论文部分内容阅读
Richard Bright 1836年报道的100例死于肾炎尸检病例中,发现有71例胸膜受累。在Bright的报导发表100年前后未见有关胸膜与尿毒症或肾炎有联系的报导。甚至主要的教课书也没有提出胸膜炎或胸腔积液是尿毒症的表现。胸腔液体是以大约0.5ml/分的速度形成的。积液来自胸膜下毛细血管的血浆。任何原因使静脉阻力增加均可使毛细血管内的静水压增高,促进液体流出。血浆的胶体渗透压可阻止液体滤过到胸膜腔内。由于有低蛋白血症致使胶体渗透压降低。此外肺不张又可使胸膜腔内负压加大,促进液体流入胸腔。胸腔内液体主要是由淋巴管引流。因此,淋巴管的阻塞可使胸腔液体的聚积加速。再者小的溶
In the 100 cases of death from nephritis autopsy reported by Richard Bright in 1836, 71 cases of pleural involvement were found. There were no reports of pleural involvement associated with uremia or nephritis 100 years after Bright’s report was published. Even the main textbooks did not suggest that pleurisy or pleural effusion is a manifestation of uremia. Pleural fluid is formed at a rate of about 0.5 ml / minute. Accumulation of plasma from subpleural capillaries. Any reason for increased venous resistance can make hydrostatic capillary pressure increased, to promote the liquid outflow. The colloid osmotic pressure of the plasma prevents fluid from filtering into the pleural space. Due to hypoproteinemia resulting in decreased colloid osmotic pressure. In addition, pulmonary atelectasis can increase the negative pressure within the pleural cavity, and promote liquid into the chest. Thoracic fluid is mainly by the lymphatic drainage. Therefore, obstruction of the lymphatic vessels can accelerate the accumulation of pleural fluid. Another small solution