even pouched.

This is known as

This is known as "stasis" or "stagnation" (Fig. 20). If stasis persists, coagulation or thrombosis occurs, because the vessel-walls have been so injured by the irritant as to be practically dead material, and they are no longer able to prevent clotting of their contents. Stasis is chiefly due to paralysis and damage of the vessel-walls. We can then sum up the vascular changes of inflammation by stating that they consist in a dilatation of the vessel-walls, in a primary acceleration, a secondary retardation, and a subsequent stagnation of the blood-current with adhesion of leukocytes to the walls of veins and capillaries, and the aggregation into masses of the red blood-cells. If stasis persists, the vessel-walls become profoundly involved in the inflammatory change, and they may rupture or be completely destroyed.

FIG. 20.-Stasis of blood and diapedesis of white corpuscles in inflammation.

Exudation of Fluids. It is to be remembered that in the process of nutrition serum and even white cells pass into the tissues through the walls of veins and capillaries. In inflammation the same thing happens, but the exudation is vastly greater in amount and is different in composition. In a slight inflammation, and in the early stage of any inflammation, there is an increase in the fluid exudate, and we speak of the condition as "serous inflammation." This fluid is really not serum, but is liquor sanguinis. We find true serum in passive congestion, not in active inflammation. The fluid in a serous exudation contains very few white cells, and hence little or no fibrin can form in it, and coagulation does not take place; and if the inflammation goes no further, it is absorbed by the lymphatics. A blister is an example of serous inflammation. If the inflammation continues to intensify, the exudation is altered in character-it becomes thicker, turbid, and very coagulable. It contains

white cells and fibrin-elements, and coagulates in the tissues. This fluid is known as "lymph" or plastic exudation, and when it is present we speak of the condition as "plastic inflammation." The lymphatics endeavor to absorb the fluid, but become occluded by coagulation, and the area they drain becomes swollen, hard, and "brawny." Lymph can be seen in the anterior chamber of the eye in cases of plastic iritis. The slighter the inflammation the less albuminous is the fluid-the higher the inflammation the more albuminous is the fluid. The focus of an inflammation feels brawny because of coagulation of a highly albuminous exudate-the periphery of an inflammation is soft and edematous because of the presence there of thin and non-coagulable exudate.

Diapedesis or Migration.-Even early in an inflammation some few white corpuscles pass through the vessel-walls;

FIG. 21.-Stages of the migration of a single white blood-corpuscle through the wall of a vein (Caton).

but when the inflammation is well established large numbers, and when it is severe vast hordes, pass into the perivascular tissues. This process is known as "diapedesis" or "migration." The leukocytes throw out protoplasmic arms, insert themselves between the cells of the walls of the vessel, and pull themselves through by their power of ameboid movement. They do not pass through existing open doors, but form openings which close after them. This is readily accomplished, because the vessel-wall is itself damaged, weakened, and convoluted. The escape of leukocytes takes place chiefly from the venules, though some migrate through the capillaries and even the arterioles (Fig. 21).

In very acute inflammation the vessel-walls are so damaged that red corpuscles also escape, making the tissue ap

pear as if infiltrated with blood. The white corpuscles often greatly increase in number in the blood of a person who has an acute inflammation (leukocytosis), and the blood-making organs, such as the spleen and lymphatic glands, are often enlarged. The blood-plaques or third corpuscles are found to be present in increased numbers. These blood-plaques are not seen in moving blood, but are found in blood-clot, their usual proportion to red cells being as I to 20, and they are especially numerous at the height of fever-processes and during convalescence from an extensive abscess.

Changes in the Perivascular Tissues.-The exuded liquor sanguinis coagulates, and as a result of the exudation of elements of the blood the tissues are softened, separated, and overfed. The abundance of food causes tissue-cells to multiply, and this process is known as "cell-proliferation." To the proliferating cells of the perivascular tissues are added the migrated leukocytes, the individual tissue-elements are separated and their identity is destroyed, and a mass is formed consisting of small round or oval cells held together by gelatinous intercellular material. The newly formed cellular mass is called "embryonic tissue," inflammatory new formation, indifferent tissue, juvenile tissue, or plastic infiltration. The tissues have reverted to a condition identical with the tissues of the embryo, as the first step in repair. Embryonic tissue may be absorbed by the lymphatics. It may be converted into pus if infected with pyogenic bacteria. It may be vascularized by the extension into it of capillary loops derived from adjacent capillaries. When embryonic tissue is filled with blood-vessels, that is to say, when it is vascularized, it is called granulation-tissue. Granulation-tissue is finally converted into fibrous tissue. The above complicated processes, vascular and perivascular, are not accidents nor haphazard freaks, but are Nature's efforts to bring about a cure. The acceleration of the circulation is an attempt to wash away offending material; when this fails ensuing congestion is relieved by exudation and migration, the blood becoming fibrinous and more corpuscular in order that foreign bodies may be encapsuled or extruded, so that damaged parts may be amply repaired and vital structures may be protected and shielded. The exudation of germicidal blood-serum may destroy bacteria in the perivascular tissues.

