Part 6

Symptoms and results. If on a mucous membrane or white skin the color becomes dark red, or violet (cyanotic) with evident distension of the capillaries and veins, the latter of which may stand out as knots or cords, there is an appearance of swelling or enlargement and sometimes coldness of the part. Soon the watery part of the blood transudes in excess, constituting dropsy, with increased swelling and pitting on pressure. On the mucous surfaces it determines an abundant serous secretion. The color is deepened by the escape from the vessels of red globules as well as white. The transudation contains little albumen and only exceptionally fibrine. In connection with the marked deoxidation and high carbonization of the blood, the nutrition of the part is largely arrested together with the functions, secretory, motor or otherwise. The imperfectly nourished vessels may give way, leading to hæmorrhage, or nutrition may be definitely arrested producing moist gangrene or ulceration. Sometimes a thrombus is formed in a congested vein. The changes in the affected organs depend much on the degree and duration of the hyperæmia. If slight and lasting it causes permanent induration and thickening, from connective tissue hyperplasia as frequently seen in the hind limbs of the horse. In case of blood transudations the altered coloring matter gives the various shades of gray, brown or black. If long continued the organ may shrink and atrophy occur from defective nutrition and contraction of the fibrous hyperplasia.

In making post mortem examinations mistakes may be made through the occurrence of changes after death. Thus a hvperæmia which was quite considerable during life may virtually disappear through the contraction of the arterial and capillary coats forcing the blood on into the veins. A minute point of extravasation here and there may be the only macroscopic lesion left. Again a marked venous and capillary hvperæmia in a dependent part of the body or of an organ may be entirely due to hypostatic conditions, the blood having settled into the lowest part of the vessels since the death of the animal. To avoid this source of error one must always carefully note the position of the carcass after death. Under other circumstances the superficial veins and capillaries may fill up with blood through the occurrence of decomposition and the evolution of gases in the internal cavities, which empty the splanchnic and parietal vessels by compression.

Treatment. The general principles of treatment may be stated thus: 1st. Remove the cause of the hyperæmia if possible, especially any mechanical cause; 2d. Secure the influence of gravitation in favor of the return of blood to the heart; though not so available in animals as in man, it is of great value in congestions of the head, ears, tail, and to a less extent of other parts; 3d. Correct any fault of blood pressure, excess or deficiency, which may act so as to cause active or passive hyperæmia; 4th. Establish derivation by cupping, leeches, fomentations, pediluvia, sinapisms, etc.; 5th. Apply cold, astringents, bandages, to empty the hyperæmic vessels, or kneading, rubbing, or electricity, to hasten the flow of blood; 6th. To improve the quality of the blood and general health, in plethora by low diet, purgatives and diuretics, in anæmic or debilitated conditions by iron, bitters, nourishing food, fresh air, sunshine and exercise.

It is especially important to check passive congestion in febrile diseases, and mechanical congestion at an early stage of its progress (Roberts).

INFLAMMATION. PHLOGOSIS. PHLEGMASIA.

Definitions. Relations to active hyperæmia. Redness. Heat. Pain. Swelling. Forms: in vascular tissues: in nonvascular. Changes in tissue elements. Death of cells. Cloudy swelling. Granular degeneration. Cell proliferation. Karyokinesis. Embryonic cells. Amœboid functions. Migration of leucocytes. Red cells escaping. Changes in innervation. Vaso-motor disorders. Fever. Changes in circulation. Contraction of capillaries, dilatation, rapid flow, tardy flow, stasis, oscillations, thrombus, collecting of white globules in periphery of current, migration of leucocytes, blood plates, and red globules, massing of red globules, exudation, softening of the capillary walls, nutrient artery more rigid and transmits more blood, heart contracts more forcibly, increase of fibrine, increase of waste products. Buffy coat, physiological causes. Microbes. Ptomaines. Toxins. Chemiotaxis. Phagocytosis. Polynuclear and mononuclear leucocytes. Exudates, unlike dropsies. Mucous exudate. Serous exudate. Fibrinous exudate. Blood exudations. Croupous exudation. Chyliform exudate. Results and Products. Resolution. Delitescence. Metastasis. New formations. Suppuration. Pus microbes. Pus. Healing by 1st intention. Healing by 2nd intention, granulation. Granule corpuscles. Interstitial neoplasia. Degenerations in lymph. Fatty degeneration, melanotic. Softening. Ulceration. Gangrene.

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.

=Cell Proliferation and Change.= In the nonvascular organ attacked by inflammation the multiplication of tissue cells and their resumption of amœboid movements is a constant phenomenon. Virchow insisted on the fundamental relation of the cell to the morbid process, and Goodsir and Redfern showed the rapid increase of the cells of articular cartilage in attacks of arthritis. There is first a sensible increase of the nucleus of the cartilage cell which shows a more extended and deeper staining in carmine or aniline; then by a special method of division (karyokinesis) the cell and nucleus divide in two; by a similar process these divide in four and so on in regular order. Meanwhile the cartilaginous substance becomes softened and finally dissolves and disappears, leaving in the place a mass of closely aggregated cells.

