Page:Encyclopædia Britannica, Ninth Edition, v. 18.djvu/422

 PATHOLOGY ceived ; and in many cases globules of pus, known by their larger size and freer motion on one another (and, when observed in mass, by their yellow colour), soon appear in this effused matter ; and it assumes more or less rapidly, and more or less generally, the form of purulent matter. . . . Along with the semi-fluid lymph effused in the earlier stage of inflammation there is often extravasation of the colouring matter of the blood, and sometimes of entire blood.&quot; This, then, is the central fact of inflammation, the incontinence of the vessels and the exudation from them. Addison adopted the theory that the pus of inflammation was nothing but the colourless cells of the blood tliat had been washed out with the plasma ; and that doctrine has been revived by Cohnheim with little or no reserve. There have been serious objections to this doctrine of the origin of pus ; practical surgeons have always failed to understand how all the pus could come from the blood, which has not only a mere trace of colourless cells in it, but, moreover, contains neither more nor less of these cells during suppuration than at other times. Again, in cases of leukaemia, where the number of them is enormously increased, the course of inflammation does not appear to be affected thereby. Lastly, it is pointed out that we cannot infer altogether fully from the extremely susceptible transparent membranes of the frog to the subcutaneous and other connective tissues which are the usual seats of the in flammations met with in practice. So far, then, we are justified in admitting only the incontinence of the vessel-walls, the escape of some colourless cells, and of plasma, the latter yielding fibrin under some circumstances, in combination with the paraglobulin and the ferment known to reside in the white corpuscles. The cause of the incontinence of the vessel -walls naturally engrosses attention. In an experiment of Cohnheim s a. similar condition was produced in the vessels of the frog s tongue by liga turing the tongue bodily at the root, so as to stop the circulation in it altogether. If the ligature were kept on for six days the tongue began to mortify, and the circulation showed no power to re-establish itself; if it were removed after forty-eight hours the current slowly resumed its flow, the arteries returned from their dilated condition, but not the veins, and the colourless cells began to escape from the latter ; on removing it after twenty-four hours only, the circulation quickly resumed its normal course without any transient emigration of cells. The conclusion was that the walls of the vessels suffered a certain loss of &quot; integrity &quot; if the circulation through them were stopped beyond a certain limit of time, and this loss of integrity seemed to be analogous to the altera tion of the vessel-walls under the blow of an inflammation. On the other hand, it has been pointed out that not the vessel-walls only, but the cells in closest proximity to and in intimate nutri tive relation with them, are affected by the stroke of inflammation ; where such cells have processes, and can be seen, they are found to draw in their processes under an irritant. In the exposition of Cohnheim, however, these changes in the cells of an inflamed part are not admitted to be other than regressive or passive ; according to him, the walls of the vessels only are affected, and affected in their molecular constitution. Suppura- Suppuration. We have seen that there still remains the difficulty tion. of accounting for the large quantity of pus ; and it will probably be found that to account for the pus we shall have to ascribe a more than passive attitude to the connective -tissue corpuscles of the inflamed area. Where the suppuration is diffuse, as in phlegmon, and still more where it is discontinuous, as in secondarily inflamed lymphatic glands, it is not to be supposed that the pus is a mere aggregate of blood -cells brought thither. Something from the primary seat of inflammation has caused the more distant parts, whether they be continuous or discontinuous, to take on the in flammatory and suppurative action ; but it is quite clear, if we examine a lymphatic gland beginning to suppurate, that its own cells yield the pus. There has been an action of presence on the parenchyma of the lymphatic gland ; and it will be difficult to account for the production of pus in acute primary inflammation without assuming the same action of presence. In inquiring after the catalytic agent suspicion falls on the substances exuded from the vessels, and mostly upon the emigrated colourless cells. Sup puration, when it occurs, is subsequent to and secondary to the exudation. When no suppuration occurs, as in what is called (tdhcsive inflammation, which is the commonest kind on free sur faces, the exuded blood-plasma simply coagulate!