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The old cicatrix ulcerated, and left the portion of skin newly introduced attached by a small base, peninsulated. This portion of skin, however, remained unaffected by the ulceration, and ultimately again re-united to the skin of the old cicatrix. In such cases, the arterial impulse through the transplanted portions of skin must be very slight; and in the face of such well-known facts, the want of arterial impulse can hardly be seriously maintained as a sufficient cause in itself for mortification. When a portion of skin is frozen, it turns white; and when great heat is suddenly applied, it does the same. Strong nitric acid placed on the surface of the skin or of the mucous membrane, will leave the centre of the slough which results of a dirty white colour. In these instances, it is reasonable to imagine that there may be an actual want of blood in the affected part. In some cases of spontaneous gangrene, the same may in all probability happen. But in these latter cases, which are comparatively very few in number, some unusual obstruction to the transmission of the blood through the arteries has generally been manifest; and it may fairly be presumed, from the want of pulsation in the arteries, and from the coldness of the affected part, and other symptoms, that in these cases of mortification a deficient supply of arterial blood was a principal cause of the mortification.
In the vast majority of instances the parts affected with gangrene afford the strongest contrast to such appearances. The mortified part is commonly of a deep livid colour, evidently surcharged with blood, which it has not the power to propel. This is equally true, whether there be a mechanical cause to the return of the blood, or whether no such apparent cause exist. In either case, the deep livid congestion precedes mortification—a condition quite compatible with obstructed circulation in the affected part, but utterly inconsistent with a deficient supply of blood. But, it will be asked, do not the cases in which a ligature has been applied to an artery in cases of aneurism, show that obstruction to the flow of blood through a large artery is often followed by mortification in the limb which it supplies? To this it must be replied, that it is a remarkable fact that mortification, in such cases, has only occurred when the ligature has been placed between the aneurism and the heart, and where, consequently, any softened fibrin or cther morbid products which the aneurismal sac may have contained, have had an opportunity of becoming mixed with the blood of the limb upon the distal side of the ligature, and of producing their effects upon the nutrition of the parts there situated. Upon this subject we need only observe at present, that in thirty-three cases of aneurism collected by Paul Broca, * where the ligature was placed on the distal side of the sac, no instance of inortification occurred.
Inflammation of the Arteries has, by nearly all the ablest writers, past and present, been assigned as one of the causes of mortification ; aud the way in which this result is produced is by them ascribed very generally to the blocking up of the arterial tubes by inflammatory effusion from their lining membrane. Tiedemann, Gendrin, Hasse, Hodgson, Travers, and many other celebrated names, may be quoted as
. Des Anévrysmes et de leur Traitement. 1856.
holding the doctrine of the obliteration of arteries by inflammatory effusion of lymph upon their lining membrane. “If an irritating injection,” says M. Gendrin, “ be thrown into an artery included between two ligatures, the inflammation which follows is characterized by the formation of a plastic layer, which ultimately fills up the cavity of the vessel.”* This opinion was currently received, and the prevalent notion for many years was, as expressed in Mr. Travers' most valuable treatise · On Inflammation,' that these fibrinous layers were “secreted by the capillary vessels under inflammation.”
Having reason to doubt the correctness of this theory, the author entered upon some researches wbich led him to the conclusion, that while the lining membrane of the arteries remains entire, no inflammatory effusion of lymph can take place upon its free surface. The following experiments will illustrate this point: A dog was placed under the influence of chloroform, and the carotid artery exposed low down in the neck. A ligature was then placed upon it, and the vessel was opened on the distal side of the ligature. Several small portions of cotton wadding (as large as could be introduced into the vessel) were then saturated with a solution of sulphate of zinc, and propelled, by means of a probe, along the artery towards its distal extremity. A portion of the artery was thus left obstructed, on the one hand by the ligature, and on the other by the plugs of cotton wadding. Little blood would, it was thought, under these circumstances, find its way into the vessel. The experiment was performed on September 4th, and the animal was killed and the parts examined on the 8th. The internal and middle coats had been divided at the points where the ligature had been applied. The outer cellular coat and the surrounding parts were here much inflamed, and a large abscess had formed in the immediate neighbourhood. At the part of the vessel in which the cotton wadding had lodged, the coats of the vessel had also given way, and an abscess had formed in the surrounding tissues. The intermediate portion of the artery, over which the saturated cotton wadding had passed, had become considerably retracted, so as to occupy perhaps not more than half its natural length. The lining membrane in this portion of the artery was entire, and of its natural colour. On its surface was a very small coagulum of blood, and at another point a very slight thickeniug or elevation of the lining membrane. With these exceptions, the inner surface of the vessel presented its natural appearance. The contact of the cotton wadding soaked in the solution of sulphate of zinc had therefore not produced any appearance of inflammation, or of effusion, in those parts over which it had passed, but where it had not been allowed to lodge.
