Pneumonia passes from the stage of red hepatization through several scarcely distinct transition-stages till it finally attains the true third stage. These transition-stages are characterized by alterations of consistence and especially of color. The red, hepatized lung gradually becomes paler, assumes a brownish-red, then a grayish-red or gray, and finally a yellowish color, and thus presents the condition to which the term gray hepatization has been appropriately given. We can recognize this coloration externally, but far better on examining a cut surface; and we can perceive that in many cases, the tint is not monotonous, but that the black pulmonary tissue is more or less uniformly sprinkled over the grayish-red, gray, or yellowish-gray ground, which is also marked by the white projecting cut vessels, so that the whole presents a granitelike appearance.

The granular texture is still present, and even becomes decidedly more distinct at the commencement of the third stage, especially when the progress of the disease has been rapid and tumultuous; the consistence diminishes and the decoloration increases the nearer the disease approaches to the third stage; although the lung feels tolerably firm, it remains pitted after pressure, and is yielding and easily torn, and a grayish-red, very turbid, flocculent, viscid fluid exudes from its cut or torn surface.

If we examine the granulations in these transition-stages, we perceive that they have become more marked, larger, and more independent of the surrounding structures; and that they can be more easily separated and removed, as they only adhere loosely by a glutinous substance to the walls of the cells.

Third Stage, Purulent Infiltration

At its commencement the change of color of the hepatized tissue to a yellow tint (to which we have already adverted) becomes more or less uniform, the granular texture very rapidly disappears, and is succeeded by a purulent infiltration of the parenchyma. The lung then becomes heavy; any pressure on it forms and leaves a distinct pit; the cut surface is yellow or straw-colored, with interspersed spots of black pulmonary tissue, and effuses a large quantity of a very viscid, purulent fluid of the same color as the surface, and of a sickly odor; the parenchyma is extremely yielding, gives way on the slightest pressure, so that if not carefully handled, cavities are easily formed in it, which are the more likely to be taken for abscesses, as they actually are very similar to fresh accumulations of pus. The granular texture has now altogether disappeared, and, on removing the pus from a piece of lung by careful pressure and washing, we perceive that its substance has again assumed its spongy, cellular tissue.

The bronchi present several changes, especially in their final ramifications; in the first stage their mucous membrane is reddened and swollen, subsequently however it becomes paler; and they almost always contain first a reddish, and afterwards a whitish, purulent, fluid exudation. The vessels are frequently clogged by exudations of this nature.

These are the three stages through which well-marked cases of acute pneumonia run; the last is the ordinary and natural mode of termination, and is frequently although by no means necessarily fatal, for, partly by expectoration and partly by resorption of the pus, the lung may return to its normal condition. There is no other and earlier stage than that which we have described as the stage of stasis, for the condition described as such by Stokes is in no respect inflammatory. The bright-red color of the lungs or of portions of them, which Stokes regards as the earliest stage of inflammation, and attributes to arterial injection, is; -

(a.) Always dependent on anaemia, which is frequently very highly developed.

(b.) The lungs, or the affected parts of them, are puffed up, but are devoid of turgor and resistance in consequence of their capillary vessels not being duly filled; they collapse readily, and not a trace of a swelling of the tissue remains.

(c.) This condition always occurs when, in consequence of paralysis of the heart or of excessive thickness of the blood, the capillaries of the lungs can no longer be injected, and the little blood occurring in them is repeatedly exposed to the chemical influence of the atmospheric oxygen by the inspirations during the death-struggle. In this way we observe this condition either distributed over large portions of the lungs, or confined to small spots of lungs otherwise healthy, or associated with hyperemia and stasis in many cases of asphyxia in new-born children and adults, in consequence of rapidly exhausting diarrhoeas, of Asiatic cholera, after extensive burns of the general integument, etc.

Before entering into any further discussions, it will be most expedient that we should add to the above sketch the conclusions regarding the seat and nature of the pneumonic process, at which we arrive from an accurate anatomical investigation after death, and a review of the physical phenomena during life. These conclusions will not only find an influential application in what is to follow, but will also receive corroboration from it.

In relation to the first point, we have already stated, in our remarks on the formation of the granular texture of the hepatized lung, that the granulations are formed by the inflammatory product deposited in the cavity of the air-cells. Their formation, or, in other words, the exudation, is preceded by the secretion of a viscid, tough, reddish-brown fluid in the cavities of the cells, which gives rise to the crepitation well known to auscultators: as the stage of hepatization advances this fluid disappears, and the air-cells become filled with plastic exudation. The granulations are roundish, and at first of a dark-red color, hardish, and fragile; they appear to have uniformly coalesced with the swollen, dark-red walls of the cells, from which it is difficult to isolate and extract them. The inflammatory turgor and the redness of the tissue become then moderated; the granulations become paler, of a grayish-red, and finally a grayish-yellow tint, while they appear less dense in structure, and become somewhat swollen. The secretion of a glutinous mucus is established around their circumference, which loosens their connection with the cell-wall, thus rendering themselves and the swelling more obvious: they appear surrounded by a light reddish cell-wall, and their distinctness is proportional to its paleness. Finally, they break down into a purulent fluid, mixed with this glutinous, mucous secretion. Hence the seat of the pneumonic process is on the walls of the air-cells - that is to say, on the pulmonary mucous membrane, and its product is deposited in the cavities of the air-cells; from this period - that is to say, from the stage of red hepatization - the process consists in a metamorphosis tending to the fusion and breaking down of the exudation, under the influence of an inflammatory process, which is now declining in intensity. These conclusions are further strengthened by the following considerations: