Discussion on the pathology of phthisis pulmonalis.

  • Gairdner W. T. (William Tennant), Sir, 1824-1907.
Date:
1881
Catalogue details

Licence: Public Domain Mark

Credit: Discussion on the pathology of phthisis pulmonalis. Source: Wellcome Collection.

Provider: This material has been provided by the Royal College of Physicians of Edinburgh. The original may be consulted at the Royal College of Physicians of Edinburgh.

    17/62 (page 13)
    It is to be noted that in both lungs the lower lobe is almost free from cavities, but there are isolated patches of condensa- tion in the form of groups of nodular projections. Examined roughly in the fresh state, these are found to present rounded bodies supposed to be tubercles and containing distinct giant cells. The]-e are now one or two points which must be considered here in relation to the more immediate anatomical conditions. Hamilton has recently in the Practitioner given an account of the processes concerned in this disease, with much of which I am in full accordance; but there are certain parts of this account with which I cannot agree, and while taking advan- tage of his excellent descriptions, I do not rigidly follow his account of the processes. There are three principal situations in which connective tissue is present in the lung—namely, under the pleura, between the lobules, and around the bronchi, so that we may speak of sub-pleural, interlobular, and peribronchial connective tissue. These are all in intimate connection by means of. the lymphatics, which communicate so thoroughly throughout these parts that the connective tissue in these three situations may be regarded as one. As evidence of this, Hamilton has shown that foreign material, such as dust inhaled, if it finds its way into the peribronchial connective tissue, is carried about in the lung and deposited in all three situations. In interstitial pneumonia there is great new-formation of connective tissue, in the usual fashion of productive inflam- mation, in all these three situations. Just as in the liver the inflammatory new-formation occurs where there is existing connective tissue, the so-called capsule of Glisson, so here the inflammation produces primarily a thickening of the existing connective tissue. There is great thickening of the sub-pleural and pleural connective tissue, great peribronchitic new-forma- tion, and the interlobular connective tissue is converted into thicker bands. But the inflammation does not confine itself to these structures, and the walls of the lung alveoli are invaded, and become thickened. The bronchial mucous mem- brane, on the other hand, becomes the seat of catarrhal inflammatory changes, and forms a muco-purulent discharge. The new-formed connective tissue, like other inflammatory connective tissue—like the cicatrix—has a marked tendency to contract, and the flattenning of the chest which is so marked in this disease is a result of this. By the formation of the connective tissue and its contraction there is great