Pulmonary Tubercles originally appear either (1) as the well-known gray, semi-transparent granulations of the size of a millet or hemp-seed, or in many cases of acute tuberculosis as still smaller-sized granules, which are clear, transparent and vesicular; or (2) in high degrees of tuberculous disease, especially when it is running an acute course, they are separated from the blood as yellow tubercle. On a cursory examination they appear almost or quite round: on closer investigation, however, we find that their outlines are not sharply defined, but that delicate prolongations extend from their surface into the surrounding tissue, which according to their size, may enclose one, two or more air-cells. These cells are most commonly obliterated, but not unfrequently appear dilated.

In examining the lungs we not unfrequently meet with extensive, roundish, or irregularly ramifying or lobulated tuberculous masses, which are produced either by the confluence of several tubercles which were originally in the same group, or by the subsequent deposition of tubercles in the same immediate neighborhood. The tissue at these points is completely wasted away, so that nothing but the pigment remains, and the air-cells and extremities of the bronchial tubes are obliterated. These tuberculous masses must be distinguished as carefully as possible from tuberculous infiltration. The whole of the upper lobes are not unfrequently so thickly strewed with tubercles as to present the appearance of having degenerated into a tough, resistent, uniform tuberculous mass.

In the ordinary course of the disease the principal seat of the tubercles is in the upper third or apices of the superior lobes; it is here that they are deposited first and in the greatest quantity, and that they first begin to undergo their ordinary changes. The apices of the lungs must therefore be regarded as the usual starting point of tuberculosis, which gradually extends from thence to the lower portions of the lungs. Exceptions to this rule are, however, not unfrequent; we sometimes meet with tubercles in the apices and others far away from them, even in the lower lobes, or they may even occur in the latter portion while the upper parts are perfectly free from them. In this respect there is a contrast between pulmonary tuberculosis and pneumonia, at all events in a great majority of cases, for pneumonia most commonly commences in and starts from the lower lobes, while tuberculosis has its origin in the upper lobes, and even in their highest parts.

Many attempts have been made to account for the preference which tubercles exhibit for the upper parts of the lungs, but none of them satisfactorily explain it; they are based either on mere hypothesis, or the cause and the effect have been confounded. We confess our ignorance on this point, and can no more explain it than we can account for the preference shown by certain exanthematous and impetigenous affections for particular regions of the general integument.

Pulmonary tubercles pass through the different metamorphoses which are described in the first volume.

1. They very frequently soften, and this change gives rise to tuberculous suppuration of the lungs, tuberculous ulcers, tuberculous abscess (vomica pulmonis tuberculosa, caverna tuberculosa), and tuberculous phthisis. The separate, gray tuberculous granulations begin to soften in their centres, which become turbid, opaque, yellowish and cheesy, and finally undergo purulent solution. The groups of tubercles break down at several points simultaneously, corresponding to the different separate tubercles of which they are composed. Hence, in the first case, we have a small primary tuberculous ulcer; and in the second case, after the final solution of the whole mass, a much larger one, whose further progress we shall consider in the following remarks.

It is especially important to understand the manner in which the primary tuberculous ulcers enlarge, and give rise to such peculiar and extensive destruction of the lungs. This is elucidated by the process which goes on in the tissue surrounding the softened tubercle. The breaking down of tubercles is always followed by a secondary deposition of tubercle in the surrounding parenchyma, the extent of this secondary deposition being proportional to the intensity of the general disease. Moreover these secondary tubercles and the tissue in which they are deposited likewise break down with a rapidity which stands in a direct ratio to the intensity of the dyscrasia, and in this way the tuberculous ulcer becomes enlarged. If this process goes on in so tumultuous a manner as to exhaust the powers of reaction and the supply of organic matter, the ulcer usually extends unequally in various directions, and forms an irregular, sinuous, and apparently lacerated cavern whose walls consist of lung substance plugged up with softened tubercle, and whose internal surface presents, as it were, a gnawed appearance, without a trace of any inner lining except a coating of adherent tuberculous pus. The small quantity of parenchyma occurring between the tubercles is in a state of compression and dirty brown discoloration (carnification), while that in the surrounding neighborhood exhibits no trace of reaction, except a certain degree of hyperemia. If this, as is usually the case, takes place simultaneously at several spots, two or more caverns will come in contact and will finally unite, and we then have either a number of caverns communicating with one another by means of sinuses of varying width, and either straight or tortuous in their course, or else the whole represents a large abscess with sinuosities in various directions. This cavity is intersected in various directions by bridges or rafters of rotten tuberculous lung-substance, which is likewise dependent in the form of shreds from its roof and walls.

