We have seen that whenever any form of inflammation comes to the. surface of the lung it causes inflammatory changes in the pleura; there is acute pleurisy in acute pneumonia and in caseous phthisis, and chronic pleurisy is a constant accompaniment of all forms of phthisis pul-monalis. On the other hand, the pleura seems to have intimate connections with the peritoneum, as there are lymphatic channels passing through the diaphragm which form communications between the two sacs, and so pleurisy often follows on peritonitis.

These channels are doubtless intricate and narrow, so that the diaphragm acts to a certain extent as a barrier between the two sacs, but it is not sufficient to prevent the passage, for instance, of the tubercular virus from the one to the other. A tubercular peritonitis is nearly always accompanied by a tubercular pleurisy, perhaps limited to the lower parts of the sac. Similarly a septic peritonitis has usually a dependent pleurisy. Tumours of the peritoneum also frequently lead to similar formations in the pleura.

Besides these we may have pleurisy occurring in the course of some acute diseases, such as acute rheumatism, pyaemia, etc. In addition to these there seems to be a more independent pleurisy, produced, as it is said, by cold. Whilst cold applied to the chest may doubtless lead to a pleurisy, yet it is probable that many case of apparent simple pleurisy either owe their origin to tuberculosis of the lung (see ante) or are themselves tubercular in character.

There is often a localized pleurisy occurring in a limited area, just where the pleura is most directly exposed to the effects of cold, namely, in the left lower lateral region. In this position the chest is not covered by any considerable layer of muscles, as the fleshy masses of the latissimus dorsi and pectoralis major passing upwards to the arm leave, as it were, an unprotected space covered by the comparatively thin origins of the serratus magnus and external oblique muscle of the abdomen. This part is also removed from the centre of heat in the heart, and on the left side instead of the liver there is the hollow stomach. On the. right side the liver is a source of heat, and renders the corresponding part on this side less exposed to cold than that on the left, but still more exposed than most other parts of the chest. It is probable that, in these localities especially, cold, acting directly on the chest wall, may cause an inflammation of the pleura by depressing the temperature.

In its Anatomical details acute pleurisy is closely analogous to acute pericarditis. There is hyperemia, soon followed by a thin fibrinous deposit. This fibrinous exudation, forming a soft yellow layer, often attains to a considerable thickness, forming shaggy projections from the pleural surface especially in the region of the lower lobe. Serous fluid is also exuded, sometimes in considerable abundance. The exudation in some cases is haemorrhagic in character.

If the inflammation goes on there is a new-formation of vascular granulation tissue which may come to replace the fibrine. If two such surfaces are in contact, by absorption of the serous fluid or otherwise, coalescence occurs and complete union of the surfaces, the granulation tissue afterwards developing into connective tissue. We have already seen that the fluid accumulated in the pleural sac frequently compresses the lung greatly, producing collapse.

Empyema is a suppurative inflammation of the pleura. It may develop from an ordinary pleurisy or the inflammation may have been suppurative from the outset. In the latter case there has usually been some specially virulent irritant present in the pleura, as where a metastatic abscess in the lung has approached the pleura, or where pleurisy is one of the phenomena of septicaemia. In these cases the disease is generally rapidly fatal, and we may find remains of the fibrinous exudation mixed with abundant pus.

Where the suppuration has come on in the course of a simple pleurisy the disease is often greatly prolonged, and the pleura undergoes great thickening, being converted into a bulky layer of granulation tissue like the wall of an abscess. The granulation tissue may undergo partial transformation into connective tissue with occasional adhesion, and as the lung has been compressed by the exudation we may have drawing together of the chest to an extreme degree, should the pus be discharged or partially absorbed. The pus may dry-in instead of being discharged or absorbed. In that case it is, in course of time, impregnated with lime salts, so that considerable masses of calcareous matter may be found free in the pleura or embedded in adhesions. Very striking results are sometimes brought about in this way. The lung may be in great part surrounded by a cuirasse of flat calcareous plates.