53.4% partial and in 11.1% no recanalization. At nearly all sites of venous occlusion preformed collaterals can be found. A hemodynamically meaningful occlusion causes an increase in the peripheral venous pressure. On use of Doppler ultrasound examination, there is absence of respiratory modulation as well as a high-frequency continuous signal which disappears as soon as collateral function is optimal. As the venous circulation adapts, there is dilatation in the collateral vessels, initially with preserved coaptation of the valve leaflets. This stage is designated as compensatory phlebectasia; phlebography of the great saphenous vein shows the typical findings. If the venous valves are incompetent, under some conditions the direction of flow may be reversed. An example of secondary varicosities in the region of the great and lesser saphenous vein is shown in Figure 3. The most frequent causes of valve damage are over-extension of the valve ring through recoil pressure and volume waves during standing, coughing and pressing in addition to local thrombus formation and inflammatory processes. In association with thrombosis in the femoropopliteal region with compensatory phlebectasia of the great saphenous vein, respiratory modulation in this vein can be detected with Doppler ultrasound examination. With secondary varicosities, which have to be differentiated from compensatory phlebectasia, on use of the Valsalva test or calf compression test there is pathologic, persistent retrograde blood flow, the calf compression test shows diminished A-sounds. In contrast to primary varicosities, with secondary varicosities of the great saphenous vein the distal dilatation is more marked than that seen proximally. Retrograde blood flow can extend to the foot with no obstacles.(ABSTRACT TRUNCATED AT 400 WORDS)
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