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share which the lymphatic system has in the subsidence, as well as in the development, of this class of diseases ; the corresponding lymphatic glands swelling as the reabsorbed matter passes through them. It is rare to find the bronchial glands free from disease in chronic tubercle of the lung; and I have long been in the habit of pointing to this in the dead-house, as one of the proofs of absorption of tubercle. In these chronic cases, the matter found in the glands is commonly old, being cheesy or calcareous; but the examples I have cited above are recent, and show how these glands may be first affected.

After the preceding analysis of consumptive diseases of the lungs, we shall be able to construct a table, with comments, presenting a synthetic view of the inflammatory and tuberculous lesions of the lungs which are met with in the consumptive. This may serve as a key to explain the varieties, contrasts, and complications in the morbid appearances, and the very great diversity in the symptoms, signs, course, and duration of the malady in different cases. As strictly bearing on this subject, I quote the following propositions, to which I was led more than thirty years ago, and which I venture to believe are now receiving their detailed demonstration:—

'Lymph, pus, and tubercle are the same albuminous matter, and differ from each other in mechanical condition and susceptibility of organisation, rather than in

their chemical nature We can readily perceive

that these different properties, although possessed by matter chemically the same, and from the same source, must lead to all that variety of results which we know to follow, respectively, organisable, purulent, and (yellow) tuberculous deposits. But the characters of these matters are not always distinct: lymph is not always equally organisable, nor perfectly free from the greenish colour and disintegrating globularity of pus, nor even from the GRADATIONS OF LYMPH, PUS, AND TUBERCLE. 59

lifeless curdy particles of (yellow) tubercles; and tuberculous matter often contains flakes or fibres of imperfect lymph. The diffused tuberculation or infiltration of the lung from inflammation generally presents a matter in this transition state. It is neither good organisable lymph, nor is it wholly unorganised tubercle; and the albuminous (curdy) effusions on serous and mucous surfaces not unfrequently present such an intermediate state that it is difficult to determine to which class they most belong. Lymph, pus, and tubercle pass by imperceptible gradations into each other. The history of the intermediate products has yet to be more fully studied; and it is a subject of immense importance, for they probably constitute those forms of phthisical lesions which it is most within the power of medicine to control.'1

In accordance with the view here given, it may be stated that, although the protoplasm, from changes in which all these morbid products proceed, does take the distinct forms defined in the following table, and in different examples, one or other of these forms may so predominate as to distinguish the disease into characteristic groups, yet most cases present less marked distinctions, and comprise a mixed history of various proportions of lymph, pus, and grey and yellow consolidations, in the varying course of the consumptive malady.

1 Pathology and Diagnosis of Diseases of the Chest, 4th ed., 1840, p. 166. Tabular view of Elements of Consumptive Diseases, and their results. CHAPTER VIII.

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Pus-cells, with liquid trit-
oxide of protein; pro-
liferating and assimil-
ating other tissues
into pus.

Eed, pale or grey indura-
tions of lung and other
Caseous hepatisation.

Ulterior results

C. Inactive and aplastic.
Combined with tho above, and partaking of their changes and results.

Well organised; or reabsorbed.
Well organised; or reabsorbed.)

a. Dense, tough, and contracting.

b. Degeneration and caseation.

a. Discharging from freo mem


b. Suppurating into abscess, and


c. Imperfectly suppurating and


a. Withering and cornefact ion.

b. Decay by caseation and soften-

a. Early softening and excavation.

b. Obsolescence and calcification.

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Phthinoplasms, or elements of Consumptive diseaseTheir origin and results Divided into those of the blood-vessels and those of the lymphatic systemClinical and pathological varieties of Consumptive diseases, euplastic and cacoplasticOf inflammatory Phthinoplasms ; the filyroid is the highest, tending to contract, and endure long without decay But it dwindles, and is attended with evidences of wastingEffects of fibroid in the lung; scars; dilated bronchi ; emphysema.

The preceding table will supply a key to explain the leading varieties of consumptive disease with which clinical experience makes us familiar, by referring them to the predominance of one or other of the elements here specified.

The first two on the list, representing the most healthy hyperplasms produced by inflammation, do not in themselves tend to induce consumptive disease. They are supposed to occur in otherwise healthy subjects; and, although they are morbid in their superfluity, yet they have in themselves either sufficient vitality to assimilate them to the affected tissue, or sufficient vitality and divisibility to be removed by reabsorption. But what begins as healthy inflammation may become deteriorated through mistreatment or neglect, or other unfavourable circumstances, or by the repeated application of the exciting cause; and then some of the more unhealthy results follow; and so the healthy hyperplasms may be combined with, or turned into, cacoplastic or aplastic products. The converse takes place more rarely. A person previously unhealthy recovers health; and then an accidental inflammation may produce euplastic results, to be well organised or dispersed without any evil consequences.

Unhealthy inflammations evolve two classes of hyperplasms, with less or more of a degenerative or consumptive tendency: (1) the fibroid and (2) the corpuscular, each of which has several remarkable varieties.

1. Fibroid hyperplasms are probably in part formed from the fibrillas of the fibrin exuded from inflamed vessels; possibly also by hypertrophy of pre-existing connective tissue. A great part of the tough consolidations produced in the lung by prolonged subacute or chronic inflammation consists of a fibrous material, which assumes the form of irregular connective tissue. They may owe their origin to the variety of pulmonary inflammation which I long ago1 distinguished as the interstitial kind, and leading to a non-granular form of hepatisation. To this variety, without recognising its cause, Laennec gave the term of carnification. It occurs in pleuro-pneumonia when the pressure of the pleural fluid on the lung restricts the plastic effusion to the interstitial texture, without any granular formations in the air cells. This is the most common origin of extensive fibroid disease of the lung; and its nature is evident in the accompanying proofs of previous inflammation,—the general adhesions (often of the same tough character) of the pulmonary and costal pleura of the affected lung. But there is also, probably, a peculiarly fibrinous state of the blood, which Kokitansky calls a fibrinous crasis, in certain cases, rendering the products of inflammation more fibrinous than usual, and with smaller proportion of the corpuscular element; and tending, therefore, to produce more fibroid or con

1 Cyclopedia of Medicine, Article 'Pneumonia,' 1833.

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