The Capillary Bronchi undergo the same softening as the true lung-substance, for they, or at least their walls, are the seat of tuberculous deposition, and their mucous membrane, becomes the seat of tuberculous infiltration (bronchial tuberculosis, p. 38) during the softening of the pulmonary tubercle, just as we observe in the larger bronchial tubes in the neighborhood of a tuberculous abscess. The capillary vessels become obliterated in the tubercle, and are exposed to the same softening process as the cellular strata surrounding them. If the cavern should now enlarge, the bronchial tubes become destroyed in the same proportion with the surrounding parenchyma, and it is only when the destruction of the tissue has attained a certain degree that an opening is effected into the tubes, and a communication established between the bronchi and the cavern. We only find bronchial tubes of a comparatively large size opening into the caverns, for the smaller ones are compressed by the tubercle deposited in their walls and in their immediate vicinity, or by the products of interstitial inflammation, or they are closed by catarrhal tumefaction of the mucous membrane, or by tuberculous infiltration. Their mouths remain freely open in places where compression cannot affect them, in consequence of greater and more resistent thickness of their walls, or of their having a larger calibre. The number of bronchial tubes opening into a cavern is generally proportional to its size. They constantly open with a round or an oval fissure-like mouth, according as they are more or less transversely or obliquely situated in relation to the wails of the cavern, or are only ulcerated on one side. When the bronchial opening is recent, it commonly presents an ulcerated appearance, but subsequently, when the cavern has acquired a dense callous wall, it is bounded by a puckered border of mucous membrane in a state of gelatinous infiltration, which is analogous to the serrated, puckered, and similarly infiltrated border of mucous membrane which surrounds the callous tuberculous ulcer of the intestine. The mouth of the bronchial tube opens in exactly the plane of the wall of the cavern, and never projects beyond it.

The blood-vessels present, as it were, the very reverse condition. The bronchial vessels are usually obliterated and thrust aside, and run along the walls of the cavern as ligamentous, projecting, yellowish-white, ramifying cords, and those of an arterial nature, even when in this condition, for a long time resist the destructive processes which are here in operation. A partially or entirely obliterated vessel, enveloped in atrophied lung-substance, is usually found in the bridges which run across the cavity of the abscess. It often, however, happens that, before the vessels are obliterated, they are laterally denuded of the surrounding tissue and of their cellular sheath; the two inner coats then soon give way, and occasion the pulmonary hemorrhages which, as is well known, occur in the course of phthisis.

There are two circumstances under which the caverns may reach the pulmonary pleura; either when they are originally formed in the peripheral portion of the lung, or when they were originally deep-seated, but have attained a considerable size in an outward direction. The first is very rarely dependent on the softening of tuberculous granulations, but, as we shall presently show, is much more frequently a consequence of the softening and breaking down of tuberculous infiltration. In either case the pulmonary pleura may finally be destroyed, and this may occur in different ways and with different consequences. If there are no adhesions at the point where the cavern reaches the pleura, this membrane, after being denuded on its pulmonary surface, will be converted into a yellowish-white eschar, which extends over a greater or smaller portion of the cavern, and either becomes torn or else loosened along its circumference and falls out in an entire piece; in this way tuberculous pus and atmospheric air find their way from the bronchial passages into the pleural cavity, and give rise to pleurisy with pneumothorax, and usually to speedy death. Mere cellular adhesions cannot prevent this termination; they are, in part, mechanically loosened by the effusion from the cavern, and being involved in the pleuritic process, they are, in part, likewise destroyed in the exudation. If, on the other hand, there are thick adhesions, that is to say if the lung is bound down by dense, thick, callous, cellulo-fibrous, and fibro-cartilaginous pseudo-membranes, such as occur especially about the upper lobes and their apices in consequence of previous pleurisies, then the pulmonary pleura which has coalesced and become identified with these false membranes may sometimes be laid bare to a considerable extent without perforation and the above-named consequences ensuing. But the tuberculous destruction is usually limited by these callous bands; cases occasionally occur in which even these are perforated; irritation is set up in them at one or more spots; they soften, become tuberculous, and suppurate, layer after layer; in this way they finally become perforated, and the tuberculous process attacks the wall of the thorax, insidiously advances to the ribs and soft parts, and at length reaches the outer surface of the chest, or even of the neck (Cru-veilhier), in the form of a tuberculous sinus variously combined with caries of the ribs, the sternum, and the vertebrae.