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affected part is perfectly free and unobstructed. If we therefore leave inflammation on one side and confine our attention simply to the coagulation of the blood, to the formation of the clot (thrombus), it seems most convenient to comprehend the whole of this process under the term Thrombosis. I have proposed to substitute this term for the different names, phlebitis, arteritis, &c, inasmuch as the affection essentially consists in a real coagulation of the blood at a certain fixed spot.

Upon investigating the history of these thrombi, we find that the puriform mass which is met with in their interior does not originate in the wall, but is produced by a direct transformation of the central layers of the clots themselves, a transformation indeed which is of a chemical nature, and during which, with a result similar to that which can be artificially obtained by the slow digestion of coagulated fibrine, the fibrine breaks up into a finely granular substance and the whole mass becomes converted into debris. This is a kind of softening and retrograde metamorphosis of the organic substance, in the course of which from the very commencement a number of extremely minute particles become visible; the large threads of fibrine crumble into pieces, these again into smaller ones, and so on until after a certain time has elapsed the chief l'.$, part of the mass is found to be composed of small, fine, pale granules (Fig. 70, J). In cases in which the fibrine is comparatively very pure,

Fig. 70. Puriform mass of debris from softened thrombi. A. The granules seen in disintegrating fibrine, varying in size, and pale. B. The colourless blood-corpuscles set free by the softening, some of them in process of retrograde metamorphosis; a, with multiple nuclei, b, with simple, angular nuclei and a few fat-granules, c, non-nucleated (pyoid) corpuscles, in a state of fatty metamorphosis. C. Red blood-corpuscles undergoing decolorization and disorganization. 350 diameters.


we frequently see scarcely anything else than these granules.

You see, gentlemen, the microscope solves the difficulties in a very simple manner, by demonstrating that this mass, which looks like pus, is not pus. For we understand by pus a fluid essentially provided with cellular elements. Just as little as we can imagine blood without blood-corpuscles, just as little can pus exist without pus-corpuscles. But when, as in the present instance, we find a fluid which is nothing more than a mass pervaded by granules, this may indeed, as far as external appearance goes, look like pus, but never ought to be regarded as real pus. It is a puriform, but not a purulent substance.

But now we frequently see that in addition to these granules a certain proportion of other structures shew themselves, for example, really cellular elements (Fig. 70, JB), which are round (spherical), or angular, present one, two, or more nuclei, frequently lie tolerably close to one another, and in reality exhibit a great similarity to pus-corpuscles, the distinction at most being that very often fat-granules occur in them, indicating that a process of disintegration is going on. Whilst therefore in individual cases there can, on account of the often very greatly preponderating mass of debris, exist no doubt as to what the observer has before him, in others considerable doubts may exist as to whether real pus is not present. These doubts cannot be removed in any other way than by an examination into the history of the development of the puriform mass. Now that we have already seen that colourless blood- and pus-corpuscles perfectly agree with one another in form, so that it is impossible to draw a real distinction between them, the question which suggests itself in cases where we find round, colourless cells in a clot of blood, whether these cells are colourless blood- or pus-corpuscles, can only be decided by determining whether the corpuscles were present in the thrombus from its very


commencement, or only sprang up in it afterwards, or found their way into it in some other manner. Now upon accurately following up the different stages of the process, the very positive result is obtained that the corpuscles preexist, and that they do not arise within the clot, and are not forced into it. Even when quite recent thrombi are examined, the corpuscles are found in many places heaped up in great masses, so that, when the fibrine breaks up, they are set free in such numbers, that the debris are nearly as rich in cells as pus. It is with this process, just as when water which is thoroughly impregnated with solid particles is frozen and then exposed to a higher temperature; when the ice melts the enclosed particles must of course again come to light.

