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must be freely employed; but it should ever be borne in mind that the symptoms alluded to are only the secondary effects of a great and general constitutional disorder, and the general treatment required for the relief of that disorder must on no account be neglected. In rheumatic cases, alkalies and the neutral salts must still be administered in full doses ; and in renal cases, diuretics, purgatives. Blisters and counter-irritation are also serviceable.

In certain instances of pericarditis all ordinary treatment proves unavailing to induce absorption of the effused fluid, and the pericardium remains enormously distended for weeks after all traces of inflammation have disappeared. In these cases the patient suffers urgently from dyspnea, and medicine offers no prospect of relief. It has, therefore, been proposed to puncture the pericardium and draw off the fluid by means of a trocar, and cases have been reported in which this practice has been employed with a certain amount of success. The immediate relief has been very great, and in a few instances recovery has ensued.

I have no personal experience of this mode of proceeding, as no case has occurred in my own practice requiring the adoption of such an extreme measure, but in the event of its being had recourse to, the patient should be placed in a recumbent posture, and the trocar should be introduced between the fourth and fifth ribs, about half an inch from the left edge of the sternum, and the fluid withdrawn slowly, lest the heart should be embarrassed by the sudden removal of the pressure to which it had so long been subjected. Theoretically, I am inclined to believe that the less formidable operation of withdrawing a certain quantity of the fluid by means of a grooved needle would effect the desired object of relieving the heart, and would enable absorption of the remaining fluid to take place.

There is yet one point on which a few observations are needed. It has been already pointed out how readily in most instances the occurrence of pericardial adhesion may be determined when the course of pericarditis is carefully watched, and it might perhaps be imagined that the detection of pericardial adhesions is at all times an easy matter. Indeed, I know that an impression of this kind prevails amongst those who are not skilled in physical diagnosis. But nothing can be further from the truth. In most instances in which the patient is not seen for some time after pericardial adhesions have taken place, their diagnosis is a physical impossibility. Sometimes, as already pointed out, they do not interfere with the action of the heart, nor do

they induce any structural change, nor give rise to any characteristic alteration of the sounds; and even when, directly or indirectly, they occasion atrophy, hypertrophy, or dilatation of the heart, their existence must be mere matter of conjecture, inasmuch as they are not accompanied by any change in the action or sounds of the heart which can be regarded as in any way indicative of their existence. But although this holds good in the majority of instances, it is otherwise in regard to the exceptional cases in which lymph has been effused in the anterior mediastinum, and the pericardium has contracted adhesions to the anterior walls of the chest. Patients in whom this complication has occurred almost always present symptoms of the disease they have undergone which ought not to be overlooked by the practised physician. Thus, the heart is necessarily retained in the position it occupied at the time when adhesion took place, and as the apex is usually tilted upwards and slightly outwards during the acute stage of pericarditis, it is not unfrequently retained in that position afterwards, and may be felt and seen pulsating there. Further, the heart being retained so closely and so extensively in apposition with the chest walls, its action gives rise to an undulatory movement in the cardiac region, and each systole produces a slight retraction of the parietes in the fourth interspace, just above the apex. Important corroborative evidence is also afforded by the effect of respiration. When the heart is not agglutinated to the chest walls, the lungs encroach upon the præcordial region during full inspiration, its resonance on percussion increases, the intercostal spaces expand, and the sounds of respiration are audible there; but when the heart has contracted adhesions to the anterior walls of the chest, the lungs cannot push in front of the heart, and hence there is little or no expansion of the intercostal spaces in the præcordial region, the dulness on percussion remains uninfluenced even by the fullest inspiration, and extends further upwards than even in cases of cardiac hypertrophy, and respiratory sounds are altogether absent. Add to this a peculiar tumbling action which the heart acquires under these circumstances--an action which is most remarkable when the heart is hypertrophied and dilated—and the evidence of adhesion of the two surfaces of the pericardium to each other and of the external layer of the pericardium to the chest walls, is complete.

CHAPTER II.

ENDOCARDITIS-ENDO-PERICARDITIS -CARDITIS.

ENDOCARDITIS, or inflammation of the lining membrane of the heart, is a more common, and practically, therefore, a more important form of disease than pericarditis. Originating in an irritating, unhealthy condition of the blood, it is apt to be set up in acute rheumatism, and in the whole class of diseases already referred to as associated with the production of pericarditis; nay, more, it not unfrequently happens that endocarditis occurs coincidently with pericarditis, as the result of the same agency, and that endocarditis or endo-pericarditis, is accompanied by carditis or acute inflammation of the muscular structure of the heart itself.