In like manner the left jugular vein of a donkey was exposed in two parts of its course, and two ligatures placed upon it at something less than four inches interval. After the blood had been removed, the cavity of the vein was filled with cotton wadding. The wounds in the vein and in the skin were then carefully closed with sutures. The animal was killed at the expiration of forty-four hours. The lining
- Histoire Anatomique des Inflammations. Paris, 1826.
membrane of the vein in the space included between the two ligatures was of rather a deeper colour than natural, but in no point did it present any trace of effused lymph. The outer coat of the vein was thickened and inflamed, and suppuration had commenced in its outer cellular connexions.
The conclusions arrived at from the author's experiments and observations agree with those published by Virchow-viz., that chemical and mechanical irritants, when applied to blood vessels, produce their effects only, as far as any inflammatory exudation is concerned, on the external and middle coats of arteries, or the outer coats of veins. That the epithelial and fibrous longitudinal coats of bloodvessels may become detached, and when once detached, a plastic layer from the outer coats may be poured into their cavities.
In thirteen experiments performed by Virchow, in which the lining membrane of arteries was irritated by various means, in none was there any plastic exudation from the surface of the lining membrane. Mortification of the lining membrane may be produced, but it necessitates the coagulation of the blood in the vessel to the extent of the lesion, and may be subsequently followed by effusion from the outer coats into the vascular canal.
Although effusion of lymph, as the result of inflammation, can be with such difficulty produced in the cavities of arteries, yet is there hardly any artery or vein in the human body that has not been found narrowed, closed, and impervious to blood. Professor Tiedemann, in his work on The Closure of Arteries in Disease,' has collected together a great number of instances, and these he refers to four heads-viz, Ist. To inflammation of the inner smooth coat of arteries ; 2nd. To growth and morbid excrescences of the inner coat; 3rd. To deposits of solid or earthy concretions, or purulent matter between the coats ; and 4th. To clots of blood, which, like plugs, close the sides of arteries. The first and second of these divisions we believe to be referrible to deposits from the blood. The lining membrane of an artery being a non-vascular structure, cannot be said to inflame, and so long as it maintains its integrity, lymph cannot be effused upon its surface. That which has been supposed, therefore, to be lymph effused as a result of inflammation, must in reality be fibrin deposited from the blood. Upon a microscopic examination of the white fibrinous plugs found in arteries, they may be found to consist of a delicately fibrillated material resembling that which constitutes ordinary fibrinous coagula, and in the meshes of this may be often seen an abundance of roundish corpuscles, unacted upon by acetic acid in the same manner as pus, but not unlike pus globules in general appearance. The fibrinous concretions also contain ordinarily numerous refractive globules, which, from their solubility in ether, are evidently fatty in their nature. These concretions may be very slightly, or not at all, adherent to the vessels in which they are found, or they may adhere with more or less firmness to the sides of the vessel, and sometimes they may become so intimately connected with the artery as to be with difficulty distinguished from it. In such instances they may resemble an
excrescence from its lining membrane. A thin, smooth, polished membrane often forms on the surface of these fibrinous inasses, which is continuous with the lining of the vessel, and gives the appearance of the inner coat being continued over them. These white fibrinous deposits are found in almost every degree of consistence, and they may extend to any distance along the arterial canals. When they are detained in one of the larger arteries, they commonly adhere to one side of the vessel; but they are often carried along with the current of the circulation, and lodge in the substance of the organs to which the arteries are distributed. In some rare instances the fibrinous deposit may be traced continuously from the artery to its remotest ramifications. Thus, in an experiment performed by the author, in which some viscid pus was injected into the jugular vein, fibrinous cords were found to extend from the right side of the heart to the minutest ramifications of the pulmonary artery. In a case, mentioned by Sir B. Brodie,
“In which there was mortification of the right foot, the muscular structure of the heart was soft, thin, flaccid, and easily torn; one coronary artery was impervious, and the right iliac artery, for the extent of three inches, was impervious also, in consequence of its being completely filled by a mass of firmly coagulated blood. In another case, in which there had been mortification of the right foot, the muscular structure of the heart was pale and flaccid; one coronary artery was contracted and impervious; the cavities were dilated; a mass of dense coagulum, resembling that found in the sac of an aneurism, occupied the appendix of the left auricle, and there was a similar coagulum obstructing the popliteal artery and vein of the right side, and extending some way down the branches of those vessels in the leg.”
