CONSUMPTION OF THE LUNGS. 



227 



ridges, and sometimes stretch from one wall to the other in the form 

 of ligamentous bridges. It is very seldom that, prior to obliteration 

 of the walls of a vessel, they become so eroded as to cause dangerous 

 haemorrhage. We shall take this opportunity to call attention to a 

 peculiarity in the circulation of the lungs which frequently arises in 

 phthisis. Many branches of the pulmonary artery becoming destroyed, 

 those of the bronchial dilate, and conduct arterial blood to the lungs. 

 Many newly-formed vessels, springing from the intercostal arteries, 

 also advance through pleuritic exudations into the lung. Thus the 

 phthisical lung receives more arterial blood than the sound lung. Part 

 of it passes into the pulmonary veins, a part into the bronchial veins, 

 and a third portion passes through the pleuritic adhesions into the in- 

 tercostal veins. As the discharge of blood from the cutaneous veins 

 into the overloaded intercostal veins is thereby impeded, they, too, are 

 apt to become overfilled and distended, and a blue net-work of veins 

 appears upon the skin of the thorax. A chronic form of inflammation 

 of the pleura almost always occurs as soon as the affection of the pul- 

 monary substance commences to approach the periphery of the lung. 

 The pleural surfaces become thickened and adherent. The thickening 

 may be so great, especially at the apex of the lung, that it may be 

 covered, as by a cap, with a thick, compact fibrous rind, and at such 

 places it is generally impossible to separate the two pleural surfaces 

 without tearing the lung. In many cases the two pleural surfaces 

 grow together throughout the entire extent of the lung, so that a 

 pleural cavity no longer exists, and so that pneumothorax cannot occur, 

 though the process of destruction advance to the pleura itself. It is 

 only through the rapid disorganization of superficially-seated caseous 

 deposits that perforation sometimes occurs before adhesion is estab- 

 lished, or before the adhesions have grown strong enough to prevent 

 air and debris of tissue from entering the pleural cavity. In tubercu- 

 lous consumption, and in secondary tuberculosis, miliary tubercles are 

 often found, both in the pleura itself and in the pseudo-membrane, re- 

 sulting from the chronic pleuritis. The cavities rarely enlarge in what 

 was formerly supposed to be their most frequent mode of enlargement 

 that is to say, by caseous disorganization of secondary tubercular de 

 posit in their walls. Generally speaking, no matter in what manner 

 the cavities have formed, their increase in siz'e is the result of a 

 diphtheritic process, an infiltration of their walls, with subsequent 

 decay. 



The frequent coexistence of laryngeal disease with pulmonary con-r 

 sumption has been already spoken of in detail. The equally common 

 complication of pulmonary phthisis with ulcer of the bowels, intestinal 

 tubercle, with fatty liver, with amyloid liver, with parenchymatous in- 