In the nonvascular transparent cornea, the membrane of Descemet, the epithelium of serous membranes and in the epidermis a similar cell multiplication occurs, also in the lateral cartilages of the horse’s foot.

To follow the indirect cell division by karyokinesis, we must note the cell as a semi-solid mass, formed of protoplasm and nucleus, each having as its framework a network of exceedingly fine inter-crossing filaments, much finer in the nucleus than in the cell protoplasm. The nuclear filaments stain with hæmatoxylon and safranin and are called chromatin threads. The intervening non-staining material is achromatine. The nucleus has a membranous envelope in two layers, of which the inner only stains. When about to divide two poles are formed in the cell protoplasm opposite to each other and near the nucleus the filaments concentrating to the poles. The chromatin threads in the nucleus thicken, become convoluted, split and multiply, and draw into their substance the chromatin layer of the envelope. Next the chromatin threads form long loops directed toward an achromatine centre or pole like a star, and this is followed by the progressive division of the star-shaped mass into two equal parts.

Finally they separate, together with the cell protoplasm, forming two daughter cells.

This cell proliferation under the action of an irritant is common to the vegetable kingdom in which galls, and tumors are formed in this way. It is a remarkable feature of these multiplying cells that they not only lose their power of developing the tissue in which they formerly lay, and have all their vital powers devoted to proliferation, but they acquire the amœboid power of their ancestors, the embryonic cells, which they further resemble in size. Indeed these cells are freely spoken of as embryonal cells, and the tissue formed by their massing together as embryonal tissue, and there is a widespread impression that they revert entirely to the form and characters of the embryonic cell. In some respects, however, they are unlike. The modified tissue cell of inflammation presents a nucleus of horseshoe outline, or after division of the nuclei they together retain this semi-circular outline; it has the power of actively digesting the adjacent tissues as the embryonic cells do not, and again it does not possess the power of differentiation into widely different tissues as does the early embryonic cell. It may be called a reversion, in the direction of the embryonic cell, however, since it reacquires a number of its functions.

=Migration of white blood cells.= This is another, and in vascular tissues the main source of the great cell accumulation in the inflamed tissue. This process was observed by Waller in 1846, but was given its true importance through the later observations of Cohnheim. The migration takes place through the walls of the capillaries and veins only, and the migrating cells are largely of the polynuclear variety of leucocytes. These remaining adherent to the inner wall of the blood vessel may be seen to have a small portion of their substance projected through the wall and appearing as a small buttonlike projection on the outer side. This gradually increases, while the remaining portion of the cell on the inner side of the wall correspondingly decreases until the whole cell is lodged in the tissue outside the vascular wall. The time occupied in passing through is very varied. It may be wholly accomplished in half a minute, and again hours may be required for the complete passage of a single leucocyte. The explanation of this migration has been sought in the supposed existence of stigmata (openings) in the vascular walls (Arnold), in the effect of the blood pressure within the inflamed vessels, in softening of the vascular walls and, in the contractility of the leucocyte which is strongly attracted by the pressure of certain bacteria and other irritants (chemiotaxis). The migrated leucocyte assumes in the tissues the same habit as the altered tissue nucleus. It multiplies rapidly, assists in the solution and removal of the inflamed tissue, contests the ground with infective microbes (phagocytosis), and subserves the purpose of assisting in building up new tissue, or of degenerations.

=Red Cells.= The red blood globules follow the active current in the centre of the blood vessel, yet a few of these also become adherent to the softened walls and pass through them (diapedesis). When stasis of blood takes place in the vessels, they become packed more closely with red globules which then pass outward into the tissues in much larger numbers.

=Changes in innervation.= As shown under hyperæmia the vaso-motor system of nerves exerts a potent influence on the circulation and is largely instrumental in bringing about circulatory disorders. The increase in the number and force of the contractions of the heart, and the rigid contraction of the walls of the arteries proceeding to an inflamed part, are distinctly the result of a reflex nervous action. The implication of the second eye when one has been violently inflamed from a mechanical injury is another example of this kind. The loss of power of the vaso-motor nerves is however even more characteristic. Experimentally the cutting of the cervical sympathetic or crushing of the superior cervical ganglion causes congestion and finally inflammation of the structures on that side of the head; the crushing of the semilunar ganglion similarly affects the abdominal viscera; and the cutting of the pelvic plexus, the structures of the hind leg. The contraction and dilatation of the inflamed capillaries is largely a nervous phenomenon. A certain number of irritants, like warm water, mustard, or ammonia cause contraction followed by dilatation of the capillaries, while others like dilute mineral acids, alkalies, chloroform, or sodium chloride and sugar in concentrated solution produce dilatation at once. Some poisons act variously on different parts, eucalyptol causing dilatation of the arteries and contraction of the veins, while corrosive sublimate causes contraction of the arteries and dilatation of the veins.

