In the period preceding the real exudation, an organ is, within the range of the inflammation, reddened, injected; that is, more than ordinarily vascular, swollen, and at the same time relaxed, softer, lacerable. The redness must be that of injection, and is to be carefully discriminated from redness of imbibition. The swelling and relaxation result from infiltration of the texture with exuded blood-serum.

Generally speaking, the swelling is accompanied by increase of volume; to this, however, spongy textures, and in particular the lungs, are exceptions. In protracted, and especially in hypostatic stases, the swelling of the texture frequently occasions closure of the pulmonary cells, and renders them inaccessible to atmospherical air. The volume of the inflamed part falls short of the normal.

As, however, mere hyperaemia occasions similar appearances, although in a minor degree, the question arises: "What are the criteria in the dead body which justify us in pronouncing the inflammatory stasis to be attained?"

The only true criterion in the dead subject is afforded in the changes suffered by the blood in the capillaries of the implicated texture, during the inflammatory stasis - changes cognizable, in part, by the naked eye.

Effusion having taken place, its product, exudate, affords incontestable evidence of inflammation, wherever its character is such as we know by experience to attach solely to the fruits of this process; examples are pus or croupous fibrin. The redness and injection cannot here commonly apply, having, for the most part, given way to the effusion. Even the swollen condition of the texture may in a great measure have subsided during a mortal collapse. The relaxation of the tissues still lasts, taking, however, in solid exudates, the form rather of fragility, as, for instance, in the hepatized lung.

Where, however, the exudate is a blastema, well known to exude both with and without inflammation, the question arises: what circumstances warrant us in assuming such blastema to be the product of inflammation? Such circumstances are -

(a.) Rapid and copious production of the blastema;

(6.) The concurrence of exudates, known to be exclusively generated by inflammatory stasis;

(c.) Analogy of textural destruction with that due to inflammatory exudation, more especially if coupled with analogy between the exudate and a product pertaining exclusively to inflammation, as between tuberculous infiltration of the lung and hepatization, and again between the hepatizing tubercle and the fibrino-croupous exudate.

Lastly, it is important to decide whether the appearances, in the neighborhood of a product, are residue of the inflammation that called it forth, or the rudiments of a new consecutive inflammation caused by the said product. The discrimination, so far as it is feasible at all, may be deduced from what has been already stated.

Corollary

(1.) The inflammatory process is especially fitted for displaying the primitive differences of blastemata, those inherent properties contingent upon internal (endogenous) formative processes.

(2.) It is equally adapted to demonstrate the commonly mixed character of blastemata, and the consequent variety of elementary constituents which enter into the composition of a new growth.

(3.) It is the last of a series of exudative processes, beginning with the exudation of plasma in the act of nutrition, which in degree and kind probably all bear more or less resemblance to it.

(4.) Scarcely a new growth exists, the blastema of which may not be produced by inflammation. On the other hand, inflammation yields products proper to itself alone. It is to be observed, at the same time, that where a corresponding crasis prevails, the stasis requisite for the formation of the product is in the inverse ratio of the intensity of the dyscrasial process in the general circulation. Such exudatory acts, together with other processes to be discussed in the next chapter, are wont, owing to the rapidity of the effusion and to the slightness of the accompanying stasis, to be characterized as deposits.

(5.) The homoeoplastic textures produced by inflammation are areolar tissue, a fibre analogous to that of organic muscle, transition-cartilage, bone, blood, and bloodvessels. The regeneration of nerve-fibrils, after wounds attended with loss of substance, does not take place as a new formation out of the exudate, but as growth of the nerve from its cut ends into the exudate, constituting a provisional cicatrix.

(6.) Inflammation possesses now a local, now a general import. In the latter case it is the localization of an anomalous crasis which stands to it in the relation of cause.

(7.) Inflammation may concur with a crasis either accidentally or as its symptom. This has been to a certain extent recognized by the acceptation of an arthritic, a scrofulous, a scorbutic inflammation. Custom has stamped inflammation with fibrinous exudates and a kindred phlogistic crasis, as genuine inflammation.

(8.) How ought we to estimate that view which designates inflammation as augmented, vital, and formative energy - as increased vascular activity, - as reaction?

Neither in the sense of a neuro-pathological nor of an attraction-theory, can there be any question of increased vascular activity. A vigorous formative power no doubt is at work in the inflammatory process; still, in the formative efforts, the qualitative anomaly is predominant. Even adhesive inflammation, in which one might be most of all disposed to look for an augmentation of the normal process of nutrition, produces but few, and these simple, textures.

To define inflammation as a reaction of the organism against a morbific influence, is simply begging the question. Inflammation is a morbid process, unconscious of its scope or object, evoked by a causal impulse, and sustained or repeated so long as this impulse remains in activity. Only in this general sense of cause and effect is the definition of reaction admissible.