Discussion on the pathology of phthisis pulmonalis.

Date:
1881
Catalogue details

Licence: Public Domain Mark

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

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    a sub-acute low form of inflammation, the products of which, along with the lung tissue caseate, soften, and give rise to tubercle. This, I think, is probably the course of events in many cases of hereditary phthisis. The difficulty we have been considering seems to me less easily explained by the theory of the French school, that there is a special blood dyscrasia in all cases, or, as Dr. Coats puts it, that there is a special virus in the system; for, seeing that the blood circulates everywhere, Why should the tops of the lungs be the only parts to suffer in the first instance ? Does that not point to a local weakness of tissue ? Another objection relates to pulmonary haemorrhage. It is urged that, for example, in cardiac disease blood may be effused into the lung, condensing its tissue, and yet does not caseate nor give rise to tubercle. There seems, however, no good reason to anticipate that result in such cases. For blood is one of the blandest and least irritating of fluids, so long as it is not in contact with an inflamed surface or mixed with air. In por¬ tions of lung condensed by it the air is usually thoroughly expelled, and comes in contact with the blood only in the bronchi leading to the condensed part, and there probably a protecting film is formed. Should the air get mixed with the blood decomposition is apt to set in, giving rise to severe inflammation, and even suppuration or gangrene. In these cardiac cases the walls of the air cells and the surrounding tissues being free from inflammation, and the lung not being constitutionally weak, no irritation is produced, and the san¬ guineous effusion may be gradually absorbed. On the other hand, in patients with weak lung tissue and a hereditary bias to consumption, low inflammatory action precedes the haemoptysis, and occasions it through the attending congestion, and it follows that the blood that condenses the lung at the part where the disease begins lies in contact with an inflamed surface, and both participates in and accelerates the morbid changes that are progressing there—changes that end in caseation. Should there be no preceding inflammatory action, it is easy to see that blood, though not irritating to strong lung tissue, may be so in one that is constitutionally weak, and initiate disease in such. The greatest difficulty that I have is to explain certain cases of acute general tuberculosis. Most cases of that kind are readily enough accounted for when we find caseated glands or caseated matter in walls of cavities or anywhere, as its absorp¬ tion by the blood-vessels shows how the system as a whole becomes involved. But there are cases met with where no E