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PRODUCTS OF INFLAMMATION; FIBRINOUS EFFUSIONS.

LECTURE VI.

PRODUCTS OF INFLAMMATION.

I. Fibrinous effusions; ulterior changes of fibrin; collateral illustrations from anatomy of intra-vascular clots.-II. Generation of cytoblasts.-III. Their ulterior progress; pus; glomeruli-their relation to dissolution of blood; suppuration-on mucous surfaces, in solid organs; distinctions of adhesive and suppurative inflammation, and circumstances determining them. IV. Vascularity of new tissues.

GENTLEMEN: In the present lecture I purpose sketching for you the chief changes which occur in inflammatory effusions; those changes at least which lead to suppuration, or to chronic thickening in organs.

I must begin by carrying you back to the subject of my last lecture, and by reminding you of what occurs when the capillary bloodvessels are overloaded with blood. I stated to you that, under these circumstances, the capillaries suffer a certain proportion of their fluid contents to exude. I stated likewise that they change this fluid as it exudes; and that the change thus accomplished (which distinguishes the serous fluid in question from the plasma of the blood) will vary, according as the pressure which drives it through is little or much above the healthy and normal pressure of the circulation. If the pressure be very slightly in excess, the material which transudes is a weaker solution of the salts of the blood with a trace of albumen; as the pressure increases, the proportion of albumen becomes larger; at length fibrin is found, perhaps only in flakes; a stage further, and it becomes sufficiently plentiful to impart to the transuded material the property of spontaneous coagulation; and finally the pressure may be such as to cause the rupture of the capillary vessels, and impart to the effusion a more or less considerable admixture of blood-corpuscles.

These various degrees are well illustrated in the pathological history of the kidney. If you have hyperemia of that organ induced, either by interference with its escaping blood, or by too much impulse in that which goes to it, an increased exhalation occurs into the urinary tubules, and you get the symptom called albuminuria—one precisely analogous in its method of production to that of ordinary serous effusion in the cellular tissue of the body. If the disease advance, the Malpighian tufts pour out not only serum, but fibrin; and in this stage, if you examine the urine microscopically, you find this fibrin in the shape of little threads: these are accurate casts of the minute urinary tubules into which the fibrin was originally poured, and from which it often brings down, entangled in its substance, a certain quantity of the cell-growth of the tubule, the epithelium or

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endothelium. Finally, go a stage farther, and instead of seeing these little threads transparent, colourless, and of pure fibrin, you see a quantity of blood-corpuscles entangled in them; the capillaries of the Malpighian tufts have broken with the pressure, and have let all the elements of their blood escape; so that, instead of getting a mere fibrinous mould of the microscopical tubule, you get its little mould made of a thread of coagulated blood. These changes exactly illustrate the history of congestive and inflammatory effusion in all organs of the body; and as the kidney is peculiarly liable to such diseases-diseases, moreover, which are of the utmost interest and importance, you can hardly select a more convenient organ for exhibiting the changes in question.

And now, gentlemen, the inquiry that peculiarly belongs to our lecture of to-day is-what becomes of these inflammatory effusions when they are retained in the body? How do they terminate?

In approaching the consideration of this subject, remember, as the key for its right understanding, that the serous or fibrinous, or even bloody, effusion, of which I have spoken (if it occur from increased determination of blood to the part) is, in the strictest language of physiology, only an exaggeration of that ordinary nutritive supply, which conveys to the various organs of the body, and diffuses amidst their elements, the natural materials for growth. Remembering this, you will be prepared for knowing that all the true and immediate terminations of inflammation are processes of growth; accelerated processes, it is true, or perverted processes; but still processes essentially accordant with those by which the tissues were originally formed in the embryo, and are continually renovated in the adult.

Cell-development, formation of fibre, formation of vessels-these are the true and immediate terminations and tendencies of the inflammatory process; for the destruction of parts, in their molecules or masses, by softening and ulceration, or by gangrene-this occurs only incidentally in the process, only by indirect causation, and by the introduction of other influences than those which are essential to inflammation. To those primary and natural terminations I shall therefore at present confine myself.

