Woodring J H
Department of Diagnostic Radiology, University of Kentucky Medical Center, Lexington 40536-0084, USA.
South Med J. 1997 Dec;90(12):1176-82. doi: 10.1097/00007611-199712000-00003.
The purposes of this study were to review possible causes of reexpansion pulmonary edema (RPE) and to attempt to explain atypical distributions of RPE after drainage of large pleural effusions.
Five patients had focal RPE after routine drainage of large pleural effusions. In these cases, pleural effusion did not completely fill the hemithorax, and part or all of the ipsilateral upper lobe remained aerated. Reexpansion was accomplished by chest tube drainage with -20 cm H2O suction in four cases and by percutaneous needle aspiration without application of negative intrapleural suction in one.
In all five cases, RPE developed in the portion of the lung that had been collapsed but did not develop in the portion of the lung that remained aerated.
This suggests that hypoxic injury to the atelectatic lung, rather than mechanical stress, is the most plausible explanation for RPE.
本研究的目的是回顾复张性肺水肿（RPE）的可能病因，并试图解释大量胸腔积液引流后RPE的非典型分布情况。
5例患者在常规引流大量胸腔积液后发生局灶性RPE。在这些病例中，胸腔积液未完全充满半侧胸腔，同侧上叶部分或全部保持通气。4例通过-20 cm H2O负压吸引的胸腔闭式引流实现肺复张，1例通过经皮针吸且未施加胸腔内负压实现肺复张。
所有5例患者中，RPE均发生在肺萎陷的部分，而通气良好的肺部分未发生RPE。
这表明肺不张肺的缺氧损伤而非机械应力是RPE最合理的解释。
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