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.
MICROBES, DIAPEDESIS AND PHAGOCYTOSIS.
The rôle of microbes in inflammation is much greater than was formerly supposed. It is now demonstrated that a large class of inflammations are directly caused by the colonization of microbes in the tissue and by the local irritation caused by their ptomaines and toxins. We must also admit the direct action of the latter on the heat producing and vaso-motor nervous centres, as a factor more or less potent in different cases in the causation and maintenance of inflammation. No less important is the relation of the microbe to the migration of the globules and the subsequent results of the inflammation. This influence microbes share with certain chemical agents. Migration may be greatly checked even in inflamed parts by the hypodermic or intravenous injection of sulphate of quinia, eucalyptol, salicylic acid, or iodoform. Some have thought these acted by a chemiotactic attraction, but quinia is otherwise found to repel the leucocytes. Their action on the leucocytes or capillary walls is problematic.
Chemiotaxis is that power by which a microbe or any element attracts or repels the leucocytes. When it attracts the chemiotaxis is said to be positive, when it repels it is negative. Among negative chemiotactic agents are quinia, solutions of sodium chloride (10%), and potassium salts, lactic acid, alcohol (10%), chloroform, glycerine, jequirity, and bile. To some agents, (creatine, creatinine, allantoin, peptone, phlorydzine,) leucocytes are indifferent. To gluten, wheat casein, pea legumin and the great majority of pathogenic microbes, leucocytes are positively attracted. As microbes exercise a great influence in producing local inflammation, so they are important factors in procuring an abundant emigration of leucocytes. Some of the most fatal of microbian diseases, like fowl cholera, repel leucocytes, and the benefit of their defensive work is to a large extent lost. The toxins of the chemiotactic microbe filtered from the bacteria exert the same influence as the living bacteria, as shown by Gabritchevski, Massart and Bordet.
But chemiotaxis may be exerted from within the bloodvessel as well as from without. Bouchard, Massart and Bordet have shown that a tube containing a culture of bacillus pyocyanus, introduced beneath the skin of a rabbit attracts in a few hours a great number of leucocytes. But if, immediately after its introduction, ten cubic centimetres of a sterilized culture of the same bacillus are injected into a vein, very few leucocytes enter the tube inserted under the skin. The chemiotaxis seems to operate in this case from within the blood, and the desires of the leucocytes are satisfied without leaving the vessel. It would seem that in such cases the migration and protective work of the leucocytes is best exerted at the outset of the illness and before the toxic products have been poured into the blood in any quantity, whereas in the advanced stages when the blood is charged with ptomaines and toxins migration and phagocytosis would be likely to be limited and ineffective. The same consideration would forbid the use of drugs that check migration in all cases of attacks by microbes for which leucocytes have a positive chemiotaxis.
Phagocytosis is the act by which the leucocytes englobe and dissolve the invading microbe. By its amœboid movement the leucocyte flows around, and envelopes the microbe for which it has a positive chemiotaxis, and then begins the struggle of vitality between the two living germs. If the poison (leucomaine antitoxin,) and digestive ferment (enzyme) of the leucocytes are more deadly to the invading germ, than its ptomaines, toxins and enzymes are to the leucocyte, the white cell comes off the victor, and recovery takes place, but if the converse obtains the triumph is on the side of the microbe. As a rule much depends on the more or less deadly nature of the products of the invading microbe, on the numbers of the germ, the rapidity of its proliferation, and the consequent amount of its toxic products thrown into the system, on the one hand: And on the other the potency of the chemiotaxis of the leucocyte for the invading germ, the number of white cells that emigrate into the inflamed tissue and engage in the work of phagocytosis, and on whether the particular animal system and its white cells have sustained a previous attack by the same germ and has thereby been educated to produce a greater amount of the defensive proteids (leucomaine, antitoxin, enzyme) than it naturally would (acquired immunity).
Even with an abundant emigration of the leucocytes into the inflamed or invaded tissue, a number, greater or less, are usually destroyed by the bacterial poisons and pass into degeneration or liquefaction, as in the formation of pus, and yet the attacking germ may be overcome, destroyed and devoured by the rapidly increasing survivors. In general terms the migration of the cells is in inverse ratio to the susceptibility of the animal to the microbe or the disease which it causes.
The positive and negative chemiotaxis, which determine phagocytosis or prevent it, may be seen in the action of the leucocytes toward the germs of two diseases, to one of which the animal is susceptible and to the other of which it is not. Thus the leucocytes of the pigeon take in the bacillus anthracis and suffer nothing apparently, whereas the same white cells of the dove are repelled by the bacteria of fowl cholera which are not therefore found in their interior.
