Osseous laminae are sometimes developed under the serous investment, in like manner as in the cellular tissue beneath normal serous membranes.

In these caverns an event not unfrequently takes place, which very often proves fatal on its first occurrence; this is the hemorrhage which is met with in caverns of this construction, and which always springs from the larger branches of the pulmonary artery traversing the walls; these branches often remain permeable, and become opened for a considerable extent on the side towards the cavity. There are two different conditions which may give rise to the opening of these arteries.

(a.) They either undergo an aneurismal dilatation in consequence of the absence of support in the direction towards the cavern, and finally tear at this point, without any further change in the texture of their membranes;

(β.) Or the delicate cellular sheath of the vessel participates in the irritation of the adjacent investment of the cavern; the process extends to the fibrous coat, which becomes relaxed and infiltrated with gelatinous matter; and the vessel finally gives way, a previous dilatation of its coats being sometimes but not always observed.

A circumstance deserving of notice sometimes accompanies these hemorrhages. The extravasated blood in the cavern coagulates into a fibrinous clot, which completely fills it, and is attached to a pedicle, which is seated in the rent in the vessel, and is continuous in both directions with the cylindrical clot in the artery. The cavern may certainly contract around this clot of fibrin when, in the course of time, it has become shrivelled and finally cretified; but as the cavity in its previously described state must be regarded as innocuous, and may be closed in another and a simpler manner, this method of cure, except in cases where hemorrhage takes place into a cavern which does not communicate with a bronchial tube, must always be regarded as dangerous, and only of actual use, insomuch as the fibrinous coagulum affords a support for the vessels in the walls, and prevents subsequent hemorrhages, which might occur before the cavity had closed by the ordinary way.

The above-described cavern must be regarded as a cured pulmonary abscess; but the cure may progress further, till there is perfect cicatrization.

b. This occurs in the following manner: - If the abscess be not too large, it closes by a gradual approximation of its walls, which finally come in contact and coalesce. We then find, in place of the previous cavern, a cellulo-fibrous stripe, in which the bronchi end in blind sacs. This is of most frequent occurrence in the apices of the lungs, where the coexistence of open caverns and the presence of obsolete and cretified tubercles indicate the nature of the processes that is here going on. The obliteration of a cavity of considerable size always occasions a corresponding depression of the surrounding parenchyma, and a cica-trix-like folding and puckering of the pulmonary pleura, which is most frequently and distinctly observed In the case of those cavities which are often superficially situated quite in the apices of the lungs. The thorax is also depressed to an extent corresponding with the size and number of the closing vomicae, and is obvious from the flattening and slight depression so frequently observed in the clavicular region.

This process is undoubtedly favored very essentially by certain circumstances, amongst which we may enumerate the local depression of the thorax, the contraction of its cavity in consequence of the diaphragm being abnormally pressed upwards by the contents of the abdomen, the development of emphysema in the parenchyma surrounding the cavern, and bronchial dilatation. It has been proposed and attempted to produce these conditions artificially, by way of treatment, in various and sometimes violent ways: we have already discussed (in the first volume) the admissibility of these methods of treatment, their modes of action, and the consequences to which they may give rise.

When the healing process is rapid and continuous, the cicatrix sometimes encloses chalky concretions of various sizes, formed by the inspissa-tion of tuberculous pus in the cavity.

(c.) The cavern, instead of cicatrizing in the above-described manner, may be filled up with a roundish or irregularly branched mass of fibrocartilaginous structure, in which the bronchi terminate in blind sacs. This is effected by the conversion of its cellulo-fibrous walls into a fibrocartilaginous callus, which continues to grow thicker. The cicatrix-like puckering of the surrounding parenchyma is generally in this case very inconsiderable.

This fibro-cartilaginous mass may sooner or later be converted into a very compact osseous concretion of corresponding form and size.

2. The Second Metamorphosis

The Second Metamorphosis which pulmonary tubercles undergo under favorable conditions, is their cretefaction. After their softening has began or is perfected, they gradually diminish in volume and become converted into a yellowish-white, or grayish, or blackish-gray, smeary, chalky paste, and finally into a calcareous concretion. This concretion is situated, according to the intensity and extent of the process of reaction which is set up in the neighborhood of the softened tubercle, either in obliterated pulmonary tissue, or in fibro-cellular, or callous, fibro-cartilaginous capsule. Here also cicatrix-like puckerings of the parenchyma occur over the cretified tuberculous masses.

Tuberculous infiltration may also undoubtedly undergo this metamorphosis, for we not unfrequently meet with paste-like masses of chalk, together with cretified tuberculous granulations in the apices of the lungs, and corresponding in size and form to a pulmonary lobule; they are surrounded by a very delicate sero-cellular capsule, formed of condensed interlobular cellular tissue, and most probably are cretified lobular, tuberculous infiltrations.

Pulmonary Tubercle

3. Finally, pulmonary tubercle, when in the form of crude gray granulations, may become obsolete, shrivelled up, and abortive. It is then changed into opaque, bluish-gray nodules, having the resistent power of cartilage, which are incapable of any further metamorphosis. This destruction of the tubercle is either general, or it is combined with the process of cretefaction, the central portion or nucleus being converted into a chalky concretion encysted in the obsolete peripheral layer of tuberculous matter.

From what has been already stated, it follows that pulmonary tuberculosis may be cured by phthisis with the elimination of the tubercle; but the two last-described metamorphoses, opposite as they are to one another, constitute more direct healing processes. Any one of them may take place under favorable conditions, and as a general rule, they are all found in one and the same individual, for we find associated together cellulo-fibrous caverns, their cicatrices, and cretified and obsolete tubercle. They are generally all found imbedded together in obsolete parenchyma, infiltrated with black pigment.

Tuberculosis is either an acute or a chronic disease. In acute cases it attacks both lungs simultaneously, and frequently other parenchymatous organs and membranes, giving rise to peculiar symptoms resembling those of typhus; the tubercle is the product of tuberculous dyscrasia of the blood developed in a very high degree. The tuberculous mass is, in some cases, deposited at once, and in others at different intervals, which rapidly succeed one another, and are indicated by paroxysmal exacerbations: it is formed of gray, crude granulations, which are either very minute, vesicular, and transparent, or in some cases, as large as millet-seeds. The tubercles are always very numerous, discrete, and uniformly scattered through the lung-substance; it is only rarely that we find them accumulated and confluent at individual spots, and in these cases they are all in the same stage, namely, that of crudity. Moreover the lung is in a state of hyperaeemia, oedema, and emphysematous textu-ral relaxation; the hyperemia occasionally passes into pneumonia and hepatization.

In most cases it only attacks the lungs after tuberculous disease has advanced in them to the stages of softening and ulceration (vomica), and after it has existed for a longer or shorter period in its favorite locality, - the apices of the lungs - in the state of more or less circumscribed, insidious tuberculosis. A pre-existing chronic tuberculosis of the lungs is generally the predisposing cause of the acute production of tubercles in those organs. It proves fatal in consequence of the hypersemia and of the subsequent oedema to which it gives rise, in consequence of the violent production of emphysema, or from paralysis of the lungs.