General Arteritis

General Arteritis, like general phlebitis, has no existence.

The above remarks apply to the inflammation of the arteries of the aortic system. In the system of the pulmonary artery appearances indicating inflammation of the larger branches are very rare, and probably are merely secondary processes arising from spontaneous coagulation of blood, and resembling secondary phlebitis. The occlusion of these vessels in most cases results in death, before the development of an excessive inflammation in their coats.

The smaller the arterial vessels are, the more dependent are they on the condition of the surrounding tissue. They likewise participate in this inflammatory process, which either penetrates directly into the vessels of their cellular sheath, or affects them indirectly, in consequence of the inflammatory products penetrating through and saturating the delicate, permeable coat of the vessel. Hence arise the occlusion of the arteries of an inflamed parenchyma, and the obliterations arising from inflammation terminating in induration, as we see in the walls of healing cavities of the lungs.

Although there exists no true chronic arteritis of the form here indicated, acute arteritis having products of an adhesive nature may persist for a prolonged period; the textural metamorphosis of its products may be effected slowly, and the terminations we have already indicated may be only very gradually brought about; while arteritis with purulent exudation may terminate in protracted ulceration. That which is commonly regarded as chronic arteritis or as one of its sequelae, is not originally or essentially inflammation, although it constitutes one of the most frequent and most important diseases of the arteries, as we shall presently have occasion to show.

There is, however, a chronic inflammation of the arteries, manifested as inflammation of the cellular sheath of the arteries (which consists of a layer of elastic, and a layer of cellular tissue), to which its products are limited, and which merely exerts a secondary disturbing action on the normal relation of the inner arterial coats of arteries, viz., the circular fibrous, and the true lining membrane. This constitutes a very frequent, and, at the same time, a highly important phenomenon in arteries of large calibre, as, for instance, the trunk of the aorta and its branches.

It is occasionally a primary, but more frequently a secondary disease, and as such constantly accompanies the morbid deposition on the inner coat of the vessels and its metamorphoses. Its anatomical appearances are in general those of chronic inflammation of the cellular tissue, as-, for instance, unusual vascularity of the cellular sheath, with dilatation of the injected vessels, and, corresponding to the degree of its injection, a more or less uniform, saturated coloration, varying from a dark red to a purple, while the cellular sheath is infiltrated with a grayish, or grayish-red, watery or adhesive and gelatinous fluid.

This disease terminates in hypertrophy, thickening, and condensation of the cellular sheath, which is converted into a tough, apparently lar-daceo-fibrous, and callous, white stratum, varying in thickness from 3 to 6 lines. (Sclerosis).

It induces paralysis of the diseased tissue, more especially of the elastic layer of the vessel, and consequently dilatation, which appears, according to its degree, either diffused, local, or partial. The circular fibrous coat, which is loosened in texture by the dilatation of the vessel, exhibits a morbid brittleness in cases of callous condensation of the cellular sheath, is stratified in appearance, and is of a dirty yellowish, faded color, which indicates a tendency to spontaneous lacerations, owing very probably to the deranged nutrition of the coat of the vessel. Dilatation of the vessel moreover induces the excessive formation of an anomalous inner coat, and its further consequences.

This inflammatory process and the modes of its termination that we have already indicated, are accompanied by two different conditions of the cellular sheath.

In the one case, the vascularized, infiltrated, cellular coat of the artery, together with the elastic layer, admits of being detached with unusual readiness from the circular fibrous coat - a condition which may degenerate into spontaneous detachment, and give rise to spontaneous laceration of the lining membrane (dissecting aneurism).

In the other and more commonly observed case, the callous and thickened cellular sheath has coalesced with the circular fibrous coat. This most commonly occurs in dilated aneurismal arteries.

Special reference must be made to the inflammation of the cellular sheath at the origin of the two arterial trunks, which depends on pericarditis. It would appear from the milk-spots and adhesions found at this point, that inflammation of this portion of the pericardium occurs very frequently, either partially or associated with general pericarditis. By affecting the subserous cellular substance, it also implicates the cellular coat of these arterial trunks. This inflammatory condition very frequently extends beyond the period of the acute pericarditis, and in the form of chronic inflammation of the cellular sheath gives rise to dilatation, more particularly of the aorta.

In reference to the pulmonary artery, this chronic inflammation sometimes attacks the trunk and its two branches, and it is commonly present in an inferior degree associated with a similar condition of the cellular sheath of the aorta.