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.
In very imperfect monsters, as for instance, in cases of acephalia, the lungs as well as the central organs of circulation, are altogether absent. In lower degrees of monstrosity, and even in cases in which, in other respects, the organization is normal, there may occur a considerable deficiency of one or both lungs, that is to say, an arrest of development. The development may be arrested at so early a stage, that we can barely observe them as roundish little bodies seated on the bronchi. It generally happens that this condition is a consequence of the contraction of the volume of the thorax, or of pressure exerted on the lungs either hy the displacement of the abdominal viscera into the thorax, in cases of absence of the diaphragm, or by the accumulation of fluid in the thorax.
An excessive formation occurs in double monsters, as more or less duplication of the lungs, either with or without a simultaneous duplication of the pleural sacs. The occurrence, of an extraordinary number of lobes is apparently due to an excess of development.
Hypertrophy and Atrophy.
The manifest differences in the size of the lungs are, for the most part, dependent on the number and the capacity of the air-cells. As an individual structure, the lung will attain a large size when there is a large number of air-cells, and at the same time their volume is well developed; while under opposite circumstances, the lung will appear small.
The former usually occurs in the male sex, and is generally associated with well-developed muscular and osseous systems, and with a low state of development of the abdominal viscera, whilst the latter is most common in the female sex, and is associated with a weak state of the muscular fibre, fragility of the bones, and a preponderating development of the abdominal viscera.
The lungs may appear large either within the normal limits or beyond them, when a certain number of the air-cells are dilated; and under opposite conditions they may appear small or abnormally diminished; indeed, the former may occur when the number of dilated cells is comparatively small, and the latter when the number is comparatively great. In the former condition the pulmonary tissue is rarefied, in the latter it is compressed and dense.
Hence in forming an opinion of the size of the pulmonary organs in any individual case, the density of the parenchyma should be especially noted, since it alone determines the respiratory capacity of the lungs; and the two extremes, excessive rarefaction and excessive condensation, constitute very important morbid conditions, of which we shall speak in our observations on changes of tissue.
Hypertrophy of the lungs undoubtedly arises from a remarkable combination of dilatation of the air-cells, with a simultaneous augmentation of their tissues; we sometimes observe it as a vicarious development of one lung, when the other, for any reason, is no longer able to discharge its proper function. It is incontestable that this hypertrophy does not consist in an increase in the number of the air-cells, but in their dilatation, in the increased thickness of their walls, in the enlarged calibre of the capillaries, and in the development of new vessels. The pulmonary tissue is thus rendered denser and more resistant, and the lung exhibits a singular power of resisting external atmospheric pressure; it has become larger, and its thoracic cavity wider.
Atrophy of the lungs is the exact reverse of this condition. It is most marked in advanced age, when it is known as atrophia senilis; sometimes, however, it occurs in the earlier periods of life, constituting a premature involution of the respiratory organs, and it is only in these latter cases that it strictly falls within the domain of pathological inquiry. It consists in a dilatation of the air-cells (emphysema), and an alteration from their angular or polygonal into a round or elliptic form. The dilatation is the consequence of the emaciation and attenuation of their walls, the vessels of which become obliterated. The atrophy of the cell-walls may proceed to such an extent that several cells may coalesce; the interlobular areolar structure has then disappeared, and hence the lobular structure no longer exists; the pulmonary tissue then represents an irregular, perforated network; the lung itself is of a pale, light-gray color, generally dotted with numerous specks of black matter, conveys a soft downy sensation to the hand, is light and small, and collapses on the opening of the thorax; on cutting into it the air escapes tardily, with a dull and diffused sound. Its tissue is dry and bloodless.
Thus marasmus of the pulmonary organs is, for the most part, associated with an equally well-marked atrophy and dilatation of the trachea, emaciation of its walls and deficient moisture of its mucous membrane, the nature of the changes being in both organs the same. Moreover, as a general rule, it is most highly developed in the superficial portion of the upper lobes, giving rise to a singular displacement of the interlobular fissure, and causing it gradually to assume a vertical position (Hourmann).
The thorax becomes depressed over the atrophied lungs, exhibits distinct lateral flattening, and assumes a conical form; there is an arched curvature of the vertebral column in a backward direction; the sternum is thrust forward, and there is a diminution in the vertical diameter in consequence of the curvature of the spine, and the absorption of the intervertebral cartilages, and partially even of the vertebrae themselves. The soft parts about the thorax disappear; the muscles become emaciated and pale; the diaphragm thin, lax, and plicated; and the heart small.
On these changes are based the difficult respiration, and, in a great measure, the collapse, pallor, and lividity of the tissues, - in short, the general atrophy of old age. The impaired state of the respiratory muscles renders the act of inspiration difficult and imperfect; the deficient contractility of the pulmonary tissue, together with the above-named muscular weakness, opposes similar obstacles to the act of expiration; while the surface of the lungs presents to the atmospheric air so obliterated a capillary network, that only a small quantity of blood can be submitted to the vivifying process of arterialization.
If this change occur at an earlier period of life, and an abnormal relation be then established between the degree of involution of the lungs and that of the other organs concerned in haematosis, the disease will assume much more importance if active dilatation of the right side of the heart should supervene.
A remarkable enlargement of the lungs takes place in emphysema; a less marked and usually only partial enlargement also occurs in hepatization, in highly advanced tuberculosis, in cancer of the lungs, etc.
Diminution of the lungs is chiefly induced by contraction of the thorax, the pressure of gases or liquids that have accumulated in the thoracic cavity (pneumothorax, hydrothorax, empyema, &c), and by obliteration of the bronchi.
Congenital anomalies in the form of the lungs are, for the most part, confined to some irregularity in regard to the lobes, which present a position of lateral inversion.
Amongst the acquired deviations, we must notice the displacement of the interlobular fissure in atrophia senilis, the pit-like depression of the surface in obsolescence of a portion of a lung, or in cases of cicatrization after loss of tissue, the flattening of a whole lung, or of a circumscribed portion, and the impression produced by the accumulation of gas in the thorax, by circumscribed exudations, aneurisms, or adventitious products.
Again, when the lung has been for a long time surrounded by a pleuritic effusion, and has acquired a thin, although resistant, fibro-serous investment which hinders its perfect re-expansion, it sometimes undergoes a singular change of form. It loses its sharp borders and the concavity of its base, and reminds us of the corresponding alteration of form presented by the liver after inflammation of its peritoneal coat. It sometimes, but not very frequently, happens that, if the pseudo-membranous investment be thinner at some spots than at others, the pulmonary parenchyma bulges out at those places into teat-like processes connected by a pedicle to the base.
Deviations in position, when congenital, are seen in the protrusion of the lungs through a wide fissure in the thorax, and in their lateral displacement. Under the acquired deviations we must notice the protrusion of the lungs in penetrating wounds of the chest, their displacement in various directions from dilatation of the abdomen and enlargement of its viscera, from copious effusion in the pericardium, from enlarged heart, from aneurism of the aorta, or adventitious structures in the mediastina, and generally from any kind of accumulation within the thorax. If there be no pre-existing adhesions in the last-named case to oppose the displacement, the lung, as has been already remarked, is constantly pressed inwards and upwards towards the mediastinum and vertebral column. A similar change in position occurs when obsolescence takes place from internal conditions, since the lung is then retracted on the bronchus.
We shall commence with a description of two very simple alterations of tissue, which, although not very striking in themselves, lead to very important consequences, which, singularly enough, resemble each other; these are rarefaction (vesicular emphysema) and condensation of the pulmonary tissue.
 
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