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vertical, they are straight. They have an appearance of curvature from their forining a part of the curved brim of the pelvis. But, in fact, they spread out below into the higher part of the broad acetabula, and acquire, as they spread, a concavity on their external as well as on their internal side, not a convexity, as would be the case if they were currel in the manner described by Dr. Duncan.
The converse of this principle is, with equal error, applied by the same author in the explanation of the deformity of the oblique pelvis descriled by Nägele. The sacro-iliac synchondrosis is obliterated in that form of pelvis, the innominatum is considerably bent between the anchylosed part and the acetabulum, whilst from the bent portion to the symphysis pubis, the bone is not curved, as in the brim of the natural pelvis, but straight. Dr. Duncan attributes the want of curvature of the linea arcuata to the want of the outward pressure of the sacrum at the points of its attachment against the innoininatum. It is indeed true that the sacrum no longer exerts an outward pressure against the cotylo-sacral beam, for as the joint is anchylosed, the ligaments and the posterior iliac tuberosities are useless; but it is not correct to describe the innominatum as straight. In that part which should be straight, according to the reasoning of Dr. Duncan—viz., the cotylo-sacral beam—the bone is in fact unnaturally curved, and the straight part is the anterior portion of the brim, which could not be affected by any lateral pressure of the sacrum. The theory of the effects of outward pressure therefore falls to the ground. First, its alleged effects cannot reasonably be expected, and next, the very opposite take place. For where the joint and the pressure exist, the cotylo-sacral beam is straight, and when neither exists, that beam is curved.
The deformity of the brim in Nägele's pelvis probably occurs in the following manner. The anchylosis renders useless all the articular ligaments and the posterior iliac tuberositics. The weight of the vertebræ, therefore, no longer passes from the sacrum to the femur by the superior sacro-iliac ligaments and the cotylo-sacral beam, but directly through the anchylosed joint; that is to say, from the upper to the lower extremity of a single and much-curved bone. Such a bone necessarily bends still more, and the increase of its curvature occurs about its middle, which is just external to the anchylosed joint. The only flattening which takes place is between the abrupt curvature of the cotylo-sacral beam and the pubes, and is due to the pressure of the bone itself against the top of the femur.
ART. IV. On Secondary Deposits and Mortification from Disease of the Arteries.
By HENRY LEE, Surgeon to King's College Hospital, and to the
Lock Hospital. As in some of the lower animals it may be shown that different segments possess independent vitality, so in the higher may it he as
clearly demonstrated that every part has a life of its own; and that this life is capable of being maintained for a time independent of the rest of the system with which it is naturally associated. A portion of blood, for instance, may be taken from an animal, and after remaining separate for a short time, may be again infused, so as to remain part of the living organism. Teeth, it is well known, have been transplanted in a similar way, as have also other parts of animal bodies. Such experiments clearly prove that although incapable of continued independent existence, each part may live, when separated from the rest, for a given time. Union implies reciprocal action; a dead part cannot unite with a living part. A tooth, therefore, which in its new relations shall adhere and grow, must have maintained its life when separated from its original bed; or a testicle removed from one animal, and placed in the peritoneal cavity of another, must in like manner, before it could have formed new adhesions and relations, have maintained for a time its own independent life. Mutual interchange of elements is essential to the continuance of existence. If a part cease either to receive, for any length of time, supplies from other parts, or to give off from the body, or back into the system, those elements which are redundant, it dies. The means by which this mutual interchange is effected in all the higher animals, is the circulation of the blood. The circulation, then, may be regarded as diffusing life through animal bodies; and the flowing blood may be looked upon as the life-sustaining stream of the various organs of which those bodies are composed. But as the bloodvessels are the means of conveying a life-diffusing energy to every part of the body, so may they be the means of carrying deadly influences. The stream which naturally is intended to support life, may itself contain the elements of death. The fatal influence may spread from the central and more vital organs to distant parts, or it may be communicated from any remote part to the centre, and thence again to the whole system.