So with certain microbian toxins. Introduced into the general circulation they produce active congestion or inflammation in the seat of colonization of the microbe from which they were derived, as witnessed in the use of tuberculin or mallein. Finally the chill and febrile reaction which attends on extensive inflammation is essentially a nervous phenomena in its inception and progress.

=Changes in the circulation.= The usual changes in the bloodvessels of the inflamed part may be thus succinctly stated: 1. Contraction of the capillary vessels of the affected part and hastening of the current of blood through them. 2. The succeeding dilatation of the capillaries and the slowing of the blood stream, which still flows uniformly throughout the diseased tissue. 3. The flow of blood becomes irregular, at points tardy, and at others oscillating or even recoiling between the pulse beats when it has been forced into a vessel already blocked by coagulum. 4. In the still pervious vessels the red blood globules occupy the centre of the vessel where the current is rapid, while the white globules roll slowly along the inner surface of the walls where the current is slow and become adherent to the walls and stationary, while the general current rolls on. This is a direct abstraction of the white globules from the circulating blood and greatly favors the coagulation of the blood in the capillaries. The blood plates equally collect in the periphery of the vessel and escape. 5. The adherent white globules migrate in large numbers through the capillary and venous walls into the tissues. The red globules migrate to a less extent at first. 6. Small coagula form in the affected capillaries, forming minute red points which cannot be pressed out by the finger. 7. The red globules in the area of stagnation back of these capillary emboli adhere to each other by their flat surfaces and form rolls which pack into the vessel and are enveloped in a fibrinous clot. 8. The liquid part of the blood rapidly exudes into the tissues leaving the red globules relatively much more abundant in the liquid which remains inside the vessel. 9. The walls of the capillaries become softened and allow a readier transudation of liquor sanguineous, and escape of the globules through the walls of the vessels. 10. The arteries leading to the inflamed part have their muscular coats more rigid and unyielding and transmit much more blood than the corresponding artery leading to the healthy part. 11. The heart is equally roused to more rapid and often more forcible contractions, which modify the pulse both in number and rhythm. 12. The circulating blood is found to have received a great increase in the fibrine formers, the fibrine in the shed blood amounting to 6, 8, or 10 parts per 1000 in place of 3 parts as is normal. The contraction of this causes a depression on the surface of the clot. 13. The red globules become viscous and adhere together by their flat surfaces to form rolls, which precipitate much more rapidly than single globules and leave the coagulated blood with a straw-colored upper stratum (buffy coat). 14. Increase of waste products, urea, uric acid, hippuric acid, etc.

Other changes in the blood are alleged, like lessening of the albumen, as balancing the increase of fibrine, and lipæmia, but the constancy of these in all cases of inflammation is uncertain.

By way of comment and explanation of the above changes in the circulation the following may be advanced: The primary contraction of the capillaries is by no means a necessary condition of inflammation, and contractions and dilatations within certain limits occur in health and as a purely physiological act. The dilatation of the capillaries and the increased flow of blood to the part are related to each other as in part cause and effect, yet both are due to a reflex act from the seat of irritation which inhibits contraction in the capillaries and determines a more rigid contraction in the walls of the arteries running to the part. A rigid inelastic vessel of the same calibre and under the same pressure transmits more liquid than the one with elastic walls. The movement of the white globules to the walls of the vessel depends in part on their levity, light bodies passing into the outer slow moving layer, which is less dense, from the central stream where the force and density are greater. The epithelial cells of the intima undergo cloudy swelling and are often detached, allowing the readier migration of the globules through the openings of the lymphatics and the softened and friable walls. When the capillaries are blocked the pressure necessarily increases on the arterial side, favoring laceration of the friable walls and the escape of minute masses of blood. The formation of the buffy coat is characteristic of the normal equine blood; in inflammation it becomes more abundant. In the other genera a buffy coat apart from inflammation may be shown in: (a) anæmia or oligocythæmia in which the blood is deficient in red globules; (b) in plethora in which there is an excess of blood solids; (c) in pregnancy in which there is an excess of white and small red globules; (d) in violent exertion or over-excitement, in which the blood has circulated with extraordinary rapidity. The all-sufficiency of the tissue cells in determining inflammation may be deduced from the following experiment. A ligature is tied around a frog’s thigh so tightly as to arrest circulation, and the leg amputated above the ligature; mustard is then applied to the web of the foot and a blister rises precisely as though circulation continued.