Inflammation has been variously defined as “perverted nutrition,” as a “protective reaction of the organism against irritant agents” and in other terms that express at once too much and too little, without actually defining the morbid process. Older definitions dealt with the manifest disorders of circulation, of innervation or of tissue change too often exalting the importance of one set of changes at the expense of another and thus giving in the main a one sided view of the morbid process.
Some modern bacteriologists are inclined to refuse the title to any morbid process that is not caused by the presence of microbes or their toxic products. To them the changes occurring in an aseptic wound or in a simple fracture in process of healing are purely reparatory and partake no more of the nature of inflammation than do the developmental changes in the growing embryo. While to a large extent true, this exclusive view implies exceptions, since if the chemical poisons derived from the bacteria can develop inflammation, the same must be admitted as possible for chemical irritants drawn from other sources.
As a matter of fact inflammation, occurring as it does in very different tissues, vascular and nonvascular, fibrous, cellular, parenchymatous, etc., and in connection with a great variety of irritants, must be held to include a large group of morbid processes, bearing to each other a strong family relationship and resemblance, and yet differing in many important details. Each irritant (heat, cold, electricity, chemical irritant, incised, punctured, lacerated or contused wound, rupture, fracture, foreign body, parasite, microbe, toxin, etc.,) has its own special character and mode of irritation; each tissue has its own special method of succumbing or reacting and its own amount of blood supply; and each system and organ has its own native or acquired power of resistance and reaction.
Inflammation agrees with active hyperæmia in the tendency to dilation of the vessels and an increased flow of blood to the part or if the irritated part is nonvascular like the cornea or articular cartilage, then to the parts adjacent. It differs, however, in the more active cell proliferation, and in the nature of the liquid transudation which is richer in albumen fibrine, cells and phosphates. Abstractly the inflamed part retains very active vital processes, trophic and exudative, but these, are largely changed from the normal and are, it is claimed, perverted, yet they preside over the processes of cell growth and decay, the removal of injured or useless tissue, and later, over the building up of new material, and repair of loss. Active hyperæmia on the other hand is mainly a circulatory disorder, and when it advances so as to determine changes in the cells and tissues it is held to have merged into inflammation.
The term inflammation (from inflammo, I set on fire), is suggestive of the local heat of the inflamed part, just as fever (febris) indicates an elevation of the temperature of the body at large. Celsius enumerated the features of rubor, calor, dolor and tumor (redness, heat, pain and swelling) which have come down to our own time as at least suggestive of inflammation. But any diagnosis, based on these alone, would be today woefully inadequate. Redness occurs in the transient blush, heat in the febrile state, though no inflammation can be recognized, pain is present in neuralgic and other nervous affections, and swelling in dropsy and tumor. On the other hand redness is entirely absent, for a time, after the outset of inflammation in nonvascular tissues (cornea, articular cartilage), the heat of the inflamed part may be actually lowered when there is much exudation around the capillary vessels and lessened flow of blood, pain may be absent in some circumscribed inflammations of the lungs, and swelling is not at first visible in the inflamed cornea or compact bony tissue. These phenomena which are so common in inflammation and, in general so characteristic of it, cannot therefore be accepted as infallible evidence of its existence, nor can their absence be held as absolutely implying its nonexistence.
Forms of Inflammation. This morbid process might be divided almost indefinitely according to the organ invaded, the cause, and type, yet it will be more convenient to deal with it generically and notice inflammation in nonvascular and vascular tissues respectively, and the different types of granular degeneration, exudative inflammation and croupous inflammation. It will be requisite further to notice an acute and a chronic type.
By dealing first with the changes in the anatomical elements of the tissues and in the innervation, we shall virtually cover the phenomena observed in nonvascular tissues, and later the changes in connection with the circulatory system will give the additional characteristics of inflammation in vascular tissues.
CHANGES IN THE TISSUE ELEMENTS.
Death of cells and tissue. By the application of an irritant (acid, heat, etc.,) a certain thickness of tissue with its enclosed cells is killed, and a thin layer of necrosis is usually produced. This does not constitute inflammation, but it acts as a foreign body, often septic, in producing inflammation in the parts adjacent.
Cloudy Swelling, Granular Degeneration. This may occur in the inflamed area surrounding the necrosed tissue in the seat of a burn or other injury, it is exceedingly common in the cells of inflamed parenchymatous tissue (liver, kidney), in the muscle of the heart, in the gastro-intestinal mucosa, in febrile affections and in poisoning with arsenic, phosphorus, or mineral acids. The gross appearance of the tissue is that of swelling, with a dull grayish color and a loss of its normal translucency. The cells of the affected organs are seen under the microscope to be filled with small albuminous granules which may be so abundant as to completely conceal the cell structure. The granules are insoluble in ether, but disappear under acetic acid. This condition of the cells is often associated with the exudative forms of inflammation.