The causes which induce separation, stagnation, and ultimate death of portions of the blood while in the living vessels, may therefore, as far as these affections present themselves to the surgeon, be divided into three classes namely, 1st. Those which depend upon morbid deposit in the coats of the vessels, and subsequent discharge of that deposit into the current of the blood. 2nd. Those which originate in a division of all the coats of a vessel, either from injury or ulceration, and the admission of diseased secretion from surrounding parts, 3rd. Those which originate in some morbid action in the blood itself. In the first of these divisions may be included diseases affecting principally the arteries, and in which the materies morbi is carried from the centre of the circulation towards the circumference. In the second may be considered diseases of the veins, in which the morbid products are, on the contrary, carried, in the first instance, from the more distant parts of the body towards the inore central and vital organs. The third division is alike common to arteries and veins, and to the structure of organs which intervene between their terminal branches.
Magendie, * from the experiments which he performed, was induced to believe that fluids introduced into the arteries of animals returned quickly through the corresponding veins, and that this occurred even more rapidly in the living than in the dead body. The experiments of M. Gaspard, however, show that while some fluids pass readily from the arterial to the venous system, others do so with much difficulty or only after the lapse of a certain time; and it is probable that there may be others, again, which cannot do so at all without previously undergoing certain changes. Some clear fluids—such as solution of tartar emetic, of opium, and of nux vomica, when introduced into an artery, pass readily in the course of the circulation, and produce their full effect upon the constitution. In such cases, where the passage of the morbid matter is not opposed, little or no irritation is manifested in the organs through which they first pass. The first of the abovenamed poisons produces vomiting and purging, the second stupor, and the third tetapic rigidity, when injected into an artery, exactly in the same manner as if introduced into the stomach, or injected into a vein; but no great pain or loss of power is experienced in the limb upon which the experiment is made. On the other hand, M. Gaspard found that when introduced into an artery, the infusion of tobacco neither produced vomiting nor purging; the solution of acetate of lead did not act upon the intestines, and putrid fluids did not produce those copious alvine evacuations which commonly follow the introduction of the same fluids into a serous cavity, or into the veins. The injection of acetate of lead, however, produced the signs of local inflammation in those parts to which the artery was distributed; the muscles which it supplied became of the reddish-black colour, and the whole limb had the appearance of having been affected with gangrenous inflammation. The introduction of tartar emetic, in the same way, produced slight local symptoms, but was followed by diarrhea and fatal vomiting. Experiments like these clearly indicate that some extraneous substances when introduced into the blood, expend their action by producing a local, although perhaps most severe, disease; while others which circulate more freely with the blood, leave no trace of irritation in the first system of vessels through which they pass, but expend their influence upon some part to which their action is peculiarly determined, or produce a constitutional affection.
Changes of various kinds are found after death in the coats of arteries. These consist chiefly of steatomatous or atheromatous de posit, and of cartilaginous or bony thickening. These changes consist essentially in an alteration of the nutrition of the part, and may give rise to inflammation, as a secondary effect, in the coats of the arteries." Two principal forms of atheroma may be distinguished; one consists of a gelatinous deposit on the internal surface of the vessel, the other of yellow spots either on the surface of the internal membrane, or in
Précis Elémentaire de Physiologie, tom. ii. p. 389. † The description of the morbid changes which the coats of arteries undergo is taken from Lebert's Anatomie Pathologique, PP. 312
natomie Pathologique, pp. 512–13.
its substance. The first is originally semi-transparent, grey, or reddish. It becomes subsequently opaque and white, and connected with the lining membrane. The structure of this deposit is generally amorphous and fibroid. After a time, these patches become drier, more opaque, and may assume a reticular appearance. The second form of atheromatous deposit is by far the most common. It consists of irregular patches deposited in the substance of the internal membrane or beneath it. These patches by degrees become thicker, and may extend to the middle coat, the circular fibres of which may become softened and more or less altered in structure. Subsequently these spots may become either hardened or softened, and these conditions may co-exist, at the same time that there is the gelativous deposit on the surface of the lining membrane. The pultaceous softening of the atheromatous disease commences in a small spot, and raises the internal membrane in a pustular form. This appearance has often been mistaken for an abscess. Under the microscope this softened matter is found of a yellowish-white colour, containing molecular granules, vesicles, or granules of fat, crystals of cholesterine, calcareous granules, and débris of the elements of the middle coat. The internal membrane, instead of being raised in a pustular form, is often eroded and worn away. A crack is thus first formed, then an erosion, and finally an ulcer of greater or less depth. The atheromatous ulcers present, besides the elements above mentioned, little coagula of blood deposited on their surface. Of these the only traces that often remain are the brown or blackish stains which they leave when removed by the current of the blood.
