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GENUINE FATTY METAMORPHOSIS.

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If sections are made in such a case in the neighbourhood of the surface and parallel to it, we readily obtain a view embracing the fattily degenerated tubules by the side of more normal ones, and of unaffected glomeruli. With a lower power and by transmitted light, we see close to the Malpighian bodies which appear as large, light, globular structures, the convolutions of the degenerated uriniferous tubules interlacing in various ways, and the convoluted tubules distinguished by their opaque, shaded appearance from the straight ones, which are lighter and more translucent.

I will here call your attention to the circumstance, that in all fatty parts, where, by reflected light and as we usually view objects with the naked eye, we see whitish, yellowish, or brownish-yellow parts-by transmitted light, as generally employed for microscopes, and especially with the higher powers, either black, or brownish black, or at least very dark parts, surrounded by sharply-defined shadows, appear. A granule-globule which, when lying together with several others, produces a spot white and opaque to the naked eye, will, when viewed by transmitted light, display a nearly black appearance.

We have now compared a series of examples of fatty degeneration, and may henceforth confine ourselves to the consideration of genuine fatty metamorphosis, in which the normal structure of the part is ultimately destroyed, and the place of the histological elements is gradually occupied by a purely emulsive mass or, more concisely, fatly débris. It makes no difference whether it is a puscell, a connective-tissue-corpuscle, a nerve- or muscular fibre, or a vessel which experiences the change; the result is always the same; namely, milky débris, an amorphous accumulation of fatty particles in a more or less highly albuminous fluid. But though we hold to the agreement of all cases of fatty metamorphosis in this respect, it by

no means however follows, that the importance of this change as a morbid process is in every case the same. This you may at once infer from the circumstance, that, whilst I have introduced this process to your notice in the category of purely passive disturbances, one of the very structures which we most frequently find in it, the granule-globule, has been regarded as a specific element of inflammation. For For years an inflammatory globule [exudation-corpuscle] was looked upon as an essential phenomenon in the process of inflammation, and in fact, the frequency with which cells in a state of fatty degeneration are found in inflamed parts, affords sufficient proof, that in the course of inflammatory processes, which it is impossible we should ever regard as simply passive processes, such transformations must take place. It is therefore very essential to find a means of distinguishing between the two classes. This offers indeed in particular cases very great difficulties, and according to my conviction the only possible method by which clear notions upon the subject can be obtained, consists in examining whether the condition of fatty degeneration is a primary or a secondary one, whether it sets in as soon as the disturbance can be perceived, or whether it does not occur until some other perceptible disturbance has gone before. Secondary fatty degeneration, or that in which this peculiar transformation occurs only in the second place, generally succeeds to a first and active stage; a whole series of those processes which we do not scruple to call inflammations run their course in such a way, that a fatty metamorphosis sets in as the second or third anatomical stage of the change. Here therefore the fatty degeneration does not arise as a direct result of the irritation of the part, but where we have the opportunity of more accurately tracing the history of the changes, it nearly always turns out, that the stage of fatty degeneration has been preceded by another stage, namely that of cloudy

INFLAMMATORY FATTY DEGENERATION.

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swelling, in which the parts enlarge and increase in extent and density, in consequence of their absorbing a large quantity of matter into themselves. Absorbing I say advisedly, because I hold it to be untrue that the part is in any way forced by external influences to take up this matter, or that it is inundated with exudation proceeding from the vessels, for the same phenomena present themselves also in parts which have no vessels. It is only when the accumulation has attained such dimensions, that the natural constitution of the part is thereby endangered, that a fatty disintegration is set up in the interior of the elements. Thus we may designate fatty degeneration of the renal epithelium as a stage of Bright's disease (or as I say, parenchymatous nephritis), which has been preceded by a stage of hyperæmia and swelling, in which every epithelial cell accumulated a large quantity of cloudy matter in itself, without there having been originally a trace of a drop of fat observable. Thus we see that a muscle under the influence of agencies which it is universally conceded produce inflammation, as for example after wounds, and chemical corrosions, swells up, that its primitive fasciculi become broader and more clouded, and that as a second stage the same fatty degeneration commences in them, which at other times we see primarily arise.

It may therefore certainly, when quite general terms are used, be said, that there does exist an inflammatory form of fatty degeneration; still, strictly speaking, this inflammatory form is never anything more than a later stage, a termination, which announces the commencing disintegration of the structure of the tissue, when the part is no longer in a condition to continue a separate existence, but is to such an extent abandoned to the play of the chemical forces of its constituent parts, that the next result is its really complete dissolution. Now inflammatory conditions of this kind are of very great importance, because in all

parts whose essential elements become changed in this manner, no immediate restitution is possible. When inflammation takes place in a muscle and in its course the primitive muscular fasciculi fall into a state of fatty degeneration, as a rule they also perish, and we afterwards find a loss of substance in the muscle at the spot where the degeneration took place. The kidney, whose epithelium has passed into a state of fatty degeneration, nearly always shrivels up, and the result is a permanent atrophy. In exceptional cases something perhaps occurs, which reminds us of a regeneration of the epithelium, but usually a collapse of the entire structure ensues. The same thing is witnessed in the brain in yellow softening, no matter how it may have been caused. Whether there have been inflammation or not, a vacuity is formed, which is never again filled up with nervous matter. Perhaps a simple fluid may replace the wanting tissues, but as to any reproduction of a new, functionally active part, that must ever be out of the question.

Herein you must seek the explanation of the circumstance, that conditions apparently very similar, and which from a pathologico-anatomical point of view might be declared to be identical, in a clinical point of view lie widely apart, and that the same forms of changes are met with in analogous parts, without, however, the whole process, to which they belong, being the same. When a muscle falls into a state of simple fatty degeneration, its primitive muscular fasciculi may have just the same appearance as if inflammation or permanent tension had acted upon it. Myocarditis generates forms of fatty degeneration in the substance of the heart altogether analogous to those due to excessive dilatation of the cardiac cavities. When one of these, for example, either through some obstruction to the current of the blood, or from insufficiency of the valves, is permanently much dilated,

ATHEROMATOUS AFFECTION OF ARTERIES. 353

fatty degeneration of the muscular tissue constantly manifests itself in the part which has been most stretched. This form, morphologically speaking, completely resembles the early stages of myocarditis, and in many cases it is utterly impossible to say with certainty in what way the process may have arisen.

I have, in order to clear up to some extent these difficulties, as they are presented by an important, frequent and at the same time much misunderstood process, prepared a series of specimens exhibiting really atheromatous conditions of the arteries. For it is particularly in the case of these conditions that the confusion, which has prevailed with regard to the interpretation of the change, has perhaps been the greatest.

At no period in the course of this century has a complete understanding ever been come to as to what was to be understood by the expression atheromatous change in a vessel. Some have taken the term in a wider, others in a narrower sense, but still it has perhaps been taken in too wide a sense by all. When, namely, the anatomists of the last century applied the name of atheroma to a definite change in the coats of arteries, they of course had in their minds a condition similar to that of the skin, to which ever since the days of ancient Greece, the name of atheroma, gritfollicle, (Grützbalg) [sebaceous or epidermic cyst], had been assigned. It is self-evident therefore, that the idea of atheroma presupposes a closed sack. Nobody ever called anything in the skin an atheroma that lay open and uncovered. It was therefore a curious misapprehension when people recently began to call changes in the vessels atheromata, which were not seated below the surface and shut off from the surrounding parts, but belonged to the surface. Thus it has come to pass that, instead of an enclosed deposit being, in accordance with the original meaning of the term, called atheromatous, a change has frequently

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