Part 9

Parenchymatous inflammation is manifested by a degeneration of the cells affected. This may terminate in their destruction through the conversion of their protoplasm into fat-drops, fatty degeneration; although more frequently a simple accumulation of albuminoid granules (granular degeneration) occurs. The latter represents a transitory condition, from which a return to the normal state readily takes place. This form of inflammation is met with in those organs which present a sharply-defined contrast between the functionally important cells and the connective tissue which surrounds them. The liver, kidneys, heart, spleen, pancreas, and glands in general, are consequently the most frequent seat of parenchymatous inflammation.

Opposed to this variety is the interstitial inflammation. The exudation of the latter remains within the connective-tissue framework of the organ. It is essentially cellular in character, and the number of cells is comparatively small. With their presence and the possibility of their nutrition a permanent increase in the quantity of the fibrous tissue of the organ is permitted. This becomes relatively greater in the course of time, and the parenchymatous cells become degenerated and absorbed. Interstitial inflammations are likely to become chronic in character, and, from the outset, are usually associated with parenchymatous changes.

An important clinical distinction is drawn with reference to the duration of an inflammation. Acute inflammations are those whose course is rapid, whose progress is associated with graver disturbances of function, and with a greater prominence of the cardinal symptoms. The chronic forms occupy more time in their progress, the functional disturbances, though severe, are injurious more from their protracted persistence, than their temporary violence, while redness, swelling, heat, and pain are symptoms of trifling prominence.

The exudation in acute inflammation, if recovery takes place, is rapidly removed from the place of its origin, while in the chronic variety it tends to become a part of the region in which it lies, or, if removed, slowly disappears, and may be constantly replaced. Acute inflammations may become chronic, and the chronic variety is liable to acute exacerbations.

The distinction between acute and chronic inflammations is essentially one of convenience, and, when considered from the anatomical point of view, relates rather to the persistence of the results. These may be {54} present as a variously modified exudation or as a degenerated condition of the parenchyma of the organ or tissue affected.

Inflammation terminates in resolution, production, or destruction.

For resolution to occur it is necessary that the causes of inflammation cease to act, either by their removal or their isolation, and that their results be removed. With the removal of the results there is often associated the removal of the cause. That such may take place it is necessary that the function of the vessel walls be so restored that the exudation ceases to escape. Inflammatory products already outside the vessels, if present on surfaces with external outlets, are carried along in the course of the excretions. If they lie within the cavities of the body not opening externally, their removal is accomplished through the medium of the circulating lymph and blood, by absorption. The liquid portion of the exudation becomes a part of the circulating fluids of the body. The fibrin is converted into a granular detritus, which eventually disappears from the place of its formation. The leucocytes may return to the blood-vessels or enter the lymphatics; the latter course probably being the one taken by the larger number of the corpuscles. Many undergo a fatty degeneration, and as they lie in lymph-spaces their conversion into an emulsion permits a removal of the mechanical obstruction to the flow of lymph through the spaces in which they were accumulated. The red blood-corpuscles are destroyed, their pigment being dissolved by the surrounding fluid and removed in the course of the circulation and excretions, or it becomes transformed into granules or crystals, which may remain in the place of their formation, or be transferred, within amoeboid cells, to remote parts of the body.

When the exudation is abundant, as in the great lymph-sacs of the body--the several serous cavities--and especially when the openings in the walls of these sacs are obstructed or the currents within them are feeble, absorption takes place with great difficulty, and demands a long interval of time. The fibrinous and cellular portion of such an exudation frequently becomes converted into a caseous mass, from a partial fatty degeneration and inspissation. This mass becomes isolated from the cavity in which it lies, usually at the most dependent portion, by the formation of a capsule of connective tissue. It may subsequently become infiltrated with lime salts, calcified, and thus remain comparatively inert throughout the life of the individual.

The productive termination of inflammation is manifested by the new formation of connective tissue. This tissue is variously designated, as the inflammatory process is limited to the surfaces of the body exposed to the air, or the surfaces of cavities and organs, or as it lies within organs or the deep-seated parts of the body. In numerous instances it becomes a permanent constituent of the body, and, as time is usually essential for its formation, its occurrence is indicative of a chronic, rather than an acute inflammation. Certain chronic inflammations are progressive in character, the production of connective tissue being continuous, with perhaps occasional intermissions, as in the chronic interstitial inflammations of organs and tissues. The new-formed tissue, which at the outset is rich in cells, becomes in time more fibrous, and associated with this change in structure is a physical modification, manifested by its shrinkage. This new formation may fill a gap resulting from the destruction of tissue in {55} the progress of an inflammation, when it is present as cicatricial tissue--the scar which is usually met with upon the surfaces of the body or of certain of its organs. When opposed surfaces are united by the new-formed tissue, the term adhesion is applied; the adhesions being present as fibrous bands, cords, or membranes. The pericardial milk-spots and thickenings, the tendinous or semi-cartilaginous, indurated patches of serous membranes and of the intima of arteries, are all regarded as manifestations of a chronic inflammation of these tissues. With the localization of the inflammation in the outer walls of the bronchi and blood-vessels a thickening of the external sheath results, called a peri-bronchitis, arteritis, or phlebitis, as the case may be.