Dilatation is due to the direct effect of the irritant upon the muscle or its nerve-elements. Retardation and stasis are due to paralysis of the vessel-wall, which paralysis causes resistance to the passage of the blood-stream and adhesion of

the corpuscles to the vessel, and which deprives the blood of a force which normally urges it onward, namely, contraction of the arterioles. Stasis can be increased by the pressure of an enormous exudate, producing tension. Tension may be so great as to produce gangrene.

Inflammation in Non-vascular Tissue.-A type of non-vascular tissue is the cornea, and the cornea can inflame. When it inflames the episcleral vessels dilate and pour out exudate, and the fluid exudate and the leukocytes enter into the corneal lymph-spaces. The exudate coagulates and cellmultiplication ensues as in any other inflammation. If new formation takes place, a permanent opacity mars the cornea as a consequence. When cartilage inflames it becomes filled with leukocytes, which are obtained from the vessels of the synovial membrane or the bone, and changes ensue identical with those previously studied.

Classification of Inflammations.-The various forms of inflammations are-(1) Simple or common, that which is due to any ordinary traumatic, chemical, or thermal cause, and not to bacteria, such as traumatic periostitis or sun dermatitis. It does not tend particularly to spread. As a rule, the cause of a simple inflammation is momentary in action; (2) infective or specific, that which is due to micro-organisms, as the streptococcus of erysipelas. An unsuccessful attempt has been made to charge all inflammations to bacteria. It is true that bacteria can generally be found in inflammatory areas, but that they are the only causes of inflammation is accepted by few. Infective inflammations tend to spread widely; (3) traumatic, which is due to a blow or an injury; (4) idiopathic, which is without an ascertainable cause. There is certainly a cause, even if it cannot be pointed out, and the term "idiopathic" means that we do not know the cause; (5) acute, which is rapid in course and violent in action; (6) chronic, which follows a prolonged course; (7) subacute, which is intermediate in violence and duration between acute and chronic; (8) sthenic, characterized by high action. Occurs in strong young subjects; (9) asthenic or adynamic, occurring in the old, the debilitated, and the broken-down. It is unable to reach a sufficient degree of intensity to limit itself; (10) parenchymatous, affecting the "parenchyma," or active cells of an organ; (11) interstitial, affecting the connective-tissue stroma; (12) serous, characterized by profuse non-coagulating exudation, as in pleuritis, or by marked inflammatory edema; (13) plastic, adhesive, or fibrinous, characterized by an exudation which glues to

gether adjacent surfaces, as in peritonitis; (14) purulent, phlegmonous, or suppurative, when the pus cocci are present and multiply; (15) hemorrhagic, when the exudate contains many red blood-cells, as in strangulated hernia and in black small-pox; (16) croupous, when an inflammation produces upon the surface of a tissue a fibrinous exudate which cannot be organized (aplastic lymph), and which is due to the action of micro-organisms. It occurs most usually on mucous membrane; (17) diphtheritic, which differs from croupous in the fact that the false membrane is in the tissue rather than upon it; (18) gangrenous, an inflammation resulting in death. of the part, the gangrene being due to the tension of the exudate or the violence of the poison; (19) healthy, when the tendency is to repair; (20) unhealthy, when the tendency is to destruction; (21) latent, an inflammation which for some time does not announce itself by any obvious symptoms, as the inflammation of Peyer's patches in typhoid fever; (22) contagious, when its own secretions can propagate it; (23) dry, without exudation; (24) hypostatic, arising in a region of passive congestion (as a bed-sore); (25) malignant, due to malignant growths; (26) catarrhal, affecting mucous membranes; (27) neuropathic, due to impairment of the trophic functions of the nervous system, as in perforating ulcer; and (28) sympathetic or reflex, due to disease. or injury of a distant part, as when orchitis follows mumps.

Extension of Inflammation.—Inflammation extends by continuity of structure, by contiguity of structure, by the blood, and by the lymphatics. Extension by continuity is seen in phlebitis. Extension by contiguity is seen when a cutaneous inflammation advances and attacks deeper structures. Extension by the blood is seen in the formation of the small-pox exanthem. Extension by the lymphatics is witnessed in a bubo following chancroid.

Terminations of Inflammation.-Inflammation may be followed by a return of the tissues to health, and this return may take place by delitescence, by resolution, or by new growth. By delitescence is meant abrupt termination at an early stage, as when a quinsy is aborted by the administration of quinin and morphin, and the production of a sweat; resolution means the gradual disappearance of the symptoms when inflammation has passed through its regular stages; and new growth means that an inflammation has lasted a considerable time, with ample blood-supply, and without suppuration has gone on to the formation of embryonic tissue, granulation-tissue, and fibrous tissue. Inflam