CHAPTER XXII.

THE BLOOD VESSELS.

IN estimating the morbid lesions occurring in the blood vessels, we must bear in mind that they are mere conduits for the fluid, by which nutrition and the metamorphoses of the tissues are effected, and that they therefore bear a very different relation to disease from that presented by the central organ of the circulation, or by the blood itself. It is the more necessary to urge this, as so much that has been written with regard to the main pathological condition, which we are able to excite and observe in the living tissues, inflammation, appears to have originated in the view that the coats of the bloodvessels were the most essential elements in the production and maintenance of the phlogistic process. This is owing to the experiments having been necessarily of a character to irritate the vessels from without, and produce rather a physical than a vital effect. We cannot in this way imitate those constitutional causes of inflammation to which we must generally attribute its production, and in which it is impossible not to recognize the state of the blood as constituting the first element in the production of the phenomena in question. These remarks apply more particularly to the capillaries, but we shall have occasion to see that they also bear upon many of the symptoms met with in the larger vessels. The difference in the direction of the current, in the composition of the blood, in the velocity and force of the circulation, and in the structure of their coats, are points that must not be overlooked in forming an estimate of the diseases of the two great classes of vessels, the arteries and veins. The manifestations of disease in its primary and secondary form are essentially different in the two, as we find their physiological and anatomical relations to be widely apart. The arteries exhibit between their lining membrane and cellular coat a dense fibrous layer, which contains no vessels, and therefore removes the vasa vasorum, which ramify in the cellular coat, much further from the lining membrane than is the case in the veins, nor can any vessels be detected on the lining coat, or between it and the middle tunic. To this circumstance, and not to any difference in the supply of blood vessels, we must attribute the fact that, while irritation of the lining membrane of the veins rapidly and easily produces inflammatory reaction, it is almost impossible to produce such effects in the arterial lining membrane. Hasse' is of opinion that the latter, in both instances, at first merely yields to the alternations of en

1 Pathological Anatomy, Syd. Soc. Ed. p. 11.

dosmosis and exosmosis, and does not suffer any organic change until a later period. In arguing on the effects of inflammation in the arteries, we must not forget that the laws of exosmosis and endosmosis apply chiefly to fluids occupying the opposite side of the same membrane. In the arteries, we find deposits chiefly between the middle and lining coat, and of a character to forbid our believing that they can be derived directly from the current circulating in the vessel. Here, then, the exudation from the vasa vasorum has traversed the dense fibrous coat; and there appears to be no reason for refusing to admit that, eventually, the lining coat may be involved in a similar process. Without entering further into these considerations, we may observe that we are unable to join those who look upon the reddening of the internal coat accompanying its thickened condition, which cannot be attributed to postmortem action, to mere imbibition; but that there must be some change in the nutrition of the parts analogous to inflammation in other parts.

THE ARTERIES.

To proceed systematically, we shall first examine the morbid conditions.

of the arteries.

We have seen that it is a subject of debate whether the middle and lining coats of the arteries are subject to inflammation; as they possess no bloodvessels of their own, we can scarcely assume them to present symptoms of the primary phenomena of inflammation; but that they may be secondarily involved in inflammatory affections proceeding from the cellular sheath, cannot be doubted. A most interesting case of acute arteritis, in a previously healthy individual, a gentleman, aged twenty-nine, is recorded by Dr. Romberg,' where sudden pain manifested itself in the right femoral artery, affecting the distribution of the artery in the limb, then mounting up to the aorta, passed to the left iliac and its branches. Endocarditis followed, and inflammation of the arteries in the left upper extremity; the entire illness lasted from the 20th October, 1844, to the 5th December, of the same year. The post mortem was performed by Professor Froriep thirty hours after death, and the following appearances were found in the arteries: A pale red, firm clot was discovered in the abdominal aorta, close to its division; it blocked up the artery, and adhered closely to its lining membrane, which was smooth and not reddened. This coagulum extended into the two iliac arteries, gradually became thinner, and terminated in a point. At the point at which the left external iliac is given off, there was an equally firm but lighter-colored exudation. The left external iliac, as far as Poupart's ligament, was filled up with a thinner coagulum-containing much cruor; it could be easily detached from the lining membrane, which was thickened, reddened, and friable, and could be easily detached from the fibrous coat. The middle and external coats were also thicker and more friable than in the normal state. Between the membranes

Manual of Nervous Diseases, Sydenham Society's Edition, vol. ii. p. 238. Since the above was written, a very similar case has occurred under the care of Dr. Sibsou, at St. Mary's Hospital.