The new formation of blood-vessels is essential for the production and preservation of this connective tissue, and both arise from pre-existing tissues. Pus-corpuscles represent the simple cellular product of an inflammation, and their existence is but transitory. With the new formation of blood-vessels imbedded in abundant cells there exists a granulation-tissue, likewise transitory, but out of which arises the permanent fibrous tissue. The question is still mooted as to the part played by exuded white blood-corpuscles in the production of the permanent results of inflammation. It is generally conceded, especially since the observations of Ziegler, that they are capable of transformation into lasting constituents of tissue, into blood-vessels as well as into cells and fibres. Whether all the resulting permanent products of inflammation are dependent upon their activity, or whether the pre-existing fixed elements participate, is still to be considered undecided.

What, at present, appears most probable is, that from exuded leucocytes there arise, in the course of several days, larger cells--epithelioid or endothelioid--which are eventually associated with still larger cells, more irregular in shape, and provided with projecting filaments, giant-cells. Both varieties may result from the enlargement of leucocytes by fusion or by the assimilation of nutriment. The epithelioid cells eventually become fusiform or stellate, and their projections, as well as those of many of the giant-cells, become fibrillated. The fibrils of adjoining cells, becoming united, are thus transformed into a meshwork of fibrous bundles enclosing irregular spaces, while the nuclei of the cells, with the immediately surrounding protoplasm, remain upon these bundles as the permanent cells of the new-formed tissue. The blood-vessels arise from pre-existing vessels, chiefly capillaries, and probably are also formed from the cells present in the exudation. The former method is indicated by the projection of solid sprouts from the wall of a capillary, which may unite, forming arches, and communicate with sprouts from neighboring capillaries, thus forming bridges. Both arches and bridges then become hollowed and admit the circulating blood. Ziegler maintains that the projections of the larger epithelioid cells and giant-cells become elongated, and eventually fused with capillaries, or the projections from capillaries. When this fusion is accomplished the cells become hollowed, their cavities communicating with those of the blood-vessels. These epithelioid cells, whose formation and transformation are of such importance in the history of productive inflammation, are designated by Ziegler as formative cells, and are frequently derived from the exuded white blood-corpuscles, though not identical with them.

{56} The inflammations not terminating in resolution or production, end in the destruction of the part. This result occurs when the nutrition of the inflamed territory is so diminished, by the changes in and around the vessels, as to become insufficient for its preservation. As the nutriment is derived through the blood-vessels, the more complete and the more permanent the stagnation in them the more likely is death to result. This event also depends upon the quantity and quality of the exudation. The more abundantly cellular the latter, the more likely is an abscess or ulcer to result.

As most abundantly cellular exudations are considered to be dependent upon the presence of putrefactive agencies, those inflammations of a predominant putrid character (gangrenous inflammations) are those terminating in destruction. The dead product is present as a slough or sequestrum, when dead soft or hard tissues are detached, entire or in part, from the living; or as a granular detritus contained in a more or less abundant liquid. The inflammatory process producing the slough and sequestrum is characterized as a gangrenous inflammation of soft parts or a caries of bone, while the process resulting in the formation of the granular detritus, and which has no necessary connection with putrefactive agencies, is called a softening, from the physical condition of its result.

Thrombosis and Embolism.

A blood-clot formed within a blood-vessel during life is called a thrombus. The entire process of which the thrombus is the essential element is designated thrombosis.

These terms were introduced by Virchow to avoid the confusion which resulted from regarding the process and result as synonymous with inflammation of the vessel. All writers, even at present, do not adhere to this strictness of meaning. For a thrombus of the vulva indicates a clot of extravasated blood within the connective tissue of the labium; in like manner, a vaginal thrombus is the effused and clotted blood in the loose connective tissue surrounding the vagina. These exceptions are gradually disappearing, and the word hæmatoma, tumor composed of clotted blood, is being substituted in both instances. A cancerous thrombus represents a mass of cancerous tissue whose growth is extended along the course of a vessel, its wall having been penetrated. In general, however, the term thrombus, unless otherwise qualified, is used as first stated.

Although thrombosis is commonly a morbid process, it is not uniformly so. Its physiological significance is illustrated by the part it takes in the closure of the umbilical and uterine vessels, after childbirth. The surgeon makes use of it in his efforts to overcome certain of the ill effects of amputation, and to accomplish a cure of such local diseases as aneurism, where it is deemed important to diminish the supply of blood.

The thrombus being a blood-clot, it is composed, like the latter, of fibrin and blood-corpuscles. It is presumable that the fibrinous part of a thrombus owes its origin to the same conditions which determine the presence of fibrin in blood removed from the vessels during life or in that within the vessels after death.

