<原著>胸膜腔の吸引による虚脱肺の急速な再膨張に由来する一側性肺水腫の経験

Abstract

The incidence of unilateral pulmonary edema has been reported when the entirely collapsed lung caused by pneumothorax or pleurisy was re-expanded rapidly by means of intrathoracal aspiration technique. Many of them developed to severe clitical condition or even fatal. But only few observations on this incidence have been reported in Japan. The authors will report in this paper four cases with the unilateral pulmonary edema but none of them developed to severe condition. Of the four, two had pleural effusion and two had pneumothorax. Case 1; A 47-year-old woman. Case 2; A 60-year-old woman. Both of them suffered pleurisy (Case 1; left, Case 2; right, ) with voluminous effusion for about one month before admission. During thoracentesis and removal of fluid was performed, the patients complained temporal intrathoracic sensation of unrestness and tachycardia. Chest X-ray films on that occasion revealed wide, faint and homogeneous shadow on the middle part of the affected lung, which disappeared several days later without any specific treatment. Case 3; A 20-year-old man. Case 4; A 57-year-old woman. Both of them suffered left spontaneous pneumothorax with sudden chest pain and dyspnea on four days before admission. The each chest X-ray film on admission revealed entirely collapsed lung with the mediastinum shifted to right-ward. The intrathoracic pressure was positive. Continuous air aspiration was performed by means of intrathoracal plastic tube connected with suction pump with the negative pressure of 20cm water. After very short period release of the initial symptoms, the patients complained intrathoracic sensatin of heaviness several hours later. The each chest X-ray film on that occasion revealed wide, faint and homogenous shadow in the middle field of left lung, which disappered without any treatment within a few days. From the observations of ours and other investigators, the condition of the symptom seemes to be associated with 1) collaps of entire lung for several days, 2) rapid re-expantion of the lung by removal of air or fluid, 3) edema involving the suffered lung. Although the exact mechanism is unknown, it is seemed to be that the pressure gradient between alveolar space and interpleural space induces change of permeability of cell wall of alveoli or capillary beds, which allows to transude the fluid from capillary into the interstitial space or alveolar space. It is also probable that increase of intracapillary pressure by sudden release of pulmonary circulation or lack of the alveolar surfactant of the collapsed lung may play some role in this mechanism. Considerable relationship between the pulmonary edema appeared here and acute high altitute pulmonary edema is also discussed.