Now, Mr. Gulliver has shown that the deposit which constitutes the most ordinary form of disease of the arteries is a fatty degeneration or deposit. This deposit, when it occurs in arteries, becomes softened down, causes a rupture of the thin, brittle, internal coat, and either becomes covered with fibrin, or is discharged into the blood. If covered with fibrin, this may remain firm, or it may itself become softened down, and find its way into the circulation. In old aneurismal ses such portions of fibrin may be found softened, and containing globules of various sizes, some not unlike pus, but unacted upon in the same way by acetic acid.
"Case I.-On the 14th of December last, a girl seven years of age was examined, after death, at St. George's Hospital. She had long suffered from anomalous symptoms, which were not referrible to any one origin in particular. On inspecting the heart, two aneurismal dilatations were found communicating with the left ventricle br very narrow openings. The aneurismal dilatations contained fibrin which had undergone the process of softening in various degres, and it was erident that at each contraction of the heart some of the contents of these dilatations would be impelled into the general circulation. The kidney and the spleen both contained fibrinous deposits. Around these the structure of the organs was softened, and the deposit itself, after being kept for a dar, became softened in its centre, and dissolved. The arteries at the use of the brain contained some small isolated masses of white fibrin.”
t'iss II. - A woman, agni twente-seren, died of endocarditis (so called) on the 10th of January, 1830. The mitral razlve was covered with brittle masses,
which, under the microscope, were seen to consist of dense, amorphous, highly granular, yellowish-looking lumps. Portions of fibrinous concretion (emboli) were found in the fine branches of the coronary artery of the heart. These could be recognised by the naked eye, and had produced an acute yellow softening of the muscular structure. Numerous hæmorrhagic knots were found in the spleen, in which the endocardiac emboli could with great constancy be traced into the penicilli. These emboli were also found to fill some of the little arteries of the kidneys.”*
“CASE III.-J. F. L., a boy, aged six, apparently in previous good health, suddenly fell down, without any complaint, on the 23rd of July, 1855; his limbs were found quite relaxed, and after a short time he said it was so dark that he could not see : when taken home he spoke little, and incoherently, but his extremities were then stiff and cold. In the evening he revived, became warm, and slept. During the night he complained of pain in the left foot and great toe; the latter was found to be black at the tip. Towards morning he complained of pain in the thigh and leg of the same side. On the 24th, a cord, of the thickness of the finger, was felt from Poupart's ligament downwards, in the direction of the vessels, about one inch and a balf long. This cord was tender on pressure, and the skin over it was somewhat red coloured. A black gangrenous vesicle as large as a bean, in a half-moon shape, presented itself under the nail. The toe and that next to it were swollen, and there was considerable ædema up the instep. Motion in the left leg was attended with pain. Over the aorta a doubling was heard of both sounds of the heart; these sounds were propagated into the vessels of the neck. There was here also a strong venous murmur.—July 25th. The upper part of the thigh was ædematous, 28th. The ædema of the instep had disappeared.—August 1st. The cedema of the groin was gone, but large vibices occupied its situation on the thigh.--8th. The sore on the great toe was rapidly healing.–24th. The patient was dismissed. The sore on the toe was nearly healed. The reduplication of the sounds of the heart continued.”+
“CASE IV.-James Hunter, aged forty-four, was admitted into King's College Hospital, under the care of Dr. Todd, on the 1st of June, 1854. Be had been ill for seven or eight months, and had, as post-mortem examination subsequently proved, some tubercles in the lungs, and disease of the kidneys. On the 26th of May, he had been seized for the first time with extreme dyspnea. This symptom was so distressing that it precluded the possibility of his sleeping even for a few minutes. When admitted into the hospital he had had no sleep for four days and nights, and complained only of this, and a sense of anguish about the præcordial region. He sat up at night and laid his head upon the table, that being the only position in which, as he said, he could get any ease. On the evening of the 4th of June it was noticed that the left foot was cold and livid. On the 5th, the pulsations could be felt in the left femoral artery, but not in the corresponding dorsal artery of the foot. He died on the Sth, thirteen days after the first attack of difficulty of breathing. The body was examined fourteen hours after death. The left foot and lower half of the left leg were of a livid blue colour; upon cutting open the left ventricle of the heart, a quantity of thick, discoloured fluid flowed out. Besides this fluid, the left ventricle contained many clots of semi-solid fibrin in various stages of softening. The left common femoral artery, just above the origin of the profunda, was found to contain a dirty-white fibrinous clot, which quite filled up the canal of the vessel, but which was not in the least adherent to its inner coat. Below this the vessel contained a very little red • Virchow's Archiv, Band ix. p. 307.
† Professor Gustav von Dirben.