Another feature which distinguishes the process is the occurrence of Caseous necrosis. This consists, as we have seen, in the death of the structures, accompanied by the production of finely granular fat. As this change reduces everything which it affects to a homogeneous granular condition, it greatly obscures the structure and renders the identification of the individual elements very difficult. It occurs in all the structures already described as affected by the inflammation, the plug which fills the bronchus, the bronchial wall, the contents of the alveolus, the alveolar wall, and the tubercles. If the process is not very advanced, then it may be seen that the caseous necrosis begins in the bronchus, as in Fig. 367, the outline of the tube being still visible. In this illustration the change has extended to the alveoli immediately around the bronchus, and their outlines are still obscurely visible in the midst of the general granular appearance. Outside the caseous area the alveoli are filled with catarrhal cells and their walls infiltrated with round cells. The caseous matter is visible to the naked eye as a yellow or white opaque substance which is somewhat brittle, and, like cheese, consists of nitrogenous matter containing finely divided fat.

The dead caseous matter may lie for a long time and do little harm, just as any inert dead animal matter may. It may even undergo a partial absorption, or with this may be combined an infiltration with lime salts, so that ultimately a cretaceous mass remains embedded in the lung. These processes, however, imply that the tuberculosis has ceased to be active and that the caseous matter is inert. It is more usual to have a disintegration of the caseous matter.

Softening- or breaking down of the caseous matter often shows itself to the naked eye in the central parts of the caseating areas. It can often be determined under the microscope that the softening is beginning in the situation of the bronchus, which thus again proclaims itself the centre of the process. In Fig. 367 there are indications of a crumbling of the caseous matter and a partial separation so as to leave cracks or fissures.

Fig. 366. - Tubercle with giant-cell in lung in case of caseous phthisis, x 100.

In this way Cavities are formed, and each cavity implies the death and destruction of a certain portion of lung tissue, usually involving a bronchus and surrounding alveoli. The broken-down caseous material forms a grumous turbid fluid, in which the more resisting elastic tissue of the lung may be found still retaining to some extent the form of the alveoli. This elastic tissue may be frequently recognized in the sputum of such patients by proper methods of search (see Fig. 368). At first the cavity formed is small, but by extension of the process and coalescence of neighbouring softenings, larger cavities result. These cavities are very irregular, and their walls at first ragged and ill defined, as in Fig. 363. The cavity sooner or later opens into a bronchus, and its contents are discharged. When the caseous material is cleared out the wall assumes an inflammatory character and secretes pus more or less abundantly. There may be ultimately a smoothing of the walls of the cavities by the formation of connective tissue, but there is not the regular lining membrane of the bronchiectatic cavity, nor the same relation to the bronchi. In the walls of such cavities, and in the mucous membrane of the bronchi with which they are in communication, tubercular ulcers may sometimes be distinguished.

Fig. 367. - Caseous phthisis; further stage, a, caseous centre, including plug and bronchial wall, rendered indistinguishable by the caseation; b, alveoli scarcely distinguishable; c, alveoli further out, filled with exudation and having walls infiltrated, x 35.

Fig. 368. - Lung tissue from the sputum in phthisis. The sputum was digested in caustic soda according to Fenwick's method, and then subjected to microscopic examination, x 350.

It may be that, as Hamilton suggests, the softening of the caseous matter is by a process akin to that which occurs in the ripening of cheese, in which, according to Duclaux, certain insoluble albuminates become soluble in water.

According to Prudden, mixed infection may have something to do with the formation of cavities or with the acuteness of the disease. He found that in rabbits, whilst the insufflation of the tubercle bacillus produced tubercular lesions, yet that cavities did not result, but that the subsequent insufflation of the streptococcus pyogenes produced cavities. Prudden does not carry the whole of this by inference to the human subject, but suggests the influence of mixed infection, and especially of septic contamination consecutive to tubercular infection.

The whole process is sometimes a more acute one than that indicated above. The original exudation may approach in its characters to pus, and the process of softening may present little beyond a rapid necrosis akin to ordinary necrosis or sloughing. In these cases there is sometimes a Purulent peribronchitis. Suppuration occurs in the bronchial wall and in the surrounding tissue, and, these structures being broken up, the cavity partakes of the nature of an acute abscess. Some of these abscesses may be near the surface, and by rapidly undermining the pleura cause it to slough. By the separation of the sloughs the cavity of the abscess may come to communicate with the pleural cavity and so pneumothorax may result. Sometimes there is even a gangrenous condition developed, and actual sloughing of pieces of lung tissue occurs.

Acute cases such as these bespeak a peculiar virulence of the morbid agent or a peculiar susceptibility of the patient. They usually pass rapidly on to a fatal issue with high fever. In some cases recovery takes place, the pus dries-in or is discharged, and the abscesses become surrounded* by indurated connective tissue.