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an irritating nature, as in the occupation of stone-masons, coal-miners, dry-grinders, feather-cleaners, and millers. The cold in the one case, and the dust in the others, excites bronchial inflammation, which, on continued operation of its cause, gets deeper and deeper, affecting first the bronchial membrane, then the connective tissues underneath, and eventually the pulmonary texture of individual bronchial bunches. As the inflammation penetrates deeper, the hyperplasm which it produces is less readily thrown off. The sarcophytes thrown out by inflamed mucous membrane pass off in form of mucous and pus-cells and epithelium; but those in the deeper tissues are retained in a concrete form, and by accumulation constitute the consolidations of the pulmonary texture. This latter result is favoured by any constitutional cause lowering the vitality of the sarcophytes, such as scrofula, syphilis, irregular living, and other influences which degrade the standard of nutrition.
The different forms and varieties of red and light or grey induration of the lung—texture thus induced, correspond with the carnification and grey tubercular infiltration, chronic hepatisation, red and grey, of Laennec and Andral, and with the albuminous pneumonic solidification of Dr. T. Addison; the iron-grey induration of the last author being a more chronic form of the same lesion. In those varieties resulting from the inhalation of dust, the presence of particles of the dust may add another anatomical character; and in the case of coaldust, the very striking one of completely blackening the consolidations. Without dwelling further on their details we go on to notice the ulterior results to which they tend, as mentioned in the table (p. 60)—a withering and cornefaction, and decay by caseation and softening.
It has been before mentioned that red consolidation iu time becomes pale from the multiplication of its constituent cells superseding the blood-vessels and their coloured contents; and subsequently grey by accumulation of black pulmonary matter; and if the consolidation endures in its low vitality, without going into caseation and decay, it undergoes more or less of a withering or dwindling process, somewhat like the contraction and hardening of the fibroid or scar-tissue; but being much more corpuscular than fibrous there is less shrinking and more drying up of the material, so that it becomes more leathery or horny in substance, and of darker hue, from the increase and approximation of the black pigmental matter of the lungs. The grey consolidation thus withers and darkens with age, and passes into a state of obsolescence not liable to further change. This result, to a large extent, is not very common, and occurs chiefly in old subjects, and renders them less liable to more destructive and consuming changes; the disease is therefore at this age more generally chronic. But limited specimens of this grey withering of old consolidations, without any scar or remnant of yellow tubercle, are not uncommonly found at or near the summits of the lungs in persons who die of other diseases, and may be considered evidence of phthinoplastic deposits arrested in their earlier stage.
But the more common tendency of the chronic consolidations of the lung tissues is to caseation and softening, which we now identify with fatty degeneration and disintegration, and which was mysteriously characterised by Laennec as a new stage or change from the infiltrated grey tubercle to the yellow crude and softened tubercle. That the diffused grey induration of the lung is of inflammatory origin was generally concluded, in opposition to Laennee's views, by many of his contemporaries, and this view was adopted and extended by Dr. T. Addison, who very ably traced the inflammatory origin of several varieties of solidification of the lung, distinct from tubercle, and yet
leading to the same consumptive decay.1 He described these consolidations, produced by inflammation, as persisting for a time, and then either becoming more indurated, or being hollowed into cavities resembling those of tuberculous phthisis, yet sometimes quite distinct from them; in other cases combined with them and affecting their course. He specifies the three kinds of inflammatory consolidation: the uniform albuminous, the granular, and the iron-grey induration. The albuminous and the iron-grey correspond with the pale and grey indurations which I have been in the habit of designating cacoplastic, and form the varieties of chronic induration which have just been described. The granular induration is that state of lung tissue corresponding with granular hepatisation, more aplastic, and tending to break down soon, and to form cavities. It appears to me that the albuminous and grey indurations are only different phases of the same change at different periods and in different subjects; the albuminous pale consolidation affecting younger subjects and at an earlier stage; and the grey being the result of longer duration and at an older age.
But all these consolidations are produced by sarcophytes multiplying and becoming concrete in the lung tissue, with more or less tendency to disintegration and decay in the way of fatty degeneration and softening. The least tendency to this change is in the more uniform hyaloid and fibroid indurations, which have been recently noticed in their converse disposition to chronic contraction and withering. The greatest disposition to the destructive change is manifested in opaque consolidations, commonly more or less granular on section; and under the microscope showing a great crowd of corpuscles or
1 Collection of the Writings of Dr. T. Addison, New Sydenham Soc., 1868.
granular cells, in which fat globules already show themselves in considerable numbers, portending the organic instability of the material and its proclivity to break up and decay. If with this we contrast the character of euplastic matter, as manifest in the sarcophytes or bioplasts of a healing process or of a healthy inflammation—all transparent, gelatinous, teeming with vital properties of motion and formative and nutrient power,—we can form some conception of the different tendencies of the two products—the one bringing new life and living material to a work of reparation, the other clogging the tissues with opaque, sluggish, inorganisable corpuscles, either lifeless or of the weakest vitality, and doomed to speedy dissolution and decay. Let us bear in mind also how these cacoplastic products of inflammation injure the nutrient power of the textures in which they are crowded. Compressing the blood-vessels, they deprive the nuclei or bioplasts of the tissue cells of their pabulum from the blood, these consequently starve and waste, and soon partake of the decay of the encroaching material; and all break down together into a caseous mass, which softens and makes its way into the bronchi for expulsion.
VARIETIES OF CONSUMPTIVE DISEASE. INFLAMMATORY PHTHINOPLASMS—continued.
Caseous Hepatization—Sarcophytes lifeless—Scrofulous Pneumonia—Soon softening and excavated, or drying and calcifying — Infecting, or encysted.
The advanced or caseous stage of the pulmonary indurations, noticed in the last chapter, is in some cases presented from the first in what may be called the aplastic or caseous consolidation of the lung, the direct result of acute scrofulous pneumonia. The effused matter is at first in a curdy opaque condition, without signs of plastic activity or capacity in its constituent elements, which are numerous granules, irregular cells, and their fragments, so loosely cohering together that they form only a soft cheesy mass, choking up the proper tissues, and speedily running into fatty decay and partial suppuration. This caseous consolidation, being not circumscribed by induration, may extend to a large part of a lobe, a whole lobe, or more; but sometimes it is confined to lobules, not extending through the interlobular divisions. A variety of it seems to have its seat in the bronchial tubes and alveolar texture; and it has been stated that the effused matter consists chiefly of epithelium; but this is of rare occurrence, and does not warrant the assertion which has been made, that all cheesy deposits are to be referred to 'catarrhal pneumonia.' In all probability, any acute form of pneumonia or broncho-pneumonia in a scrofulous subject may