there was an exudation of lymph, which was also distinctly perceptible in the cellular tissue surrounding the arteries. The latter was particularly inflamed under Poupart's ligament, and the neighboring lymphatic glands were tumefied and reddened. The crural artery contained a firm coagulum at the point at which the profunda is given off, which could only be detached with difficulty from the dark red lining membrane, and which extended into the profunda. Further on, the crural artery was filled with a grumous coagulum, and the lining membrane was villous, rough, and much reddened. Then came a free spot, but at the part where it passes through the adductor, it was again closed by a firm coagulum, and the corresponding lining membrane was much reddened, softened, and pulpy. The tissues here were in a state of gangrene, the right internal iliac was unaffected. A firm, pale clot, strongly adhering to the lining coat, was discovered in the external iliac close to the point at which it is given off by the common iliac artery. The crural artery of the same side was narrow and contracted; the lining membrane thrown into folds, containing a solid plug at the site of the profunda; the lining and other membranes being much reddened and thickened. A similar coagulum was found in the left branchial artery at its division, extending into the radial and ulnar. The heart was hypertrophic, and a roundish excrescence was found attached to the mitral valve, which was proved by Professor Müller to consist of fibroid tissue, and to be subjacent to the endocardium. The same author confirmed the fact that a thin layer of plastic exudation matter was found on the arterial coagula, which at many points also invested the lining membrane. For further particulars, and for the author's views on the case, we must refer the reader to Dr. Romberg's work. We have extracted so much of it as refers to the subject under consideration, and because it offers a combination of all those phenomena which writers attribute to acute arteritis, and which are found in the inflammations of other parts of the system as a result of a peculiar derangement of the circulating fluid. In this respect, the case quoted might form an appropriate text for the development of the whole theory of the phlogistic process. Bizot' describes as the result of acute inflammation of the arteries, an albuminous exudation of greater or less thickness, of the consistency of jelly, transparent, smooth, sometimes rose-colored, at others colorless, covering the lining membrane. It is occasionally so transparent as to escape attention unless very carefully examined. It occurs in patches, solitary or numerous, and diminishes the caliber of the vessel; in one case, Bizot saw it entirely plugging up the anterior tibial artery. In the aorta, this exudation is formed mostly at the orifice of the arteries arising from the arch, at the mouth of the cœliac, mesenteric, and renal arteries, and at its posterior surface, so as to block up the mouths of the intercostal arteries. An instance of acute inflammation of the aorta is recorded by Mr. Hodgson; it is to this effect: A man was seized with violent pneumonia, which proved fatal in five days; the cadaveric inspection exhibited all the thoracic viscera in the highest

degree of acute inflammation; the aorta was also involved; its internal coat being of a deep red color, and a considerable portion of lymph being effused into the cavity. The effused lymph was very intimately

Fig. 148.

Fig. 149.

Plastic deposits in aorta.

Plastic plugs occluding the axillary artery.

connected with the internal coat of the vessel, and a plug of it had extended into the left subclavian artery, and nearly obliterated the cavity of that vessel. In reference to this subject, some experiments performed by Gendrin' are of considerable importance in demonstrating the capability of the coats of the artery giving rise to inflammatory exudation in the strict sense of the word. He found that on injecting an irritant substance into a portion of an artery included between two ligatures, and deprived of blood, a deposit of coagulable lymph took place, which arrested the internal coat, and at last formed a plug filling up the channel. The lining membrane at first was only slightly discolored, and through it a network of injected capillaries might be distinguished on the adherent surface of this tunic to the middle coat. When the

1 Histoire Anatomique des Inflammations, vol. ii. p. 13.

inflammation had advanced, this was no longer seen, the external coat having become pulpy, rugous, and dull. The suppuration that followed did always coincide with ulceration of the inner coat; the pus, however, was not necessarily deposited in the vessel, but infiltrated into the cellular sheath, forming small abscesses. We may reasonably conclude that in arteritis the morbid products are derived from the vasa vasorum as well as from the contained blood. To sum up: The symptoms of acute inflammation of the arteries are more or less extensive, reddening, softening, thickening, and detachment of the lining coat which exhibits an opaque, plicated condition; the middle coat becomes hypertrophied and friable, and in the external coat we find distinct signs of congestion and exudation. Within the vessel, a coagulation of fibrin and the deposit of coagulable lymph from the blood is seen, and as secondary effects we have to deal with ulceration, laceration of the coats, hemorrhage, and gangrene of the distal parts of the system.

2

From the time of J. P. Frank,' who first drew attention to the subject of arterial inflammation, to the most recent periods, various pathological conditions have been attributed to it; the acute forms have been repeatedly asserted to be the cause of trismus neonatorum, a disease which at present is one of very rare occurrence among ourselves. Dr. West denies this cause, but Dr. Collis, and recently Dr. Schöller33 satisfied themselves of its real existence. The latter found inflammation of the umbilical arteries in fifteen out of eighteen cases of trismus neonatorum. There was tumefaction of the umbilicus, reddening and congestion on the external surface; the channel contained pus, and the lining membrane was eroded and invested with an albuminous exudation. Dr. Schöller has carefully examined these parts in all other new-born. children who died shortly after birth, and has never succeeded in discovering similar lesions. It does not appear that traumatic tetanus in the adult, to which we may compare trismus neonatorum, is accompanied by similar lesions.

The formation of a coagulum in the artery is a well-known physiological effect of the laceration by mechanical or other means of the lining membrane, and the atrophy or gangrene of the part nourished by the artery is an illustration of the effects following similar obliteration of the channel from disease. We have alluded to the cerebral affections resulting from an arrest in the arterial circulation; senile gangrene is another morbid condition which has been ascribed, by Dupuytren and Cruveilhier, to arteritis. In this there is a marked distinction between inflammation of the two sets of vessels; that phlebitis induces secondary deposits and oedema, while these occurrences are not met with in arteritis. It is even doubted whether the latter ever gives rise to suppuration, but, independently of the cases of suppuration in the umbilical artery quoted from Dr. Schöller, Andral and Hodgson's authority' de

1 De curandis Hominum Morbis, vol. ii. p. 363.

Dublin Hospital Reports, vol. i. p. 285.

Neue Zeitschrift für Geburtskunde, herausgegeben von Busch, d'Outrepont und Ritgen, vol. v. p. 477. Anat. Pathologique, tom. ii. p. 379.

On the Arteries, p. 10.