Under proper treatment, and in the absence of other complica tions, the fluid is generally absorbed. As it diminishes in quantity, the region of cardiac dulness also decreases. The two layers of the still roughened pericardium once more come into contact, and fric tion may be again heard for a clay or two. Here, as in the case in which recovery takes place at the end of the second stage, the friction gradually disappears, and ultimately everything seems to return to its natural state, recovery being apparently perfect. It is doubtful, however, if the pericardium ever quite regains its natural condition. It may possibly do so in some cases ; but in most instances more or less extensive adhesions are formed between its two layers. Where the inflammation has been severe, such adhesions are formed over the whole surface of the heart, and the sac of the pericardium is ob literated.
Such obliteration has been regarded by some as a source of much embarrassment to the heart's action, and a cause of hypertrophy and dilatation of that organ. By others it has been said to produce some degree of atrophy of the heart; while a third set of observers main tain that an adherent pericardium gives rise to no symptoms during life, and to no morbid change in the muscular substance of the heart.
It is probable that the age and mode of life of the patient have much to do with the variety of the results noted by different observ ers. In young and excitable persons, and in those whose habits or tastes lead them to take much exercise, obliteration of the pericardial sac will cause inconvenience. The function of the pericardium is to provide for the free and active movements of special occasions and unusual efforts. If such occasions do not arise, and such efforts are not made, the obliteration of its sac causes no embarrassment, and no change in the heart. The ordinary work of that organ can be quite well done without the pericardium; and so long as this work is not unduly increased, and extraordinary efforts are not required, no harm results from the obliteration of its sac. It is for the free movements of special occasions that it is required.
There is one fact in the history of rheumatic pericarditis which has a most important bearing on the pathogenesis of the disease. This fact is that the disease almost always commences iu the visceral layer of the pericardium and at the base of the heart.
The evidence of this is as follows : 1. In slight and circumscribed attacks, the inflammatory change is, as a rule, confined to this portion. Affecting only the visceral layer, and only a small part of it, there may be no physical signs or symptoms by which its existence may be diagnosed. But we know that such slight attacks do occur: for in the post-mortem room it is not uncommon to find some thickening and opacity, the result of in flammation of this part of the pericardium, without any other evi dence of the disease having existed.
2. In cases in which the disease spreads over the body of the heart, and affects both layers of the pericardium, the friction sound is generally heard first near the base.
3. In cases in which death takes place in the early stage of the disease, it is found that while that part of the membrane which is situate over the body and apex of the heart is merely hyperzemic is still in the first stage of inflammation—that which surrounds the origin of the great vessels at the base has reached the second stage, and is covered with shreds of lymph. "In ordinary acute pericar ditis the earliest stage is seen as a minute injection of its vessels, causing a blush of redness, which close observation resolves into a beautiful red network. This injection is almost a, certain proof of pericarditis, but when you see it you should look at the base of the heart about the great vessels, where you will always find some shreds of inflammatory lymph" (Milks and Moxon).
Is there any possible explanation of these facts—any reason why the rheumatic poison should act primarily and chiefly on this part of the pericardium? There is no structural peculiarity to account for it. It cannot be clue to greater functional activity; for movement is freer at the apex than at the base. The only peculiarity of that por tion of the pericardium which seems specially liable to rheumatic in flammation, is that it is situate over and in near contact with the fibrous textures of the heart—in near contact, that is, with that particu lar portion of the cardiac structures which is specially liable to suffer from the action of the rheumatic poison. The inference is inevitable that inflammation of the pericardium may, sometimes at least, be due not to the direct action of the rheumatic poison on that membrane, but to the extension to it of an inflammatory process originating in the subjacent fibrous textures. We have already seen that inflamma tion of the inner lining membrane of the heart is limited to that part of it which is in direct relation with the fibrous rings and valves, and is secondary to inflammatory change in these structures. There is not a little evidence to show that in many cases inflammation of its outer investing membrane has primarily a like limitation and a sim ilar pathology.
When considering the pathogenesis of the joint troubles of acute rheumatism we saw good reason to think that inflammation of the synovial membrane was secondary to inflammation of the ligaments and tendons. There is equally good reason to believe that inflamma tion may in like manner extend to the pericardium from the fibrous textures of the heart; and that to such extension rather than to the direct action of the rheumatic poison on that membrane many cases of pericarditis are clue.