This section is from the book "A Manual Of Pathological Anatomy", by Carl Rokitansky, William Edward Swaine. Also available from Amazon: A Manual of Pathological Anatomy.
There are certain conditions under which hepatization does not pass into a state of purulent solution, but into induration. The red inflammatory product becomes of a grayish-red tint, and finally gray, but instead of becoming dissolved, it becomes compact and indurated. This is what has been termed indurated hepatization, a condition which has sometimes, but incorrectly, been regarded as chronic pneumonia. The lung is compact, but fragile and pale, and has lost some of the increased size which it has attained during the stage of red hepatization; it still, however, retains its granular texture, which even becomes more obvious, in consequence of the granulations becoming more marked owing to their increased density, although they are somewhat smaller.
This condition may exist for a long time, and is always followed by cachexia, and especially by dropsical symptoms, and it often proves fatal; or the induration may be gradually resolved, or merge into obliteration of the air-cells and atrophy of the tissue.
The curative process in indurated hepatization is somewhat analogous to the resolution of the pneumonia in the second stage, for an exhalation of serous fluid takes place from the inner wall of the air-cells and acts as a menstruum, which gradually corrodes and absorbs the indurated granulations. As the granulations become smaller it becomes turbid and flocculent, and when the pulmonary cells are again permeable to air, it gradually assumes a frothy appearance.
In other cases the air-cells contract over the granulations, coalesce with them round their circumference, and become obliterated, their tissue being changed into a cellulo-fibrous structure, in which from the similarity of their organizations, the granulations are most probably also merged. Unless a serous effusion occupy the empty space, this termination causes a depression of the thorax, or bronchial dilatation, or both simultaneously; and it appears to be on the whole less frequently the result of the croupous pneumonia which has already been described than of an insidious inflammation of the interstitial tissue, - interstitial pneumonia.
The above is a sketch of croupous pneumonia in general, when it occurs as a primary disease; but it also very frequently occurs as a secondary process. It most commonly runs an acute course, usually passing through its different stages in from two to three weeks, and in extremely rapid cases even in three or four days; these are, however, of rare occurrence. Sometimes, on the other hand, it runs a chronic course, being either nearly uniformly prolonged in all its stages, or one or other of them being especially protracted. It presents, however, no special relations essentially different from the sketch we have already given; for, like the acute form, it usually ends in purulent infiltration, and rarely in abscess or induration; and it is totally different from the affection which we commonly find described in pathological treatises as chronic inflammation of the lungs, and with which we shall become acquainted when treating of inflammation of the interstitial tissue.
We observe variations in regard to the original extension of pneumonia, which are of importance chiefly in consequence of their connection with the inner nature of the disease.
Pneumonia, according to its variety, attacks, as we have already described, the whole of one of the larger divisions of the lung, that is to say, a whole lobe, or a great part of one, and it is then termed lobar. It often attacks a whole lobe, and extends to the adjacent ones, and does not prove fatal till at length the remaining healthy lobes begin to be affected. It usually appears in this form as a primary affection; its most common seat is in the lower lobes, and the right lung is more frequently attacked than the left; both these rules present, however, many exceptions.
Or it attacks only smaller portions of the lungs, a number of individual lobules or single aggregations of lobules, between which we find the parenchyma in a comparatively normal state. It is then termed lobular pneumonia; it must be distinguished from the lobular hepatizations which are produced by irregularity in the progress of a lobar pneumonia in the individual lobules, while the rest of the parenchyma remains in a state of inflammatory engorgement.
Or, finally, the seat of pneumonia is confined to single air-cells; we then have what is termed vesicular pneumonia. The disease passes through the stages of inflammatory engorgement, of hepatization, and of purulent infiltration in a single air-cell, or it causes induration, and, finally, obliteration of it. The indurated hepatization of single air-cells is undoubtedly the same condition that has been described by writers on pathological anatomy, as Bayles pulmonary granulations, and regarding whose nature there has been much unnecessary dispute. It is undoubtedly the result of inflammation, and so far Andral is correct in his view; but inasmuch as the inflammatory product, under certain conditions, assumes the character of tuberculous matter, it may also be regarded as partaking of the nature of tubercle (Laennec and Louis). It represents, as we shall presently show, the tuberculous infiltration of single air-cells.
 
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