The first changes which arise in an inflammatory effusion-changes often almost synchronous with the very act of effusion, are (1) the coagulation of its fibrin, and (2) the origination of cytoblasts.

1. Fibrin seems to coagulate in inflammatory effusions (just as in blood extravasated either within or without the body) by reason of its own specific physical qualities, and independently of any vital influence derived from surrounding parts. Indeed, I may go may go farther than this, and may say that the coagulation of fibrin occurs in spite of the influence of the surrounding living textures; for, just as effused blood will often remain for a long while uncoagulated within the body, while in contact with living parts, and while maintained at their temperature (as, for instance, in a serous cavity) and will soon become clotted when you let it flow forth into some dead receptacle;

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ULTERIOR CHANGES OF FIBRIN.

just so will many inflammatory effusions refuse to coagulate while maintaining their original contact with an atmosphere of living parts, but will rapidly gelatinize, or at the least will precipitate flakes of fibrin, when artificially withdrawn from the body, and placed at rest in some foreign vessel. Even in so chronic an effusion as hydrocele, it is by no means infrequent to see transparent fibrinous clots form in a fluid which, at the moment of its traversing the canula, was perfectly free from such deposits. In short, the coagulation of fibrin is its rigor mortis, a change which essentially belongs to it as part of its process of death-a change which befalls it (1) when the whole bodily life ceases; or (2) when the blood in which it is contained dies prematurely and separately by withdrawal from the body; or, (3) under the circumstances now before us, when, either with or without the coloured elements of the blood, it is exuded or otherwise discharged from within the vessels, and is set stagnant and moribund amid the living textures of the body.

Under the microscope, you can commonly recognize coagulated fibrin by its clear, colourless, homogeneous, refractive substance; by its firmness and extreme elasticity; by the interspaces which are left in its mass, giving it the character of a network; and by a fallacious appearance of fibrous structure which is connected with its reticular coagulation. Sometimes you find the same material coagulated in small, separate flakes, which are perfectly structureless; and often you may see some such flakes as these lying unchanged amid the progressing products of inflammation.

You probably remember that, in speaking to you of the blood, I assigned some reasons for considering its fibrin an excrementitious product in the circulation, and consequently for hesitating to believe that it contributes to renovate the tissues of the body. I described to you its occasional increase in the blood, under circumstances apparently quite incompatible with its possessing the higher significance imputed to it by some writers; and I offered you an explanation of those endocardial valve-deposits which occur in rheumatic fever, to the effect that they might plausibly be considered as mere passive precipitations of fibrin, derived from a fluid overcharged with that product, and attaching themselves to a spot which offers mechanical facilities for their adhesion. These topics, relating to the natural offices of fibrin in the blood, are brought before us again to-day by our having to determine, what is the function fulfilled by it when it enters into true inflammatory effusions, and of what ulterior development does it become susceptible in its various abnormal relations.

On these points it is difficult to speak with certainty. Taking the fibrin separately, I should say that its tendency is to contract closer and closer together, with a vague appearance of striping, sometimes reticularly, sometimes with a disposition to tear in one direction rather than in another; but that this character is lost in the progress of contraction, and the nodule of pure fibrin becomes at length converted into a structureless granule of gristly firmness, which often becomes the seat of calcareous deposit. Such material

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is often found in the peritoneum (where it is very wrongly confounded with the products of scrofula, under the name of tubercular peritonitis) and in a variety of other situations, besides forming those vegetations and thickenings, to which I have already adverted, in the interior of the vascular system. In this state, with very little change, small nodules of fibrin may be retained as permanent concretions; possessing, perhaps, just enough participation in the nourishment of the adjoining surface to maintain their half-vital existence. Or, on the other hand, there may occur in fibrin the changes which I have already spoken of, as its softening and fatty degeneration changes in which it becomes diffluent, presenting, under microscopical examination, an infinite number of the minutest granules, many of which are fatty, some, perhaps, proteinous. This is no doubt the final death and decay of fibrin; and it becomes matter of exceeding interest to know whether it be in this way that the fibrin of the blood naturally degenerates, previously to its elimination; and it is from their relation to this question that great interest is given to some recorded cases, in which a large proportion of fatty matter has been found in the blood, under circumstances which would rather have led the observer to anticipate an excess of fibrin.

