Aorta

The ascending aorta, like the pulmonary artery, was very wide; the valves of the former were thickened at their insertion and their nodules, and were partially ossified. The cellular sheath (the elastic and cellular coats) of the aorta was loosened throughout its entire length round the ascending portion, at its arch and on the whole of the thoracic and abdominal aorta, over full a third of its circumference, where there adhered to it either a thin layer or partially exfoliated thicker portions of the yellow coat. This condition extended upwards over the arteria innominata to the common carotid, the right subclavian and its larger branches, and downwards over a portion of both the iliac arteries; in the former the cellular sheath was entirely separated over the whole circumference of the artery, while in the latter it was only partially loosened, or admitted of being easily detached all round, together with the external layer of the middle coat. The same condition was observed in most of the small and large branches of the thoracic and abdominal aorta for a considerable extent of surface from their points of departure. The cellular sheath was of a bluish-red color, infiltrated with blood at many parts of its detachment, and very thick; at those points, however, at which a layer of the yellow coat still adhered to it, and where the two were not entirely separated, it was paler and less thick from a deficiency in the suffused blood, and was intersected by a highly developed network of vessels. The free space between this and the yellow coat of the vessel was filled with a considerable quantity of coagulated and fluid blood.

Within the cellular sheath, which was detached, as we have already seen, from the ascending aorta, the yellow and lining membranes were torn transversely over an extent of an inch and three-quarters above the valves, so that there remained only a spiral strip of their posterior wall (about two lines and a half in breadth, and equal in length to about half the circumference of the aorta), which connected together the two extremities of the rent, and was raised along the concavity of the trunk of the aorta from its original horizontal position, in consequence of the displacement of the upper extremity of the rent, which we shall now proceed to notice.

While the lower extremity of the rent was turned upwards with an almost circular opening, in consequence of the exposed transversal rent, the upper one was almost entirely enclosed by the convex wall and driven into the cavity of the arch of the aorta as far as the left subclavian, the entrance of which was even obstructed by a conically rolled portion of the tube of the aorta, so that a communication was opened from the subclavian into the inserted vessel, and through this into the cavity of the cellular sheath.

In this manner, both the extremities of the rent were from about an inch and a half to an inch and three-quarters from each other, while within the almost saccularly expanded cellular sheath at this spot, as well as over the whole extent of the aorta and the branches already referred to, the space between it and the yellow coat of the artery was completely filled with coagulated and fluid blood. This accumulation of blood had compressed the aorta and the coeliac axis at different points, and completely detached from their origin several small branches of the aorta and a large branch of the renal artery on the left side.

The blood had been further extravasated from this space into the pericardium and the mediastinum, in the following manner. The cellular sheath of the ascending portion of the aorta was torn outwards and backwards along the descending Vena cava, near its opening into the auricle, in a longitudinal direction, together with the portion of the pericardium by which it was invested. This sheath was also considerably attenuated at several points along the descending aorta, where it readily admitted of being torn.

The yellow coat of the artery could be easily peeled off in all parts, but more particularly at the aorta itself; it was also very brittle. Several small bony plates were observed in the lining membrane of the arch of the aorta.

The intestines were pale throughout, although this pallor was especially perceptible at some circumscribed portions of the ileum where the mucous membrane was perceptibly attenuated, and had even wholly disappeared.

When we consider the appearances here presented, with a view of ascertaining the relation of the different coats of the artery in their physiological and pathological condition, we arrive at the following theory, viz., that a detachment of the cellular sheath occurs spontaneously at a certain stage of its disease, giving rise at the same time to laceration of the two inner coats. These coats are usually torn transversely along the course of the yellow fibres, in consequence of the artery being deprived, at the moment when the cellular sheath is detached, of the support which had limited its further expansion and stretching. Such a laceration is also the more readily effected, when the two inner coats, notwithstanding the integrity of their texture, are unable to resist this expansion and tension from having become soft and brittle, owing, as is commonly the case, to advanced age, or to the dilatation of the vessel which is observed in all such cases.

The detachment of the cellular sheath must, therefore, constitute the 'primary agent or cause, while the laceration of the inner coats is the consecutive effect of this condition.

It is, however, probable that this may admit of a different explanation. Thus, for instance, we are unable to apply this theory when, in addition to the cellular sheath, an adhering layer of the yellow coat is loosened with it at the spot of the laceration, and when, therefore, the rent itself affects only the inner layer of this coat (with the lining membrane of the vessel). Another theory suggests itself when we consider that dilatation of the vessel is present in all cases. This dilatation depends, in all probability, upon the paralysis of the elastic layer, owing to a chronic inflammation of the cellular sheath; and the laceration of the yellow coat of the artery might therefore be the final result of the greatest dilatation it was capable of resisting without any considerable disturbance of texture of the whole arterial wall. Laceration will, moreover, be the more readily effected in proportion to the brittleness of the yellow coat dependent on the advanced age of the patient.

In accordance with this view, the rent in the lining and yellow coats must be the primary occurrence, and the loosening of the cellular sheath, either with or without an adhering layer of the yellow coat, must be regarded as a secondary result owing to the forcible escape of blood from the rent. The following conditions appear from our observations to be worthy of notice as controlling causes:

The heart is hypertrophied in all cases, and its left ventricle is in a state of active dilatation. In most cases the laceration is effected without any special excitement of the heart's action, so that the occurrence must be regarded as the final result of the diseased condition of the vessel.

The integrity of the detached cellular sheath, that is to say, the hinderance thus opposed to the free extravasation of the blood, occasionally postpones the fatal termination for a few hours; in Laennec's case death was delayed for four days.

The cellular sheath is generally lacerated in consequence of its distension by extravasated blood, usually in the vicinity of the lining membrane of the artery, but occasionally, however, at one or more spots remote from that rent.