The leucocytes that migrate from the bloodvessels are in the main, the most numerous, (the neutrophile or polynuclear) form; the mononuclear leucocytes with horseshoe shaped nucleus also migrate but in much fewer numbers and are as a rule less occupied in phagocytosis. At the same time, these two forms may show each a preference for a particular microbe, the polynuclear cell sometimes devouring one which the mononuclear cell rejects, and the mononuclear cell taking in one which the polynuclear refuses.
The small round white cells (lymphocytes) and the eosinophile leucocytes take no prominent part in phagocytosis.
EXUDATION.
In inflamed vascular tissues one of the most important results is the exudation. This is not, however, a mere transudation of the liquid parts of the blood, as takes place in dropsy, but it is to a large extent a selective process determined apparently by the condition of the capillary walls, and the nature of the inflammation is stated according to the character of the exudate. The dropsical effusion contains little albumen, fibrine or cell forms, and does not coagulate. The inflammation exudate contains abundance of fibrine, cells and other solids and coagulates spontaneously in contact with inflamed tissue, or when removed from the body, by reason of the transforming leucocytes. Inflammatory exudate usually contains 6 to 8 per cent. of solids whereas the normal canine lymph contains 4 to 6. The exudate varies not only in different inflammations, but in successive stages of the same inflammation. The exudate may be mucous, serous, fibrinous or hæmorrhagic.
Mucous Exudate. In inflammation on a mucous or synovial surface the inflammatory exudation, mingled with the more or less altered secretion of the mucous glands, and the epithelial cells and leucocytes forms a viscid fluid, rich in mucin, and characterizing the mucous or catarrhal inflammation. The nature of the discharge varies greatly, the serous character predominating at the start of the inflammation, and a thick, opaque creamy or semi-solid muco-purulent material appearing as the disease advances. It contains filaments of precipitated mucin insoluble in acetic acid or alcohol and cells in all stages of change from the exudation leucocyte and mucous cell to the pus corpuscle, the latter being characterized by its bipartite or tripartite nucleus rendered visible by contact with weak acetic acid.
Serous Exudate. This consists of the liquid elements of the blood with only a limited amount of fibrine formers and consequently little tendency to clot firmly. The presence of fibrinogen however serves to distinguish it from the liquid of mechanical dropsy, as does also the greater quantity of cells and nuclei of common salt and phosphates. It is usually straw colored in mass, but is sometimes slightly opalescent by reason of the numbers of cells and floating filaments of fibrine. Serous exudations take place in the early stages of inflammations (as in catarrh) and in inflammations of serous membranes (pleura, peritoneum, joints), in strong, vigorous subjects. They constitute the liquid contents of blisters whether raised by medicinal irritants, chafing, or heat. They clot under heat and nitric acid with a firmness proportionate to the amount of albumen.
These effusions are dangerous by reason of their interference with the functions of organs by pressure as with the dilatation of the lungs, the movements of the heart, the action of joints, or the integrity of the brain or spinal cord. When the causative disease has subsided they are usually speedily reabsorbed, the cells passing into the lymph vessels, or becoming degenerated, liquefied, and absorbed. Yet serous effusions often remain as permanent accumulations. For the blood staining of serous effusions and their clearing up, see under pleurisy.
Fibrinous Exudate. This is characterized by the amount of fibrinogen and fibro-plastin in its composition and by the comparative absence of leucocytes. It oozes through the vessels and coagulates in the tissues or on the surface of inflamed serous or mucous membranes. The more liquid part separating from the coagulum escapes from the free surface or accumulates in the lower part of the serous cavity. The coagulation is doubtless caused by the fibrine ferment derived from the rapidly proliferating cells and degenerating leucocytes. It usually occurs promptly in or on an inflamed tissue, but in contact with healthy structures only (as in a serous sac) it may remain fluid for an indefinite length of time. This exudate constitutes the false membranes that form on the pleura, pericardium or arachnoid, the coagulum of fibrinous pneumonia, and the plastic lymph on the surface of a granulating wound. It is especially injurious by reason of its enveloping organs (lungs, heart, bowels, iris) and subjecting to permanent compression by reason of its contracting, also by binding them to adjacent structures by false membranes. In coagulating it becomes first fibrillar then granular and finally undergoes molecular degeneration (Cornil and Remvier), or development into new tissue (Paget). When organized it usually takes the form of the adjacent tissue from which its trophic cells are derived. Thus in divided tendons, in serous membranes and in granulating wounds it is fibrous, and between the ends of a broken bone it is osseous. If however, the adjoining tissue is a highly organized one, like nerve or muscle it may be replaced by a simpler (fibrous, osseous).