To this view of the matter one objection may be raised, to wit, that we do not see the red blood-corpuscles set free in a similar manner. The red corpuscles, however, perish very early; they are soon seen to grow pale; they lose a portion of their colouring matter and become smaller, whilst numerous dark granules appear at their circumference (Figs. 54, a; 70, C), and in the majority of cases they entirely disappear, nothing but these granules at last remaining. Still there are also cases in which the red corpuscles retain their integrity within the softening mass. As a rule they certainly perish, and it is precisely upon this that depends the peculiarity of the transformation, by means of which a yellowish white fluid arises bearing the external appearance of pus. And for it too an explanation may be found without any particular difficulty, if it be borne in mind how very trifling is the power possessed by the red blood-corpuscles of resisting the most various reagents. If to a drop of blood you add a drop of water, you see the red corpuscles disappear before your eyes while the colourless ones remain behind.

That therefore, which according to the ordinary nomenclature is called suppurative phlebitis, is neither suppurative, nor yet phlebitis, but a process which begins with a coagulation, with the formation of a thrombus in the blood, and afterwards presents a stage in which the thrombi soften, so that the whole history of the process is contained in the history of the thrombus. But here I must impress upon you that I do not, as has been said of me in different quarters, deny the possibility of a real phlebitis, and that I have not in any way discovered that there is no such thing as phlebitis. No ! phlebitis certainly does exist. But it is an inflammation which really affects the walls, and not the contents of a vessel. In the larger vessels the most different layers of their walls may become inflamed and enter upon every possible phase of inflammation, and yet all the while their channel remain entirely unaltered. In accordance with the views generally entertained the internal coat of the vessels was thought to be like a serous membrane, and as this readily furnishes fibrinous exudations or purulent masses, the same was supposed to be the case with the internal coat. Concerning this point a series of investigations was years ago set on foot, and I too have occupied myself at various times with it, but hitherto no experimenter, who carefully prevented the blood from streaming into the vessels, has succeeded in producing an exudation, which was deposited in their cavity. On the contrary, when the wall is inflamed, the "exuded matter" (Exsudatmasse) passes into the wall, which becomes thicker, cloudy, and subsequently begins to suppurate. Nay, even abscesses may form, which cause the wall to bulge on both sides like a variolous pustule, without any coagulation of the blood ensuing in the cavity of the vessel. At other times, certainly, phlebitis, properly so called, (and in like manner arteritis and endocarditis) is the cause of thrombosis, in consequence of the formation of inequalities, elevations, depressions, and even ulcerations upon the inner wall


which favour the production of the thrombus. Still, wherever phlebitis, in the usual sense of the word, takes place, the alteration in the coat of the vessel is almost always a secondary one, and indeed occurs at a comparatively late period.

The process runs its course in such a way that the most recent parts of the thrombus always consist of the blood which has most lately coagulated. The softening, the partial liquefaction, generally commences in the centre, in the oldest layers, so that, when the thrombus has attained a certain size, there exists in the midst of it a cavity of larger or smaller dimensions, which gradually enlarges and keeps approaching more and more closely to the wall of the vessel. But in general this cavity is shut off in an upward and downward direction by means of a more recent and tougher portion of the clot which, after the manner of a cap, takes care that, as Cruveilhier expresses himself, the "pus" remains sequestered, and all contact between the debris and the circulating blood is prevented. Only sideways does the softening extend until it at last reaches the wall of the vessel itself; this becomes altered, it begins to grow thicker and at the same time cloudy, and ultimately even suppuration takes place within the walls.

The same thing which we have hitherto considered in the veins occurs also in the heart. In the right ventricle especially we not unfrequently see what are called purulent cysts between the trabeculse of its wall. They project into the cavity like small rounded knobs, and form little pouches which, when cut open, contain a soft pulp that may present a completely pus-like appearance. People have plagued themselves to an indefinite extent about these purulent cysts and invented all possible theories to account for them, until at length the simple fact came out, that their contents are frequently nothing more than a finely granular pulp of an albuminous substance, which does not

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