Syphilis and the etiology of atheroma / by F. Parkes Weber.

  • Frederick Parkes Weber
Date:
1896
Catalogue details

Licence: Public Domain Mark

Credit: Syphilis and the etiology of atheroma / by F. Parkes Weber. Source: Wellcome Collection.

Provider: This material has been provided by The Royal College of Surgeons of England. The original may be consulted at The Royal College of Surgeons of England.

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    arteriosclerosis, and as in some cases of granular contracted kidney,' and of chronic fibroid changes in the cardiac muscle,2 the question arises in this case, also, what definition of inflammation we are to accept as our criterion in judging whether inflammation is present or not. The rubor, tumor, calor et dolor of Celsus, though still of great service as ordinary clinical tests for inflammation when occurring in extensive areas accessi- ble to touch or view, is hardly satisfactory as a scientific definition. For the present purpose I would prefer such a modification of modern defi- nitions as that suggested in my recent paper on Arterio-sclerosis, * namely, that inflammation is '' the series of tissue-changes caused by an injury or by the presence of some harmful irritant, and usually leading to an accumulation of cells in the part affected. This includes the cell-accumulation resulting from proliferation of the fixed cells as well as that resulting from the migration of leucocyte-. It includes tuberculous affections and the other infective granulomata ; it will also include cancer and sarcoma, if ultimately the presence of coccidia-like organisms should be proved to be necessary to their devel- opment. The occurrence of necrobiosis, secondary to inflammation or due to the same original cause, will not confound the definition. If we accept such a definition, does atheroma fall under the head of inflammation ? The cell-accumulation is certainly present, but an injury or irritant cause is probably not essential to the production of atheroma, unless, indeed, deficient nutrition be regarded as an irritant cause. Mere malnutrition and deficient nutrition are causes of necrobiotic and degen- erative changes, acute and chronic; but, if they should be regarded as irritants, it would become hard, indeed, to separate chronic inflammatory from degenerative processes. It is doubtful whether in many conditions it is possible to draw a hard- and-fast line between chronic inflammation of tissue and chronic de- generation of tissue. One can understand that the blood by deficiency in quantity, or, at least, by deficiency in its chief nutrient com- ponents, may give rise to a process of simple malnutrition. Besides being merely deficient in quantity or nutrient quality the blood sup- plied to the tissues may contain injurious substances owing either to excessive formation in some tissue of the body of a natural toxic product of tissue-metabolism, or to its deficient excretion from the body,4 1 Especially those cases chiefly seen in old people, in which the capsule of the kidney strips off quite readily, though the surface of the cortex appears somewhat pitted or granular, and the cortex of the whole kidney is slightly diminished in size. 2 See H. Huchard : Maladies du Coeur et des Vaisseaux, 2d ed., Paris, 1893, pp. 170 et seq. * The American Journal of the Medical Sciences, September, 1891, p. 287. * Or to deficient washing out of products of catabolism from some particular organ. Thus, the increase of fibrous tissue taking place in the liver and spleen from passive congestion may be due not merely to the passive hypersemia, per se, nor to increased vonosity of the blood, but rather to the accumulation of the products of tissue-catabolism occurring in the congested organs owing to the local stagnation of the blood.