This form of phthisis corresponds to the acute form of tuberculous intestinal ulceration, which runs its course without any reaction.

In other more common and less rapid cases, an inflammatory process, which must certainly be regarded as having a curative tendency, is established in the parenchyma around the softening tubercle or the primary tuberculous ulcer, and in the interstitial tissue amongst the secondary deposit. It gives rise to an albuminous grayish-white or somewhat reddish, tenacious and viscid product, which occasions the closure and finally the atrophy of the air-cells, and is identical with Laennec's infiltration tuberculeuse gelatiniforme. (See pp. 78, 79.) During this process the inner surface of the cavern becomes smoother and more uniform, and very often becomes covered with a thin grayish or grayish-yellow, thin, adhering investment of an apparently loose texture. This coating may sometimes, according to Andral, consist merely of the more solid portion of the pus contained in the cavity; in most instances this is, however, certainly not the case, but, as Laennec was the first to observe, there is a true exudation from the walls of the cavern like that which exposed or wounded animal tissues deposit on the surfaces of wounds or ulcers. This exudation is, doubtless, repeatedly thrown off, for if the process of tuberculous softening go on, neither it nor the adjacent wall of the cavern can meet with the conditions necessary for organization; it melts or becomes disintegrated, and mixes with the pus in the cavern, and another membrane is formed in its place, so long as the tuberculous process on the one hand, and the reactive inflammatory process on the other, continue in the tissue in a certain antagonistic degree and proportion. The caverns enlarge, in the manner we have already described, by the softening and breaking down of the secondary tuberculous deposit in the tissue of their walls, and by the confluence of several neighboring caverns into one. The parenchymatous bridges which traverse them are in a state of gelatinous infiltration, and contain tubercles, while externally they are coated by the above-named exudation.

In consequence of this process the lung-substance in the walls of the caverns becomes atrophied and converted into a more or less pigmentary, bluish-gray or blackish-blue, dense and tough layer of various thickness, the portion next to and lining the inner surface of the cavern being chiefly a whitish cellular tissue. To this the above-described exudation adheres, and through both these shine the bluish atrophied parenchyma and the vessels which are laid bare and obliterated by the cavern, and which appear as yellowish-white ramifying streaks; scattered crude or yellowish softened tubercles may also be observed. These tubercles gradually soften, and lead, on the one hand, to a gradual enlargement of the cavern, while, on the other hand, they impede any comprehensive process of consolidation, since they perforate the cellular investment of the cavity. The internal surface of the whole cavern is even and tolerably smooth, except at the spots where there are these new tuberculous excavations.

The pulmonary vomica in this condition is analogous to the tuberculous ulcer of the intestine with gelatino-lardaceous thickening of the submucous tissue on which it is situated.

The caverns naturally present the most manifold differences in reference to their size and number. The cases are not rare in which an abscess attains the size of a duck's egg, or of the fist, or even involves a whole lobe. When it is very large, the probability is that it has been formed by the confluence of several smaller caverns. The largest abscesses occur, with few exceptions, in the upper lobes, where, as we have already remarked, and especially in their upper third and at their apices, tuberculous deposits usually first occur, and where they first begin to soften.

It is a question of especial interest to ascertain how far the individual structures entering into the composition of the lung are involved in this destructive process, and above all, how the bronchi and blood-vessels within the tuberculous abscess are affected, what mode and form of destruction they undergo, and what destructive consequences follow when the cavern, in making its way outwards, finally reaches the pulmonary pleura.