This section is from the book "A Manual Of Pathological Anatomy", by Carl Rokitansky, William Edward Swaine. Also available from Amazon: A Manual of Pathological Anatomy.
We have already considered the relation of the capillaries in hyperemia, stasis, and exudation (inflammation), as well as in their modes of termination, in induration (atrophy of the tissue), in suppuration, in gangrene, and in other conditions. Although, as we must again, specially remark, these vessels cannot themselves be inflamed, they yet become the seat of an inflammatory process, and a centre for the development of its products, the deleterious effects of which they are the first, under the appropriate conditions, to experience.
The small veins and arteries beyond the capillaries are affected by the condition of the surrounding tissue, even where they had not themselves participated in the process of exudation: for their delicate and permeable coats are saturated and permeated by the product of the inflammatory process, on which, at least in part, the ordinary coagulation of blood within them and their occlusion depend. There then follows either a solution of the occluding coagulum and a liberation of the calibre of the vessel, when resolution of the inflammation occurs in a comparatively large vessel, or persistent obliteration and atrophy or a suppurative destruction of the vessel, when the inflammation terminates in induration or suppuration.
In connection with the subjects discussed under this head, we must especially refer to capillary phlebitis, although we must confine ourselves to little more than a recapitulation of what has been already stated.
Capillary Phlebitis, if it were a true inflammation, should rather be called Capillary Angioitis; but inasmuch as it does not in reality consist in an inflammation of the capillaries, neither of these names is applicable to the affection. It essentially and originally consists in no tex-tural change of the capillaries, although it very often gives rise to their atrophy or ulcerous destruction. We have already frequently referred to it, both in the general anatomy, and in different chapters of the special anatomy. It essentially consists in a coagulation of the blood in some portion of the capillary system, dependent on a spontaneous disease of the blood, or on its infection from some cause, and is analogous to the phlebitis induced by coagulation. This coagulum, which closes these vessels, at first appears as a dark-red infarctus in the affected parenchyma, and subsequently becomes decolorized, and undergoes various metamorphoses. If it be not gradually dissolved and absorbed in a finely comminuted state into the blood, it either shrivels, and assumes a rusty-brown, yeast-yellow, or perfectly bleached appearance, and the whole terminates in persistent obliteration of the affected capillaries (the adhesive process), associated with atrophy of the parenchyma, which is converted into a white fibroid (cellulo-fibrous) callus; or it undergoes, in general with considerable rapidity, a purulent and usually acute ichorous, gangreno-ichorous septic fusion, associated with a yellow, or dirty green, or brown discoloration. The walls of the vessels and the parenchyma participate in the same process, which finally results in the formation of a purulent or ichorous abscess.
Sometimes the coagulum, after it has become yellow, undergoes partial or entire cretefaction.
An exudation into the parenchyma doubtless occurs simultaneously with this process. As compared with the same process in a larger vessel, we regard it as an unessential occurrence, merely depending on the permeability of the walls of the vessels.
To these processes, considered with reference to the general condition, or to a focus of infection giving rise to it, we commonly apply the term metastases; or in the lungs, we term them lobular processes, in consequence of their usually inconsiderable extent and well-marked limitation.
Around their margin we commonly find a true secondary (reactive) inflammation of the tissue, which the experienced observer may tolerably readily distinguish from the original centre of inflammation, especially in the parenchymatous structures, which - as, for instance, in the case of the lungs - undergo a peculiarly striking degeneration (hepatization). Immediately around the inflammatory centre we not uncommonly meet with capillary hemorrhages, and suffusions of the tissue.
They occur in all tissues, but are especially frequent in certain very vascular organs which take part in haematosis, as the lungs, the spleen, the kidneys, and the liver. They are principally distinguished by their generally considerable number, by the roundish or (in the case of the spleen and kidneys) the wedge-like and angular form of their central part, and from their being seated on the periphery of the above-named organs.
When the affection terminates in obliteration or atrophy, pit-like, contracted depressions are formed on the organ, which are generally the more numerous the nearer the morbid changes are to the surface.
Cruveilhier also treats of a hemorrhagic capillary phlebitis. In reference to this name, we will only remark that the capillaries which are the seat of what is termed capillary phlebitis, cannot give rise to hemorrhage. In the lower extremities of aged persons suffering from dyscrasia, we meet with coagula, especially in the subcutaneous veins, which extend from the trunks into the branches, and may possibly at some spots affect the capillaries. The cellular tissue is then the seat of a spontaneously distributed suffusion; it appears sometimes to contain an extravasation of loosely coagulated blood, without any apparent degeneration of texture or cohesion; and sometimes it and its contained blood represent an apparently firm, but easily torn, friable, dark-red clot. We believe that this process consists in a spontaneous coagulation occurring within, and closing the trunk of the vein and its branches, and giving rise to diffuse capillary hemorrhages, in consequence of the impediment which is presented by the occlusion to the emptying of the capillary vessels, and is proportional to the extent of the coagulation, a phenomenon which we observe, on a small scale, in almost every phlebitis - that is to say, in the form of small ramifying hemorrhagic centres along the occluded vein, and, as we have already remarked, around the seat of capillary phlebitis.
It is an unquestionable fact, that very minute arteries undergo this form of disease, since their coats lose their transparency, and become opaque and thickened either uniformly or at particular parts; and, instead of remaining soft and flexible, become rigid and brittle, and not unfrequently ossified. We feel convinced that a similar condition exists in the true capillaries; and it is moreover probable, that the anomaly is here less in degree, since the arterial portion of the blood is expended in the process of nutrition.
This condition, which is duly considered in the Diseases of the Arteries, is very important, since, in consequence of the thickening of the walls of the vessels, it impedes their permeability and the nutrition of the tissues; since it also induces partial occlusion, or even perfect obliteration, of the vessels; and since, finally, it predisposes the vessels to laceration. Amongst its results are atrophy of the organs, spontaneous gangrene (mummification), and hemorrhages.
It is especially observed in the brain, in association with ossification of the trunks of the vessels at the basis cerebri, and in the uterus. On making horizontal sections through the hemispheres of the brain, and passing the finger over the cut surface, we sometimes feel roughnesses, corresponding to the exuding blood-spots, and caused by the ossification of very minute arteries.
We have already explained the relation in which the minute and true capillary vessels stand to the different adventitious products, and the changes which these vessels undergo.
 
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