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very much longer time passes than is requisite for ordinary coagulation. From this frequent phenomenon, as it is met with in the ordinary formation of a crust upon the surface of inflamed blood, gradual transitions are observed to a greatly increased prolongation of the period during which fluidity is retained.

The most extreme instance of this kind as yet known occurred in a case observed by Polli. In a vigorous man, suffering from pneumonia, who came under treatment in the summer, at a time which does not offer the external conditions most favourable to slowness of coagulation, the blood, which flowed from the opened vein took a week before it began to coagulate, and not until the end of a fortnight was the coagulation complete. In this case, too, occurred the other phenomenon which I had observed in the pleuritic exudations, namely, that decomposition (putrefaction) took place in the blood at an unusually late period in proportion to this lateness of coagulation.

Now since phenomena of this kind are observed to occur with especial frequency in chest affections, a frequency so especial indeed that the buffy coat was long since designated Crusta pleuritica, there would seem to be some grounds for inferring from this, that the function of respiration has a definite influence upon the occurrence or non-occurrence of the fibrinogenous substance in the blood. At all events, the peculiarity possessed by the lymph is under certain circumstances transmitted to the blood, so that either the whole of the blood partakes of it, and that in a higher degree, the greater the disturbance under which the respiration labours; or, in addition to the ordinary, quickly coagulating matter, a second which coagulates more slowly is found. It frequently happens, namely, that two sorts of coagulation subsist side by side. in the same blood, one early and the other late, especially in the cases in which direct analysis shows an increase of

fibrine, a hyperinosis. These hyperinotic conditions appear therefore to indicate that in them an increased supply of lymphatic fluid is introduced into the blood, and that the matters which are afterwards found in the blood are not the products of an internal transformation of its constituents, and that therefore the original source of the fibrine must not be sought for in the blood itself, but in those parts from which the lymphatic vessels convey the increased supply of fibrine.

In explanation of these phenomena, I have ventured to advance the hypothesis, somewhat bold perhaps, though I consider it perfectly able to sustain discussion, namely that fibrine generally, wherever it occurs in the body external to the blood is not to be regarded as an excretion from the blood, but as a local production; and I have endeavoured to introduce an important change in the views entertained with regard to the so-called phlogistic crasis in relation to its localization. Whilst it had previously been the custom to regard the altered composition of the blood in inflammation as a condition existing from the very outset, and especially denoted by a primary increase in the fibrine, I on the contrary have shewn the crasis to be an occurrence dependent upon the local inflammation. Certain organs and tissues have inherent in them in a higher degree the power of producing fibrine and of favouring the occurrence of large quantities of fibrine in the blood, whilst other organs are by far less adapted for its production.

I have, moreover, pointed out the fact, that those organs which with especial frequency exhibit this peculiar combination of a so-called phlogistic state of the blood with a local inflammation are generally abundantly provided with lymphatic vessels and connected with large masses of lymphatic glands, whilst all those organs which either contain very few lymphatics, or in which these vessels are scarcely known to exist, do not exercise any influence

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worth naming upon the amount of fibrine in the blood. Former observers had already remarked that there were inflammations occurring in very important organs, as for example, in the brain, in which the phlogistic crasis was, properly speaking, not at all met with. Now it is precisely in the brain that we have scarcely any evidence of the existence of lymphatics. In those cases, on the contrary, in which the composition of the blood is earliest altered, namely in diseases of the respiratory organs, we find an unusually abundant network of lymphatics. merely the lungs are pervaded by, and covered with, them, but the pleura also has extremely numerous connections with the lymphatic system, and the bronchial glands constitute almost the greatest accumulations of lymphaticgland substance possessed by any organ in the whole body.

Not

On the other hand, we are acquainted with no fact which shews it to be possible that, in consequence of a simple increase of the pressure of the blood, or of a simple change in the conditions which influence its circulation, an exudation of fibrinous fluids could in any organ take place into its parenchyma, or upon its surface, from the blood. It is certainly generally imagined that, when the current of the blood attains a certain strength, fibrine begins to appear in the exudation, but this has never been proved by experiment. Nobody has ever been able, by the production of a mere change in the force of the current of the blood, to induce the fibrine to transude directly as it is wont to do in certain inflammatory processes; for this some irritation is always required. The greatest obstructions may be induced in the circulation, exudations of serous fluids may be experimentally produced upon the largest scale, but that peculiar fibrinous exudation which the irritation of certain tissues provokes with so much ease, never ensues upon these occasions.

That the fibrine in the blood itself is produced by a transformation of the albumen, is a chemical theory, which has no other evidence in its favour than the fact that albumen and fibrine have a strong chemical resemblance, and that, on comparing the questionable formula for fibrine with the equally questionable one for albumen, it is very easy to imagine how, by the abstraction of a couple of atoms, the transition from albumen to fibrine might be effected. But our being able in this manner to deduce one of the formulæ from the other does not afford the slightest proof that an analogous transformation occurs in the blood. It may possibly take place in the body, but even then it would at any rate be more probable that it was accomplished in the tissues, and that from them the fibrine was conveyed away into the blood by means of the lymph. This is however the more doubtful, because rational formulæ for the chemical composition of albumen and fibrine have not yet been determined, and the incredibly high atomic numbers in the empirical formulæ point to a very complex grouping of the atoms.

Let us therefore hold fast the well-ascertained fact that fibrine can only be made to exude upon any surface by the occurrence of some irritation, that is, local change, in addition to the disturbance in the circulation. This local change, however, is, as results from experiment, alone sufficient to cause the exudation of fibrine, even when no obstruction arises in the circulation. Such obstruction is not therefore in any way needed in order that the production of fibrine may commence at any given point. On the contrary, we see that the cause of the greatest differences in the nature of exudations is to be found in the special constitution of the irritated parts. On the simple application of an irritating substance to the surface of the skin, there arises, when the irritation, whether chemical or mechanical in its nature, is only slight in degree, a vesicle, a serous exudation. If the irritation is more violent, a

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liquid exudes, which in the vesicle appears quite fluid, but coagulates after its evacuation. If the fluid from a blister raised by a cantharides-plaster be received into a watch-glass and exposed to the air, a coagulum forms, shewing that there is fibrinogenous substance in the fluid. But we sometimes meet with conditions of the body, in which an external stimulus is sufficient for the production of blisters containing a fluid which directly coagulates. I had, last winter, a patient in my wards, whose feet had remained in a state of anesthesia ever since they had been frozen, and I employed as a remedy, amongst other things, local baths containing aqua regia. After a certain number of these baths, blisters, which varied in diameter up to two inches, and were found, when opened, to be filled with large, jelly-like masses of coagulum, formed upon every occasion on the anæsthetic parts of the soles of the feet. In other persons probably ordinary blisters would have formed, containing a fluid, which would not have coagulated until after its evacuation. Such a difference manifestly depends upon a difference, not in the composition of the blood, but in the disposition of the part affected. The difference between that form of pleurisy, which from its very commencement furnishes coagulable and coagulating fluids, and that in which the exudation is coagulable, but not coagulating, certainly points to peculiarities in the local irritation.

I do not think therefore that we are entitled to conclude, that in a person who has an excess of fibrine in his blood, there is on that account also a greater tendency to fibrinous transudation; on the contrary, I should rather expect, that in a patient who produces at a certain point a large quantity of fibrine-forming substance, much of it would pass from that point into the lymph and finally into the blood. The exudation may therefore in such cases be regarded as the surplus of the fibrine formed in loco, for the removal of which the lymphatic circulation did not suffice. As long