{57} According to A. Schmidt, the blood and other fluids, in which clotted fibrin makes its appearance, contain two generators, called fibrino-plastic and fibrinogenous. The former is considered to be paraglobulin, a substance contained mainly in the white blood-corpuscles, while the fibrinogenous generator is held in solution in the plasma of the blood. When these materials are acted upon by a third, the fibrin ferment, clotting takes place and fibrin is formed. It is thought that the ferment is intimately connected with the white blood-corpuscles, for with the microscope coagulation is seen to advance as these become destroyed, and where the leucocytes are most abundant, there coagulation advances most rapidly. The elements of clotted fibrin are always present in circulating blood, but Brücke has shown that blood remains fluid, under ordinary circumstances, because of its constant contact with the normal vascular wall.

The general causes of thrombosis are those which produce an abnormal condition of the endothelium, a rapid destruction of the white blood-corpuscles, or a stagnation of the blood. With the presence of one of these causes there is often conjoined another, and the conditions under which they are present are conveniently used in the classification of thrombi.

Although stagnation of the blood is often an important immediate cause of its coagulation, it is apparent, from the investigations of Durante and others, that stagnant blood clots in the living vessels only when their endothelium is in an abnormal condition. With the co-existence of abnormal endothelium and stagnant blood, thrombi form with greater frequency and become more voluminous in a given interval of time.

The importance of the death of white blood-corpuscles in the formation of thrombi is generally admitted, and is especially insisted upon by Weigert. According to the observations of Zahn, the nucleus of certain thrombi is the result of the death of these leucocytes and their accumulation upon an altered intima. The experiments of Naunyn, Köhler, and others show that a thrombus may be rapidly produced by the injection into the blood of fibrino-plastic substances, and of those through which free hæmoglobin is admitted into the circulation. The former may be expressed from a fresh blood-clot; the latter may be obtained by thawing frozen blood, or by injecting such material (bile-acids, for instance) into the circulating blood as rapidly destroys the red blood-corpuscles. Although Weigert lays special stress upon the destruction of white blood-corpuscles in the formation of the thrombus, it appears, from the experiments above referred to, that indirectly the destruction of the red corpuscles is also of importance.

Although largely made up of fibrin, a thrombus also contains blood-corpuscles, both red and white, and the appearance of the mass is modified according to the variations in the relative proportions of these constituents.

Zahn divides thrombi, according to their color, into red, white or colorless, and mixed varieties. The red owes its color to a large number of red blood-corpuscles, while the white and mixed forms contain various proportions of white blood-corpuscles and fibrin and a diminished number {58} of red corpuscles. The cause of this difference in the color of thrombi is to be sought for in their method of origin. When blood clots slowly in a dish, the heavier red corpuscles settle to the bottom, and the lighter white corpuscles form a superficial layer. Stagnant blood clotting rapidly furnishes a uniformly red mass. The red thrombus, like the red clot, is the result of the rapid coagulation of stagnant blood. The white thrombus, on the contrary, largely composed of white blood-corpuscles, represents a constantly increasing deposition of these from flowing blood. The mixed thrombi arise from a combination of both conditions, and are usually white at the outset. Thrombi formed in the heart and larger arteries are usually white, those in the auricular appendages and on venous valves are mixed, while red thrombi are more common in arteries and veins, since the conditions favoring their origin are more frequently met in such vessels.

Thrombi are frequently stratified, in consequence of the successive deposition of new layers of blood-corpuscles and fibrin upon a pre-existing thrombus. Circulating blood is therefore necessary for the stratification, and such thrombi are likely to be mixed in color. Unstratified thrombi are usually white or red, the former largely composed of agglomerated white blood-corpuscles so moulded and situated as to prevent a stagnation of blood in their vicinity, while the red thrombus is rarely stratified, since its formation demands a stoppage of the blood-current. Stratification is intimately connected with the enlargement or growth of the thrombus, which takes place from the surface exposed to the flowing blood, and which is greater or less according to the seat of the thrombus.

Thrombi are usually divided into those from compression, dilatation, traumatism, and marasmus; in all of which groups an abnormal condition of the endothelium is to be met with.

Thrombi from compression are frequently formed in veins, in the vicinity of growing tumors. Their presence is most constant when the vein is compressed between a resistant surface, especially bone, and the tumor. A compression of the smaller blood-vessels within an organ, as the liver or kidney, may take place in consequence of chronic interstitial inflammation, or the growth of cancerous or other malignant tumors in such organs. The production of this form of thrombus is sought for in the treatment of certain aneurisms by direct pressure, the resulting stagnation of blood being followed by a coagulation within the aneurismal sac.

Thrombi from dilatation are met with both in dilated arteries and veins. In aneurism and varix a slowing of the blood-current is present, and the intima of the diseased region is frequently in such an abnormal condition that a clotting of the blood readily takes place. The shape and situation of the dilatation are of importance in promoting the formation of the thrombus; the more pedunculate and the more voluminous the sac the more certain is the thrombosis.