Fibrinous inflammations are especially found in connection with inflamed fibrous tissues and in strong vigorous subjects.
Blood Exudations. In all inflammations there is some migration of blood globules (red as well as white) but seldom in quantity sufficient to stain the tissues materially. Minute ruptures of the capillary vessels are not uncommon, with punctiform clots in the tissues, but extensive escape of blood is mainly seen in penetrating or contused wounds of the loose, subcutaneous connective tissue, and in infective inflammations (anthrax, Rinderpest, swine plague, petechial fever, malignant catarrh, snakebites) with destruction of blood globules or extreme changes in the walls of the capillaries. Newly formed vessels in friable neoplasm are subject to blood effusions. In acute inflammations of serous membranes the exudate is usually of a dark port wine hue at first. In such cases it may pass in succession through all the stages of dark red, brick red, yellow, reddish, and chocolate color, before becoming milky and finally transparent.
Croupous Exudate. Croupous inflammation usually occurs on or near a mucous surface and is characterized by an exudation consisting mainly of fibrinous material entangling white cells, epithelium, a few pus corpuscles and some form of bacteria. In true diphtheria of children this is the Löffler bacillus, in the pseudodiphtheria, attending on scarlatina, etc., it is streptococcus pyogenus, in the diphtheria of calves it is bacillus diphtheriæ vitulorum, and in that of chickens and pigeons it is the bacillus diphtheriæ columbarum (Löffler). Pseudo-membranous inflammations therefore constitute a group agreeing in the nature of the exudate but differing essentially in the cause. This difference in the cause has a most material effect on the course and gravity of the disease. One form like true diphtheria in man not only extends into the tissues, and tends to necrotic changes, but also poisons the nerve centres by the toxic materials absorbed inducing troublesome paralysis, while another like croup of children establishes a violent but essentially superficial disease and when that recovers it leaves no ulterior ill effects elsewhere.
A Chyliform exudate has been noted in peritonitis in the dog the milky whiteness being due to fatty granules.
RESULTS AND PRODUCTS OF INFLAMMATION.
As nearly all inflammations have significant exudations it is well to follow these in their subsequent progress through reabsorption and removal, development into new tissues, necrosis, suppuration and ulceration.
Resolution. If an inflammation, slight in character and with only a moderate exudation, subsides and is followed by a rapid liquefaction of the cells and fibrinous coagula and a reabsorption of the exudate, so as to leave the part in its primary healthy condition structurally and functionally, it is said to have terminated by “resolution.” If this occurs with extraordinary rapidity it is said to have ended by “delitescence.” This is not always an unalloyed good, as often in delitescence, coagula and infecting material may be carried on by the circulation, to block the next set of capillaries in its course and set up new centres of inflammation. This is one form of “metastasis” though a more definite metastasis is in rheumatism where the disease attacks one joint today and a distant one to-morrow.
Inflammatory New Formations. Of the growths in lymph there are two principal kinds: first, the plastic, fibrinous, granular or molecular; and second, the aplastic or corpuscular. The first form tends to develop into new structure, the second to disintegrate and decay. The tendency to one or other form depends largely on the strength or weakness of the system’s health, on the deficiency or excess of corpuscles in the exuded fluid, and on the distance of the latter from living tissues and blood supply. Much also depends on the predisposition of the genus, the tendency to suppuration in lymph being in a descending series from horse, ass, and mule, through ox and sheep, to dog, pig, and finally, the bird, in which latter suppuration is quite exceptional.
Suppuration. In inflammations of a high type, in those occurring on the skin or mucous membranes in which there is an extraordinary increase of nuclei and embryonal cells, and in lymph thrown out in excess at one point, so that its central parts are far from vascular tissue and nourishment, the cell elements undergo a rapid increase and degradation into pus-corpuscles, and its solidified intercellular lymph undergoes granular decay and liquefaction into pus.
