290 DISEASES OF THE PLEURA. 



air which has been expelled from the lung by virtue of its elasticity. 

 With the next inspiratory movement of the chest an additional quan- 

 tity of air enters the pleural sac, and, if this air can pass out again 

 with the succeeding expiration, the thorax returns to its expiratory 

 state, and the lung does not suffer compression. If, however, the aii 

 which enters the pleura during inspiration cannot escape with the next 

 act of expiration, the thorax remains dilated, and the lung is com- 

 pressed. This process is repeated until the thorax attains the utmost 

 dilatation which a forced inspiratory act can produce in it, and until 

 all air has been driven out of the lung, and its compression is com- 

 plete. Owing to the peculiar ragged character of the opening in the 

 pulmonary pleura, through which the air enters the pleural sac in most 

 cases of pneumothorax, it generally happens that the air which gets 

 in cannot get out again. The orifice opens like a valve during inspi- 

 ration, and is closed by the pressure of the compressed air when expi- 

 ration commences. Finally, after the tension of the air within the 

 pleura has reached a sufficient degree of intensity, the valve is perma- 

 nently shut, even during inspiration, and, although there is no aggluti- 

 nation or adhesion of the point of perforation, no more air enters the 

 cavity. In pure pneumothorax, the dilatation of the chest does nol 

 exceed the normal expansion which forced inspiration can produce in it. 

 The extraordinary degree to which this normal limit is often exceeded, 

 and the excessive distention which the walls of the chest frequently 

 undergo, are due to a consecutive effusion of liquid, which also takes up 

 room, or, in other words, the pneumothorax has become a pyo-pneumo- 

 thorax. In the rare instances in which the air passes freely in and out 

 of the thorax, as occurs in large wounds or fistulous openings which 

 penetrate perpendicularly, and in spacious fistulous communications, 

 with rigid resisting walls running between the pleural cavity and a 

 large bronchus, there is no dilatation of the chest, and no compression 

 of the lung, which, however, has generally been emptied of its air by 

 other causes. 



When a vomica perforates the pleural sac, the moment of perfora- 

 tion is usually distinctly perceptible to the patient. He feels as if 

 " something had given way, or burst, in his chest." Immediately after- 

 ward a dyspnoea commences, which rapidly assumes the utmosi in- 

 tensity. The patient can only lie upon the affected side, or else is 

 compelled to sit upright, so as to give the freest play possible to the 

 sound side of his chest. This dyspnoea is partially owing to the sudden 

 compression of one lung, and in part to the collateral hyperaemia and 

 collateral oedema, and obstruction of the alveoli in the sound lung, 

 consequent upon the compression of the vessels of the diseased one. 

 In all the cases of sudden pneuraothorax which I have seen, the pa- 