The edges of the atheromatous ulcer are flat, uneven, thin, detached, occasionally undermined by the blood. The base is uneven, of varying depth, extending sometimes to the outer coat, which then becomes thickened. This thickening is accompanied by a certain degree of congestion.
When the morbid product is firmly adherent to the coats of the vessel, a deposit of fibrin from the blood may take place which will then temporarily unite the torn edges of the divided lining membrane, and cover the ulcerated surface. But if the atheromatous disease in the artery has undergone any great degree of softening at the time the internal coat gives way, then its more fluid parts become necessarily mingled with the blood, and carried to a greater or less distance in the course of the circulation. The same general effects may then be produced, whether these morbid deposits be poured into the circulation as now described, whether similar morbid matters be generated in the blood itself, or whether they be brought from some distant part of the vascular system. There is this important local difference, however, that when any morbid matter is generated in an artery, it will necessarily expend its first and principal influence upon the parts to which that artery is distributed. The remainder of the system may or may not then be directly affected.
Disease of the arteries has very generally been considered as a cause of mortification, and the diseased conditions have by most authors
been attributed to inflammation of the arterial coats. Earthy concretions, for instance, in the arteries of the lower extremities, since first noticed by Cowper and Naish, have been regarded as the cause of the closure of the arterial canals, and of the consequent mortification of the extremities. But, as is observed by Mr. Hodgson," our knowledge of the power of the collateral circulation in every part of the body will not allow us to admit the obliteration of the trunks as a sufficient cause of mortification from a deficient supply of blood.” Some other cause of this kind of mortification had then to be sought, and a sufficient one was thought by some writers to have been found in the theory, that if the large arteries were diseased, the small ones would be so also; while others have supposed that the want of elasticity and organic power would interfere with the due supply of blood, in a degree sufficient to account for the effects observed in gangrene. Both these suppositions are entirely devoid of proof; for although in cases of dry gangrene the arteries are often found to contain bony deposits, and the smaller arteries are also sometimes found diseased, yet are these deposits not found in those situations in which the gangrene actually takes place, for instance, in the pulpy vascular extremities of the toes, in the lips, cheeks, or lobes of the ears. In the arteries of the size here found is there never any bony deposit detected. That gangrene is not necessarily connected with disease of the arteries, is proved by the fact that it often occurs when no such disease is suspected. And, on the other hand, M. Cruveilhier has shown* that an artery which supplies a limb may be obstructed for a very considerable distance without any mortification following. If, however, an irritating injection be thrown into such an artery, mortification may readily be produced. It is remarkable that secondary mortification seldom attacks those structures which have a scanty supply of arterial blood, but that, it almost invariably shows itself first in those parts which have the largest supply of blood vessels. The vascular cheeks and lips in children, the vascular extremities of the toes in those in advanced age, are parts very frequently affected. If a simple deficient supply of blood were the cause of mortification, in such cases we should expect to find it first developing itself in the tendons and ligaments, and we should anticipate that the cellular tissue would perish always before the skin. The reverse of all this in secondary forms of morti. fication ordinarily occurs. The parts in which mortification in general shows itself have in truth a wonderful power of sustaining their hile with a very small supply of arterial blood, and for a short time even when separated from the body. This fact is amply illustrated by the way in which portions of skin may be actually severed from fingers and reunited, or by the length of time that a flap of skin takes from the forehead will maintain its life when converted into an art... cial nose. In a case recently under the author's care, a flap of Sa, was taken from the side of the chest and placed across the neck in centre of the cicatrix of a burn. It appeared to unite favourabiy, its new position, when the patient suddenly got into very bad he
Anatomie Parlologique, rol. ii. p. 301.