While the above conditions are favorable to the formation of pus, the process of suppuration must now be recognized as an infective process due to the propogation of bacteria (mainly chain forms—Streptococcus pyogenes—cluster groups—Staphylococcus pyogenes—and rod forms—Bacillus pyogenes). These or other bacteria are found in the pus of acute abscesses, and when absent in chronic abscesses are to be considered as having perished since the abscess was recent and active. Inoculation of a rabbit with an excess of the pus of an acute abscess produces general purulent infection (pyæmia) and early death; from a medium dose an abscess is produced; while from a small dose there is no effect whatever. In the latter case the bacteria are overcome and devoured by the abundance of vitally potent white blood globules and tissue cells. This pus-forming action of these bacteria explains the great difference in results in wounds exposed to the air and those in the interior of the body and far removed from air and its floating bacteria. A broken bone, with no wound in the skin and little injury to parts around the fracture, is readily repaired without any formation of pus, if merely kept still and immovable; whereas a broken bone, continuous with a wound through the skin, always tends to form pus or become otherwise infected, and is extremely dangerous even to life. The tendency of every open sore is to form pus on its surface but this may be arrested and avoided by preventing the access of germs, or by a free use of disinfectants and a covering which shall arrest and filter out the germs. Similarly in an abscess, evacuation followed by the injection of disinfectants, without the formation of any perceptible permanent opening to the outer air, will put a stop to the pus-formation. The subjection of an inflamed part to the control of these pus-forming bacteria is dependent on the lowered vitality and power of resistance of the inflamed tissues, and of the white cells of their circulating blood. Healthy parts can successfully resist them, though they are constantly present in surrounding air and on objects, but in this as in all other cases, of bacterial infection, so soon as the tissue is injured, inflamed and lowered in its power of vital resistance, the pyogenic bacteria assail it successfully. Hence, too, the more abundant exudations of lymph, the centres of which are farthest removed from the healthy tissues and from nourishment, are the most prone to suppuration. That the germs can make their way to such deep-seated exudations in the substance of solid tissues is to be accounted for by their gradual advance through the inflamed and weakened structures from the adjacent skin or mucous membrane, or in some instances by reason of their presence in small numbers in the blood. It is further noteworthy that those animals in which suppuration does not occur readily are such as have a special power of resistance to some other organic poisons. Thus the hog, which is supposed to be proof against snake-bite, is also, to a large extent, proof against the pus-forming bacteria.
Pus. This is a white, or yellowish white, creamy-looking product, composed of a clear, transparent fluid, rendered opaque by numerous floating pus-corpuscles. These pus-corpuscles have the same size as the white globules of the blood (¹⁄₂₅₀₀ to ¹⁄₃₀₀₀ inch) and are peculiar in that each shows within it three or more nuclei, which become visible on the addition of a drop of water or acetic acid. Each of the common embryonal cells found in the inflamed tissue usually contains two nuclei, the indication of the active increase by division into two, but when the supply of nutriment is checked the nuclei continue to divide, while the cells remain unchanged, and thus every cell comes to contain several nuclei in addition to fatty granules, and constitute pus-corpuscles.
When pus is formed in a well-maintained system and tissue, the outer layer of the lymph is developed into a fibrous sac enclosing the liquid pus and constituting an abscess. In an unhealthy system, or when the inflammation depends on some injurious poison, like that of erysipelas, this sac may not be formed, and the pus, burrowing into and between different organs, destroys the connections and substance—diffuse suppuration. When an abscess has formed in soft tissues its investing sac shrinks as it assumes the fibrous character, and the confined pus being incapable of compression, presses the membrane outward on the side in which the surrounding tissues are most loose and least resistant, hence, usually, though not always, in the direction of the skin; the soft tissues become absorbed and removed in the track of the advancing pus; and, finally, the latter reaches a free surface and escapes. Thus, an abscess usually bursts through the skin, but also, at times, through a mucous membrane into the lungs, bowels, etc., or through a serous membrane into chest, abdomen, etc. When an abscess is formed in bone or dense fibrous tissues which press equally on all sides, it may remain imprisoned for months and years after all inflammation has subsided, constituting an indolent or cold abscess. When the imprisoned pus is inclosed by thick fibrous or resistant tissues at all points but one, it will make its way along the narrow passage of yielding tissue, but as the resulting outlet is constricted, long, and tortuous, the contents cannot readily escape through it nor the walls of the abscess contract so as to expel the confined pus, and the latter goes on forming and discharging through the narrow outlet for months or years. This is a fistula or sinus.
Healing by Adhesion or First Intention. When a clean-cut wound has the blood staunched and its lips brought together without exposure to the air (or contact with pyogenic germs), they adhere at once and heal without pus or almost any appreciable formation of new tissue. Here the lymph thrown out on the cut surfaces agglutinates them, and the cells, multiplying, form a thin layer of embryonic tissue which gradually develops into a fibrous structure and repairs the breach without any perceptible scar.
