The appearance of the lung in this stage is somewhat different from that in the first. It retains its red colour, both from the continuance•of the congestion of the capillaries and from the red corpuscles in the exudation, but it is now much firmer and heavier - it does not crepitate under the knife or finger, and it sinks in water - no air being any longer contained in the vesicles. On section from a sound part into a hepatized part, it is observed that the latter remains on a level while the sound part sinks away, so that the diseased part appears enlarged. Even on external examination the affected part of the lung looks bulky. On more close examination, the cut surface has not the homogeneous velvety character of the lung in splenization, but a coarse granular appearance, and this will be more readily seen on tearing the tissue and examining the torn surface with a lens. The granulations thus brought out are undoubtedly the plugs of fibrine with corpuscles which fill the air vesicles. On stroking the cut surface with the blade of the knife casts of the vesicles and infundibula may be obtained (as in Fig. 359). The finer bronchial tubes when laid open are generally found to contain casts of soft fibrine, as if the exudation had overflowed from the alveoli into them. The appearance of a section of such a lung has been compared, from its solid character, granular surface, and colour, to that of the liver, hence the name hepatization applied to this stage.

Fig. 361. - Hepatization of lung. The section is made so as to include part of hepatized lower lobe and unaffected upper lobe, with intervening pleural surfaces. The latter are coated with fibrine from the usual acute pleurisy, x 100.

The solidified lung is a much better conductor of sounds than a lung filled with air; hence, during life, we hear the sounds of the trachea and bronchi much more distinctly than usual it is as if one put the stethoscope over the trachea itself.

The third stage, that of Grey hepatization, develops naturally out of the second. In the earlier periods red corpuscles are exuded largely, but except in cases of a haemorrhagic kind the white very much preponderate, but especially in the later periods. The leucocytes swarming into the alveoli distend them more and more. The additional material in the vesicles also causes pressure to be exercised on the capillaries, which are thereby emptied. In this way we have, instead of the previous hyperemia, an anaemia of the tissue. In accordance with the much less abundance of red blood, and the presence of an additional number of colourless cells, the colour of the tissue is changed. It retains the firm character, and the granular appearance of the previous stage, but the colour is grey. The pigment of the lung intermixed with the white colour of the multitudinous cells gives the appearance which has been aptly described as marbled.

It is not to be supposed, however, that during life the vessels are empty. It is always possible to inject the vessels after death, and during life no doubt the force of the heart is sufficient to keep up the circulation. We are, therefore, scarcely warranted in saying that the grey colour of this stage is anything but a post-mortem appearance.

In the last stage, that of Resolution, the lung returns to its normal condition. The cells and fibrine in the air vesicles undergo fatty degeneration, and the plugs soften. Even in the stage of grey hepatization the leucocytes and fibrine have begun to undergo fatty degeneration, and this process advances in the stage of resolution. The fatty degeneration and disintegration of both cells and fibrine result in the conversion of the exudation into an emulsion which fills the alveoli, and, having a yellow or greyish-brown turbid appearance, resembles pus in its naked-eye appearances.

The lung is still solid, still sinks in water, but its firmness is gone, its surface is pale, yellowish, or greyish red, it has lost the granular appearance, and a greyish, dirty fluid oozes out, which makes the surface so slippery that a small portion is with difficulty lifted or held in the fingers. The tissue is also extremely soft, and readily tears under manipulation. In removing such a lung from the body, unless care is exercised, pressure of the fingers may rupture the tissue, and as the pus or emulsion flows into the cavity it may give rise to the appearance of abscesses in the midst of the lung.

The softened exudation is now in a condition to be disposed of, and this is done partly by expectoration, but chiefly by absorption. The exudation must have been thoroughly softened before it will make its way through the narrow neck of the infundibulum into the bronchus, and the fatty emulsion is for the most part absorbed. It is remarkable how rapidly an extensive exudation in the lung may be disposed of Sometimes, in the course of four or five days from the crisis of a pneumonia, the physical signs will indicate an approach to complete disposal of the exudation and return of air to the alveoli, and this may be almost entirely by absorption, little expectoration occurring in the interval. In some cases, however, expectoration materially aids in the disposal of the exudation.

After the infundibula and vesicles are emptied the blood returns in full force into the capillaries. Instead of the anaemia we have indeed a hyperaemia, for the tissue has been weakened by the inflammation, and is less able to resist the blood-pressure than formerly. It should be remembered in practice that the lungs of a pneumonic patient take some time to recover from the effects of the inflammation, and great exertion during convalescence should be warned against, till the tissue has recovered its tone.

Purulent infiltration is a termination of pneumonia which is rarely met with as compared with resolution. In some cases, instead of the inflammation ceasing, it goes on in its acute form, and leucocytes continue to be exuded. In this case, when the fibrine breaks down, its place is taken by pus, and a true purulent infiltration occurs. The condition somewhat resembles that present while resolution is in progress, the fatty emulsion in that case resembling pus in its naked-eye characters.

The purulent infiltration in some cases results in Abscess, of which there may be several present. There may be rupture of a considerable vessel in the wall of such an abscess and profuse haemorrhage. The abscess may subsequently burst into a bronchus or the pleura, in the latter case producing empyema, and perhaps pneumothorax.

Another unfortunate result which sometimes occurs is Gangrene of the lung. This is mostly met with in the haemorrhagic form and in drunkards, but it may occur where, in addition to pneumonia, there is a bronchiectatic cavity with decomposing contents.

Another rare result is Chronic pneumonia, whose description follows below.

The Pleura always takes part more or less in the inflammation of the lung (see Fig. 361). The pleural surface of the inflamed portion of lung is coated with a white fibrinous exudation, which is sometimes of considerable thickness. There is rarely any considerable serous exudation in the pleura, probably because the lung distended with the solid exudation fills the cavity, and by its pressure prevents the accumulation of fluid. Sometimes the pleural exudation takes on a purulent character, and an empyema may remain after the resolution of the pneumonia. In some cases the inflammation extends to the pericardium, on the surface of which there may be a slight fibrinous exudation.

When resolution occurs the pleurisy will become chronic and the fibrinous exudation will be gradually absorbed. The result will usually be coalescence of the two pleural surfaces, adhesion of the pleura.

Pneumonia is an acute febrile disease, and so produces secondary changes in the organs of the body, generally comparable with those in acute specific fevers. There is commonly, but not always, enlargement of the spleen. The liver is usually enlarged, and shows parenchymatous infiltration. Herpes of the lips is a frequent accompaniment of pneumonia, this condition being probably due to the action of the toxine on the nerve stems concerned.

In some cases of pneumonia the connective tissue of the mediastinum and sub-pleural tissue are the seats of inflammatory oedema, which may extend to the loose tissue between the oesophagus and trachea, up to the retropharyngeal tissue, the soft palate, the tonsils, and even to the nares. Sometimes this inflammation assumes a phlegmonous character. This probably occurs by propagation of the specific microbe in these loose tissues (Weichselbaum).