CHAPTER III
INFLAMMATION

Inflammation may be defined as the series of vital changes that occurs in the tissues in response to irritation. These changes represent the reaction of the tissue elements to the irritant, and constitute the attempt made by nature to arrest or to limit its injurious effects, and to repair the damage done by it.

The phenomena which characterise the inflammatory reaction can be induced by any form of irritation—such, for example, as mechanical injury, the application of heat or of chemical substances, or the action of pathogenic bacteria and their toxins—and they are essentially similar in kind whatever the irritant may be. The extent to which the process may go, however, and its effects on the part implicated and on the system as a whole, vary with different irritants and with the intensity and duration of their action. A mechanical, a thermal, or a chemical irritant, acting alone, induces a degree of reaction directly proportionate to its physical properties, and so long as it does not completely destroy the vitality of the part involved, the changes in the tissues are chiefly directed towards repairing the damage done to the part, and the inflammatory reaction is not only compatible with the occurrence of ideal repair, but may be looked upon as an integral step in the reparative process.

The irritation caused by infection with bacteria, on the other hand, is cumulative, as the organisms not only multiply in the tissues, but in addition produce chemical poisons (toxins) which aggravate the irritative effects. The resulting reaction is correspondingly progressive, and has as its primary object the expulsion of the irritant and the limitation of its action. If the natural protective effort is successful, the resulting tissue changes subserve the process of repair, but if the bacteria gain the upper hand in the struggle, the inflammatory reaction becomes more intense, certain of the tissue elements succumb, and the process for the time being is a destructive one. During the stage of bacterial inflammation, reparative processes are in abeyance, and it is only after the inflammation has been allayed, either by natural means or by the aid of the surgeon, that repair takes place.

In applying the antiseptic principle to the treatment of wounds, our main object is to exclude or to eliminate the bacterial factor, and so to prevent the inflammatory reaction going beyond the stage in which it is protective, and just in proportion as we succeed in attaining this object, do we favour the occurrence of ideal repair.

Sequence of Changes in Bacterial Inflammation.—As the form of inflammation with which we are most concerned is that due to the action of bacteria, in describing the process by which the protective influence of the inflammatory reaction is brought into play, we shall assume the presence of a bacterial irritant.

The introduction of a colony of micro-organisms is quickly followed by an accumulation of wandering cells, and proliferation of connective-tissue cells in the tissues at the site of infection. The various cells are attracted to the bacteria by a peculiar chemical or biological power known as chemotaxis, which seems to result from variations in the surface tension of different varieties of cells, probably caused by some substance produced by the micro-organisms. Changes in the blood vessels then ensue, the arteries becoming dilated and the rate of the current in them being for a time increased—active hyperæmia. Soon, however, the rate of the blood flow becomes slower than normal, and in course of time the current may cease (stasis), and the blood in the vessels may even coagulate (thrombosis). Coincidently with these changes in the vessels, the leucocytes in the blood of the inflamed part rapidly increase in number, and they become viscous and adhere to the vessel wall, where they may accumulate in large numbers. In course of time the leucocytes pass through the vessel wall—emigration of leucocytes—and move towards the seat of infection, giving rise to a marked degree of local leucocytosis. Through the openings by which the leucocytes have escaped from the vessels, red corpuscles may be passively extruded—diapedesis of red corpuscles. These processes are accompanied by changes in the endothelium of the vessel walls, which result in an increased formation of lymph, which transudes into the meshes of the connective tissue giving rise to an inflammatory œdema, or, if the inflammation is on a free surface, forming an inflammatory exudate. The quantity and characters of this exudate vary in different parts of the body, and according to the nature, virulence, and location of the organisms causing the inflammation. Thus it may be serous, as in some forms of synovitis; sero-fibrinous, as in certain varieties of peritonitis, the fibrin tending to limit the spread of the inflammation by forming adhesions; croupous, when it coagulates on a free surface and forms a false membrane, as in diphtheria; hæmorrhagic when mixed with blood; or purulent, when suppuration has occurred. The protective effects of the inflammatory reaction depend for the most part upon the transudation of lymph and the emigration of leucocytes. The lymph contains the opsonins which act on the bacteria and render them less able to resist the attack of the phagocytes, as well as the various protective antibodies which neutralise the toxins. The polymorph leucocytes are the principal agents in the process of phagocytosis ([p. 22]), and together with the other forms of phagocytes they ingest and destroy the bacteria.

If the attempt to repel the invading organisms is successful, the irritant effects are overcome, the inflammation is arrested, and resolution is said to take place.

Certain of the vascular and cellular changes are now utilised to restore the condition to the normal, and repair ensues after the manner already described. In certain situations, notably in tendon sheaths, in the cavities of joints, and in the interior of serous cavities, for example the pleura and peritoneum, the restoration to the normal is not perfect, adhesions forming between the opposing surfaces.