Healing by Second Intention. Granulation. When a wound has caused destruction of tissue, or when a simple incision is left exposed to the air, the breach is filled up by new tissue through the process known as granulation. The superficial layer of lymph thrown out on the raw surface becomes oxidized and degenerates into pus, while the deeper layers become solid, fibrillated, the seat of cell growth, and are finally transformed into a fibrous structure. New bloodvessels form in loops in the developing lymph and constitute the bright red granulation-points which cover the raw surface. The fibrous tissue into which the lymph is transformed undergoes gradual contraction in development, and thus, day by day, the edges of the adjacent healthy skin are drawn in, so as to cover the wound more or less perfectly, and a slight scar only is left when healing has been accomplished.
Granule Corpuscles and Masses. This is another degenerative transformation in lymph and, is seen mainly in inflamed glands and brain and lung tissue. The cells found in the exuded lymph are made up of granules ¹⁄₁₀₀₀₀ inch in diameter, and besides these, large, irregularly shaped masses of granules are extended along the capillary bloodvessels. After the lymph has coagulated these granular masses soften and liquefy preliminary to reabsorption and removal, and the restoration of the tissue to a healthy condition. When in excess this softens and disintegrates the tissues, leading to permanent loss of substance. See granular degeneration.
Interstitial Development of Lymph into Tissue. This is equivalent to what takes place in the formation of the sac of the abscess or of granulation-tissue. The liquid lymph in coagulating, becomes fibrillar, and the cells and nuclei of the adjacent tissue, having an abundant supply of blood and nutriment, multiply first as simple, rounded embryonic cells, then deposit around them new tissue, becoming elongated, spindle-shaped, branching, etc., and thus get imbedded in a fibrous material of their own formation. These new formations are usually of a low type of organization, like white fibrous tissue or bone, and hence, although breaches in the higher structures like muscle, nerve, gland, skill, are filled up, it is usually only by the drawing together of the remaining healthy parts by these new formations without the restoration of any of the original tissue which has been destroyed. The cicatrix (scar), alone is made up of new material.
Lymph developing in this way may undergo any degeneration to which normal tissues are subject. Thus it may undergo black pigmentary (melanotic) degeneration, it may become impregnated with lime-salts (calcified), it may wither up into a hard gelatiniform or horny mass, or it may undergo fatty degeneration.
Fatty degeneration is the most common form, and consists in the excessive deposit of fatty granules, first in the cells which are in excess or badly nourished, and next in the adjacent tissue, the normal elements of which are replaced by fatty granules.
Softening is an almost constant result of inflammation. The exudate infiltrates and separates the tissue elements, destroying their cohesion; the liquefaction of these elements impairs this still further, and the more or less perfect transformation of the tissue into embryonic tissue entails the loss of its rigidity and power of resistance. Thus the inflamed brain-tissue may become a mere pulp, and the inflamed bone may be cut with a knife.
Ulceration is closely allied to softening. On the surface of a sore there is an excessive exudation of lymph, which loosens and disintegrates the layer of lymph that is already in process of development, and also a part of the tissue beneath. The cells in these parts fail to develop naturally and to build up good tissue; they become fatty, die, and together with the tissue in which they lie, break down and pass off as a pulpy debris. Thus the sore constantly deepens and widens, or at least refuses to contract and heal. It is usually the result of bacterial infection.
Gangrene or death of a part is another effect of inflammation. It results usually from the cutting off of the blood supply through the obstruction of the bloodvessels; by the pressure of excessive exudation in unyielding structures, as in bone, or under the hoof; by implication of the inner coats of the bloodvessels in the inflammation, when the contained blood will clot and obstruct them; or by blocking with the blood clots that have been formed at a distance and washed on in the blood current to be arrested when they reach vessels too small to admit them. Like suppuration, gangrene is associated with and often caused by a bacterial growth. The dead mass remains as an irritant, and is slowly separated by the formation around it of embryonal tissue, granulations and pus. A second form is molecular gangrene, in which the cells and minute elements of the tissue die, and are cast off, leading to phagedenic (eating, extending) sores, as noted above under Ulceration. When gangrene occurs on an exposed surface, that may be altered from the normal color into shades of yellow, brown, green, red, or black, according to the amount of blood and the stage of decomposition, and may be cut without pain, if the subjacent parts are not pressed upon; it may be soft, may pit on pressure, may crackle under the hand from the evolved gases of decomposition, and may be covered with blisters (phlyctenæ) with red, grumous liquid contents (moist gangrene); again, it may be white, as after freezing, or it may be dark colored, dry, and horny, as from ergotism (dry gangrene).