It

appears, then, that fibrin may remain stationary, and be nourished; or it may degenerate and decay: thus much is certain. But, may it advance? may it be developed into any higher form? into any tissue?

Notwithstanding the prevalence of a very general opinion to the contrary, I believe I may venture to question its possession of this power, and may say that I entertain extreme doubt whether, of itself, it ever shows the slightest disposition to cell-formation, or to any process of self-development.

Unfortunately, our opportunities of watching its solitary behaviour are very few; for, in almost every instance that can be thought of, albumen (which is probably the real regenerator of the tissues) is likewise present; and that great developmental activity, so often and so glowingly ascribed to fibrin, may, with at least equal probability, be considered the work of this associated albumen, for which (on this latter assumption) the fibrin could merely be considered to furnish an inert mechanical support. For think, gentlemen, if fibrin were that restless element of growth and vital expansion which some have fancied it, what a world of activity there would be in an aneurismal sac! A large aneurism, filled with laminated clot, has almost as much fibrin in it as the whole body put together; and yet it shows, on microscopical examination, no evidence of activity or of growth. At its circumference its pressure may have irritated surrounding parts, and may have provoked inflammatory effusion from them, but in the interior all is stationary and quiet. Towards the cavity, where the formation is most recent, lie the blood-corpuscles in a net-work of fibrin -the former in such numbers that the latter can but very imperfectly be seen; but in passing outwards, as the corpuscles seem more and more wasted, the fibrin begins to show more distinctly,

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always adapting its meshes to the material within them, so that innumerable blood-cells are seen, each in its separate setting of fibrin: in getting still nearer to the circumference of the sac, the arrangement becomes confused, from the closer consolidation of the fibrin; but in no part of the structure have I been able to see any trace whatever of new organization.

There is a similar reluctance to the initiation of organic development in those other intra-vascular clots which form in tied arteries. They undergo changes referable to their blood-corpuscles, and they become pale and contracted; but their fibrin may remain for many weeks, or perhaps permanently, unaltered, except for some increase of density. I have seen it after the lapse of six weeks, showing only a vague appearance of longitudinal striation, with no essential change of physical character, and without the slightest trace of new development in its substance.

In an elaborate paper written by Dr. Zwicky on the metamorphosis of the arterial clot, a series of observations is given, which might appear to conflict with this opinion, but which, in reality, I think, confirm it. Where organization of the thrombus has occurred, he finds that it has been preceded by the following steps: first, there was the well-known clot with coloured corpuscles embedded in its reticular interstices; then gradually (while conglomerate bodies collected chiefly towards the apex of the clot, and while the coloured corpuscles diminished in number) the mass lost its appearance of striation, becoming amorphous and porous; together with this change, its base became very capable of infiltration from the blood-vessels about the seat of the ligature; next (a fortnight after the operation) it began to show cytoblasts; and from that time onward, as blood-vessels gradually became demonstrable in its substance, it proceeded to develop nucleated fibres at an increasing rate. Now the extreme tardiness with which the development of cytoblasts occurred in these cases, contrasts remarkably with their quickness of growth in inflammatory exudation; and for this reason it seems to depend on some new influence being imparted to the clot by the prolongation of blood-vessels into its substance (a process with which it is apparently simultaneous) much more than on any specific faculty of organic development residing in the fibrin itself.

I do not wish it to be understood as, in my opinion, a proved and certain thing, that fibrin is insusceptible of ulterior development; but I find, as yet, a want of sufficient evidence, to establish its possession of this power; and in the examination, both of intravascular clots and of inflammatory exudations, I find several facts which apparently militate against such a conclusion. In all such products, the fibrin has shown itself either stationary or retrogressive; either lying as first deposited, or contracting more and more densely; or altering, only to undergo degradation. So far as my knowledge extends of adhesive inflammation, and of the several reparative processes, I see no evidence that fibrin takes a more important part in them than that of holding the true albuminous blas