*, forming a fibriu- ous layer, in the meshes of which are a larger of smaller number of colourless blood -corpuscles. In the further development these blood-cells are probably themselves the active elements ; they pro duce the tissue of adhesions, which is a form of the tissue of repair. In situations which are not free surfaces that is to say, in the subcutaneous tissue, or more generally in the tracts or planes of the common binding tissue the exuded substances are less apt to coagulate or to take the adhesive fibrinous course. It is in these deeper situations that we ordinarily get suppuration, an event subsequent to exudation and undoubtedly dependent thereon. It is true that &quot;inflammation&quot; may be excited on tlie surface of articular cartilages and in the cornea, where there are no blood vessels to yield an exudation ; but the inflammation is not of the ordinary kind, and in particular there is no true suppuration until the nearest blood-vessels have projected their system as far as, or close up to, the irritated area. Artificial keratitis has been tho chosen ground of controversy to determine whether it is the vessels, or not rather the cells, of the part that are primarily and actively concerned in the inflammatory process ; but it will probably be found that the two sides of the controversy correspond to two dif ferent sets of facts. The transparent superficial ulcer of the cornea has hardly anything to do with inflammation ; it does not sup purate, although there is some formative action in the cells of the part to enable it to heal. Whenever there is true inflammation of the cornea it is accompanied by or preceded by extension of the nearest vessels to the transparent and non-vascular surface. Changes in the Connective Tissue. In the events of true inflam mation, therefore, exudation from the vessels precedes suppuration ; and it can hardly be doubted that they are cause and effect, to the extent, at least, that exudation is a necessary antecedent. At the same time the connective-tissue cells of the part can hardly have escaped that molecular injury, or injury to their nutrition, which the elements of the vascular wall would appear themselves to have suffered ; they are, as Rindfleisch points out, intimately bound np with the plasmatic circulation or the ultimate diffusion of the juices ; they are in closest relation with the terminal nerve-plexuses ; and, histogenetically, they are the remains of that &quot;parablastic&quot; embryonic tissue from which the blood-channels themselves were made. It would be surprising, indeed, if they escaped the shock which had deeply affected the integrity of the cells in the vascular wall. A concurrent alteration, at least, must be postulated for them ; but that can hardly account for more than a preparedness in them to form pus. According to Strieker, the elements of the connective tissue revert to an embryonic character before pus is formed from them. If the hardness of the central core of an inflam mation under the skin be analysed, it will be found to depend, says Strieker, upon the following things : the tissue is thickened, the network of cells in it is swollen, the intercellular substance is re duced, the network of cells has broken up into independent pieces of nucleated protoplasm. This is the swelling of the tissues which precedes abscess-softening ; it is essentially a return to a more pro toplasmic and less fibrillar state, and accordingly to a more embryonic state. Of this power of reversion to an embryonic state, which the common binding tissue of the body retains as a memory of develop ment, we have already had illustrations in the processes of repair, of tumour formation, and of cancerous infection. In all these cases the tissue falls back upon a more elementary condition, or we may say that it retreats to broader ground, where, however, it cannot stand still. Its special destiny is settled for it in each case by the circumstances, and, for the particular case of inflammation (as dis tinguished from the process of repair), its special destiny is to form pus. If the analogy adduced in the section on &quot;repair&quot; has any value, pus is the by-product of a kind of blood-making from the embryonic cells, a ha-matoblastic activity in which no red disks are formed, but only pus-corpuscles and a fluid, the corpuscles stand ing for the residual nucleus of the hasmatoblast (with evidence of cleavage in it) and the liquor pur is for both the red disks and the plasma. This ha&amp;gt;matoblastic doctrine of pus would correspond, in form at least, to Hunter s conjecture that &quot; the new-formed matter peculiar to suppuration is a remove further from the nature of the blood.&quot; So long as the intensity of the process lasts, the connective tissue uses its reacquired embryonic powers only to make pus ; when the effects of the blow have subsided (or if they have been from the first slight, as in the reparative process) the formative powers of the tissue make granulation-cells and new blood-vessels (including even new blood within the vessels), and so the incident ends in repair. The pus of a granulating surface would thus differ from the pus of acute inflammation only in degree. In like manner, common inflammation with a moderate degree of fever differs only in degree from phlegmon, or diffuse suppuration, with its peculiar fever. The diffuse suppuration of phlegmon is the case where tho infection or action of presence extends by continuity along tho tracts of connective tissue ; the implication of lymphatic glands (it may be at the outset) is the case where the infection is carried to a distance by the lymph-drainage of the tissues. Contrasting with such cases, the area of suppuration in a healthy subject (where there has been no extrinsic poison introduced) is a limited one ; but, however limited the focus, it seems necessary to resort to infection of the connective tissue for an explanation if the exuded fluid turn to pus or the inflammatory swelling turn to abscess. It is in this sense that every inflammation may be said to be infective. Assuming, then, that pus-formation is due to an infective influ ence impressed upon the protoplasmic connective tissue, and know ing, as we do, that the exudation from the blood-vessels is an invari able antecedent, the role of infecting cells would precisely suit those elements of the exudation about whose share in the inflammatory process there has been much controversy, namely, the emigrated colourless cells of the blood. As a material contribution to the pus all the cells that escape from the blood would go but a little