广泛肺血管之血栓形成(PVT)引起肺动脉分枝阻塞是各种严重ARDS 的共同特征,血管造影证明PVT 发生于其早期,预期死亡率为90%。PVT 可减少气体交换,增加肺血管阻力,且产生右心室功能障碍,以及由于引起局部肺缺血后坏死,增加血管的外渗(?)导致肺损伤。作者对5例严重ARDS 伴有PVT患者用静脉注射纤容剂治疗,并用动脉造影和临床表现作比较。用链激酶经中心静脉导管定量持续输入,首剂25万单位,以后每隔20分钟10万单位/小时,如有明显出血发生立即停药,其血栓溶解作用在30分钟内即可消失。在治疗前和治疗中均作抗凝治疗的常规血液监测。由于ARDS 常伴有一些促进血栓形成和阻碍血栓溶解的因素:即炎性裸露的毛细血管内皮细胞减少小血管流量,抑制血管内纤维蛋白溶解,血小板聚集, Extensive pulmonary vascular thrombosis (PVT) causes pulmonary artery occlusion is a common feature of all serious ARDS, angiography showed that PVT occurred in its early stage, the expected mortality rate was 90%. PVT reduces gas exchange, increases pulmonary vascular resistance, and produces right ventricular dysfunction, as well as increased pulmonary extravasation (?) Leading to lung damage due to local ischemia-induced necrosis. The authors treated 5 patients with severe ARDS accompanied by PVT with fibrinolytic agents and compared them with angiography and clinical presentation. With streptokinase through the central venous catheter quantitative continuous input, the first dose of 250,000 units, after every 20 minutes 100,000 units / hour, if significant bleeding occurs immediately discontinued, the thrombolytic effect within 30 minutes to disappear. Routine blood monitoring of anticoagulant therapy was performed before and during treatment. As ARDS is often accompanied by some factors that promote thrombosis and prevent thrombolysis: inflammatory bare capillary endothelial cells to reduce the flow of small blood vessels, inhibition of intravascular fibrinolysis, platelet aggregation,