The pathology of endocarditis is somewhat obscure, in consequence of the rarity of cases which prove fatal in the earlier stages of the disease, and of the difficulty, therefore, which is experienced in investigating its earlier pathological effects. It appears, however, from the few opportunities I have had of inspecting after death the changes which it produces in the human subject, as also from the valuable experiments of Dr. Richardson, who induced endocarditis by injecting lactic acid into the peritoneum of dogs,* that the first effect of inflammation of the endocardium is the production of intense vascularity of the membrane, with a swollen condition of the valves, and, occasionally, the exudation of transparent lymph, or the deposit of fibrin on their surface. At a subsequent stage the vascularity of the surface begins to subside, the valves are still swollen, but the exuded matter within them is more solid than before, and any existing fibrinous deposits are more firmly adherent to the surface. At a still later stage, the abnormal vascularity entirely disappears; the exudation within the valves is partially and irregularly absorbed, so that the edges of the valves become thickened and beaded; the fibrinous deposits become firmly agglutinated to the valves, and the natural transparency of the membrane is replaced by whiteness and opacity.

* I had the privilege of witnessing these experiments of Dr. Richardson, and the results were most remarkable. Not only was acute articular rheumatism produced, but endocarditis which was recognised by auscultation during life, and resulted in the production of its usual post-mortem appearances, was observed in several cases. For full particulars, see Richardson On the Coagulation of the Blond,' p. 371, et seq. * Many of the following remarks are taken from the chapters “On Inflammation of the Heart,” contained in my work on ‘Rheumatism, Rheumatic Gout, and Sciatica.' My views on the subject remain unaltered, and I therefore venture to quote them here.

The changes just described are those which occur in the milder forms of the disease; but they convey no adequate idea of the mischief produced by the more formidable attacks, nor of the extent to which fibrinous deposition may proceed, nor of the transformations through which the fibrinous deposits or vegetations may pass. Therefore, as fibrinous deposits constitute the most common form of endocarditic valvular lesion—especially in connection with rheumatism—it may be desirable to examine the subject a little more in detail.

Fibrinous vegetations* are sometimes found in all the different chambers of the heart, and they are especially apt to be so in the left auricle, but in most instances they are confined to the valvular apparatus, or its immediate vicinity, and the mitral and aortic valves—the valves, which are constantly bathed in highly fibrinised arterial blood-are those which are peculiarly liable to suffer. The right cavities, however, with the tricuspid and pulmonary semilunar valves, are sometimes, though rarely, affected.+

Fibrinous vegetations are often very numerous, and commonly vary in size from that of a pin's head to that of a millet seed. In one case they are isolated and distinct from each other, at another, partially confluent; and when several spring from a common base, they may form a mass of considerable size. Sometimes when fibrinous accretion has taken place rapidly, as it does in certain conditions of the blood, their form is changed, and the action which in other states of the system might have resulted in the deposition of small warty granules along the edges of contact of the valves gives rise to the production of long, filamentous growths, or of large pedicled masses, forming pendulous tumours, which hang loosely into the ventricle, and are moved to and fro by the current of the blood. I When the vegetations assume the former character, they are usually confined to the valves, and chiefly affect their edges of contact; so that in the sigmoid valves they are arranged in a double crescentic form ;* but when their growth is more luxuriant, as in the instances last alluded to, they are more widely distributed over the endocardial membrane. The surface of the valves against which the current of the blood is directed is often thickly studded with them; on the edges of contact of the valves they form festoons or fringes; the chordæ tendineæ attached to the mitral valve are sometimes loaded with an abundant crop of them; and, occasionally, in the different chambers of the heart, more especially in the left auricle, they are scattered profusely over the entire surface of the lining membrane. Judging from my own experience, the cases in which these last forms of vegetation occur are just those in which, either from some constitutional peculiarity, or from some other cause equally beyond our ken, these accretions manifest a strong tendency to decay, and in which arise the formidable erosions and ulcerations, to which I shall presently have to refer.

of For cases in point, see · Edin. Med. and Surg. Journ.,' vol. v.; also, a case recorded by my late colleague, Dr. Wilson, in the Lancet' for 1844, vol. ii, p. 217.

I Some of these masses, measuring from half an inch to an inch in length, are preserved in the museum of St. George's Hospital.

The microscopic examination of these fibrinous deposits establishes the identity in nature of their different forms, and shows that they are sometimes granular, but more generally imperfectly fibrinous in texture, presenting somewhat of a laminated appearance; and that throughout their structure are numerous granules and oil globules in varying proportions. In many old-standing cases, cartilaginous and calcareous matter is found in the valves, and in the fibrinous vegetations, as the result of earthy or atheromatous degeneration which has taken place subsequently to the attack in which the valves were injured, or the fibrin first deposited.

In colour and consistency these concretions vary just as much as in size and in position. At first, they are of a pink or reddish colour, soft, and easily broken down, and can be readily detached from the smooth surface of the membrane on which they are deposited; subsequently, they become less coloured, and of a much firmer consistence, but still admit of being separated from the membrane, whilst, after a still longer period, they become perfectly colourless, and so firmly adherent, that they can be removed only by tearing the membrane to which they are attached. At a still later date, these warty growths or bead-like accretions cease in most cases to exist, as such, upon the valves ; they become by degrees incorporated with the structure of the valve, and, merging gradually into one another, until the divisions between the several granules are effaced, they are ultimately replaced by a laminated ridge of fibrin. This at first is marked by serratures corresponding to the divisions between the original granules; but after a time it also loses

* For explanation of this, see Dr. Watson’s ‘Lectures, ed. i, vol. ii, p. 267.

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