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is regarded as an immediate consequence of the hyperæmia, and in which it is assumed that inflammation, when it has once declared itself, is characterized by the presence of a substance more or less foreign to the natural composition of the part. The only question is whether the hyperæmia really forms the actual commencement of these processes.

If inflammation were necessarily dependent upon hyperæmia, you can well imagine that it would be logically impossible to speak of inflammations in parts which do not stand in an immediate relation to vessels. We could not imagine an inflammation taking place at a certain distance from a vessel. It would be completely impossible to speak of an inflammation of the cornea (excepting as occurring at its border); of an inflammation of cartilage (excepting as occurring in the parts immediately adjoining the bone); or of an inflammation in the internal substance of a tendon. But if we compare the processes which present themselves in these parts with those which are ordinarily seen in inflamed parts, the result is unquestionably that the same inflammatory processes may occur everywhere alike, and that the changes in the vascular parts can in no essential particular be distinguished from those which take place in the non-vascular ones.

The term inflammatory (i.e., according to the common definition, fibrinous) exudation, has, as you are aware, been somewhat loosely applied, inasmuch as it has been taken to include different kinds of exudation (fibrinous and nonfibrinous) furnished by different processes, upon all of which, however, the common name of inflammation has been bestowed. When, for example, inflammations of mucous membranes are spoken of, it is not generally supposed, that the mucous membrane will furnish a fibrinous exudation. We are indeed acquainted with mucous membranes, where fibrinous exudations are of pretty frequent

occurrence, for example, the mucous membrane of the respiratory organs. But we know also that free (superficial) fibrinous exudations are scarcely to be met with on the mucous membrane of the digestive tract, and that they at most accompany the more serious, and especially the gangrenous and specific, forms. When laryngitis is spoken of, the presence of croup is not immediately inferred. In a case of cystitis, we do not expect to find the inner surface of the bladder covered with a fibrinous layer. In the whole series of the so-called gastric inflammations we find, especially at the commencement of the process, scarcely anything more than an abundant secretion of mucus. If therefore we still call these catarrhal inflammations, inflammations, if we do not wish entirely to cast them out of the class of inflammations, we must admit that there may exist a mucous as well as a fibrinous exudation in inflammations, and that the inflammations with a mucous exudation form a special category, appertaining to certain organs. For, as is well known, we do not find them in all the tissues of the body, but nearly exclusively on mucous membranes.

If now you consider the fibrinous exudations a little more closely, there can be no doubt at all, but that in this point they entirely agree with the mucous ones. For we do not meet with fibrinous exudations in all parts of the body; we know of no form of exudative encephalitis, for example, which furnishes a fibrinous exudation. Just as little is there a form of hepatitis known, in which fibrinous exudations occur. There is indeed an inflammation of the investing membrane of the liver (perihepatitis), just as there is an inflammation of the membranes of the brain, in which fibrine may be set free, but nobody has ever met with fibrine in a case of genuine hepatitis. Just as little is there fibrine to be found in the ordinary inflammation of the substance of the heart (myo-carditis).

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On the other hand, you must bear in mind that, starting with certain preconceived notions, observers have imagined fibrinous exudations to take place in many parts, where they are not really to be seen. If because pus has been obtained from a fibrinous exudation, it is therefore imagined that, wherever pus shews itself, a fibrinous exudation must be regarded as its source, no very great power of observation is required to convince oneself, that this is an error. Take any ulcerated surface you please, wipe off the pus, and collect what then comes out; you will either have a serous fluid or pus, but you will not see that the surface you have wiped becomes covered with a fibrinous layer. If we confine ourselves to those parts, where inflammations with real, unquestionable fibrinous exudation do occur, we have a category nearly as limited as that of the mucous inflammations. In such a category the first place is occupied by the serous membranes proper, which even upon slight inflammatory irritation generally produce fibrine; the second place is filled by certain mucous membranes, in which, in a great number of cases, fibrinous inflammations unmistakeably arise, as an aggravation, out of mucous ones. Ordinary croup does not generally at its very outset manifest itself in the form of fibrinous croup; at the commencement, at a time when the danger may already be very considerable, there is often nothing else found than a mucous or muco-purulent false membrane. Not until after a certain lapse of time does the fibrinous exudation set in, and then it does so in such a manner, that we can trace the transitions in the same false membrane, and see that a certain portion is manifestly mucus, another manifestly fibrine, whilst in a third part it can no longer be affirmed with certainty whether the one or the other is present. Here therefore both substances appear as substitutes for one another. Where the inflammatory irritation is more violent, we see fibrine, where slight, mucus, appear.

With regard to mucus, however, we know, that it does not exist in the blood like fibrine. Although a mucous membrane produces incredibly large masses of mucus in a short time, they are nevertheless products of the membrane itself; the membrane is not infiltrated with mucus coming from the blood, but the peculiar mucin matter, the principle of mucus, is a product of the membrane, and is conveyed to the surface by means of the fluid oozing through (transuding) from the blood. In the same manner I have also attempted, as I intimated to you on a former occasion (p. 162), to overthrow the opinion, which is wont to be entertained with regard to the origin of fibrine. Whilst until now fibrine has been regarded as a real transudation from the liquor sanguinis, as the outflowing plasma, I have proposed the explanation, that the fibrine, like the mucus, is a local product of those tissues, on and in which it is found, and that it is conveyed to the surface in the same way as the mucus of the mucous membrane. I then shewed you, how we have in this way a most ready explanation of the fact, that in proportion as, in a given tissue, the production of fibrine increases, so also the amount of fibrine in the blood increases; and that the fibrinous crasis is just as much a product of the local disease, as the fibrinous exudation is a product of the local metamorphosis of matter. Never has any one-any more than it is possible for him by a change of pressure directly to produce mucus from the blood in any place which does not itself produce mucus-been able to produce fibrine by any change in pressure of the blood; what transudes never consists of anything but serous fluids.

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I am accordingly of opinion, that, in the sense in which it has usually been assumed to exist, there is no inflammatory exudation at all, but that the exudation which we meet with, is essentially composed of the material which has been generated in the inflamed part itself through the change in

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its condition-and of the transuded fluid derived from the vessels. If therefore a part possesses a great number of vessels, and particularly if they are superficial, it will be able to furnish an exudation, since the fluid which transudes from the blood conveys the special products of the tissue along with it to the surface. If this is not the case, there will be no exudation, but the whole process will be limited to the occurrence in the real substance of the tissue of the special changes which have been induced by the inflammatory stimulus.

In this manner, two forms of inflammation can be separated from one another; the purely parenchymatous inflammation, where the process runs its course in the interior of the tissue, without our being able to detect the presence of any free fluid which has escaped from the blood; and the secretory (exudative) inflammation (which belongs more to the superficial organs) where an increased. escape of fluid takes place from the blood and conveys the peculiar parenchymatous matters along with it to the surface of the organs. That there are two different forms is clearly shewn by the fact that they occur for the most part in different organs. There are certain organs which, under all circumstances, only suffer from the parenchymatous affection, and others again which in nearly every instance exhibit a superficial exudative inflammation.

The distinction into adhesive and purulent forms, which has generally been made in accordance with the example of Hunter, has reference to a much later stage in the process; the first point to be considered is always, how far the tissues themselves become changed and their products assume a degenerative character, or how far, through the passage of the fluids, the part is again freed from what it has generated in itself, and how far thereby the degeneration of the part is avoided. Every parenchymatous inflammation has from its outset a tendency to alter the