Pathology.
—In regard to the pathology of these conditions it does not vary from that mentioned in the earlier portion of this work in connection with the general subject of Surgical Tuberculosis. The deposit of tubercle in the tissue whose resistance has been weakened is followed by the formation of granulation tissue, which, so long as the germs survive, tends to increase and to make room for itself at the expense of surrounding tissue. At the same time there occurs a tissue struggle by which the attempt is made to throw around an active focus a protecting barrier, which in soft tissues consists of condensed fibrous and connective tissue, and, in bone, of a sclerotic capsule, as though the intent were to imprison the disturbing cause, and, by completely enclosing it, effect protection. When this attempt at encapsulation is successful spontaneous recovery follows. It will be made successful, to some extent at least, by treatment whose most important local feature is physiological rest. On the other hand, when the attempt is unsuccessful and the barrier is transgressed by granulation tissue, the lesion will advance in the direction of least resistance, while its progress will be made known, especially as it approaches the surface, by very significant signs: adhesion of the overlying structures and finally of the skin, with purplish discoloration of the latter. Finally softening occurs with escape of granulation tissue, which, so soon as it is freed from pressure, will grow more luxuriantly and with more color, constituting the fungous granulation tissue, to which German pathologists so often allude, or so-called “proud flesh.” When this appears upon the surface it is soon infected with pyogenic organisms, breaks down, and an abscess cavity results, connecting with the original focus and its extensions. This may be so placed as to lie outside the joint capsule, which, in some respects, is fortunate for the patient. The joint function may then be compromised to only a minor degree.
Fig. 202
Central sequestrum. (Ransohoff.)
Often the direction of least resistance is toward the joint cavity, this fungous tissue loosening and perforating cartilage or periosteum before it enters the joint. Having penetrated it again it grows extensively until the cavity is distended, its rapidity of growth diminishing with the degree of pressure produced by its surroundings. This pressure will also make it less vascular, and when such a joint is opened it at first appears pale and anemic. In proportion as the joint distends it loses in motility, while should recovery occur spontaneously or as the result of treatment this tissue will to some extent disappear, to be replaced by adhesions by which pseudo-ankylosis is produced. The extent of the intra-articular involvement will cause obstruction to the deeper return circulation, and thus is brought about the prominence with which the subcutaneous veins appear. The degree of hydrarthrosis is apparently not limited except by the distensibility of the joint. In the articular or arthropathic forms there is always more or less synovial outpour.
Fig. 203
Tuberculous panarthritis. (Ransohoff.)
To the condition already described may be added the destruction produced by suppuration, infection occurring either through the circulation, as is quite possible, or through some trifling surface abrasion. In more chronic cases caseation may occur, especially in bone foci. Finally, as the result of a combination of morbid processes, there is produced more or less complete disorganization, all of which is summed up in the term tuberculous panarthritis. To that condition in which the articular surfaces are more or less studded with fungous patches the term pannus of the joint is often applied. To reiterate, then, as between a chronic hydrarthrosis and a destructive panarthritis, perhaps even with necrosis of epiphyses, it is but a difference of degree and of combination of infectious processes ([Figs. 203], [204], [205] and [206]).