disintegrated tissues; the sides appear hard and infiltrated. If these substances are thrown off by suppuration, the bottom of the ulcer is covered with granulations which fill up the gap. Often, indeed, they protrude beyond the edges (ulcus elevatum), and represent an elevation, rather than a depression.

As long as the ununited condition of the connective tissue continues, there is, of necessity, a secretion of pus, which accounts for the close connection in the popular mind between ulceration and suppuration. The disunion is encouraged, and, as it were, nourished, by the presence in the bottom of the ulcer of moribund matter, which can only be separated by suppuration from the organism, and is so closely connected with it that this so-called "sequestration" is a process of time.

For this reason, ulcers of the osseous system readily become chronic, because the exposed trabeculæ and lamellæ in the bottom of the ulcer, although practically dead, are closely united with other deep-seated and living constituents of the bone. Tuberculous, syphilitic, leprous, and lupous ulcers all require a disproportionate amount of time to throw off their deep-rooted, specific products of inflammation. The worst of this is, that as rapidly as the suppurative process throws off these products, new capita mortua take their place.

There are still other agencies by which the ulceration may be prolonged; chiefly, by a telangiectatic condition of the diseased part (phlebectasia), the consideration of which would at present lead too far.

(f) Inflammatory Connective Tissue Hyperplasia (Chronic Interstitial Inflammation). -Either of the above headings applies to the inflammations caused by an inflammatory irritation of moderate intensity, which is continuous, or of frequent recurrence. The most frequent mechanical causes are pressure and tension; the chemical irritations are mostly exciting ingredients of food, such as alcohol, etc. The action of the irritants upon the tissues does not immediately threaten their stability, but it creates a want to which, according to known physiological laws, the organism responds with a vigorous and prolonged hyperæmia. This latter is arterial in character, but if an arterial hyperemia continues, or is often repeated, permanent alterations in the vascular wall are effected, which react, not alone on the arterial, but, in a heightened degree, on the venous part of the circulation.

The arteries dilate and lengthen, their walls becoming thicker by hypertrophy of the muscular coat and thickening of the adventitial connective tissue. The veins, on the contrary, are, and remain, largely dilated; the elasticity of their walls is exhausted, and therefore it is not possible for them to return to their normal calibre. Whether such a condition can be rightly termed an arterial hyperemia remains an open. question.

In the further course of the disease, we usually find newlyformed connective tissue in the neighborhood of the blood vessels. This resembles granulation tissue, and may also be converted into cicatricial tissue. We may then expect considerable displacement, especially shrinkage of the organs involved (cirrhosis of the liver, contraction of the kidney). In some cases the newly formed connective tissue is more like the normal connective tissue substances, and occasions thickenings, depositions, etc.; in others, the microscope shows only a round-celled infiltration of the connective tissue, especially that forming the blood vessel wall, which does not lead to further changes.

Lastly, I would state that purely local thickening of the connective tissue without demonstrable hyperæmia, occurs as the result of slight mechanical disturbances (maculæ albæ of the pericardium).

(g) Inflammatory Hypertrophy.-Inflammatory hypertrophy is a remarkable deviation from the regular process of inflammation. It shows us how physiological growth may lead in the latter to the permanent enlargement of certain organs. The elements of the process are: hyperemia effected by pathological irritation and local increase of colorless blood corpuscles. However, as both seem to concentrate at points where the normal growth of the involved organs is taking place, and as hyperæmia and cell formation represent in these organs the normal process of growth, we find inflammation and growth to be identical, and the result is an excessive growth hastened and increased by inflammatory changes.

Inflammatory hypertrophy is most frequently observed in the skin and bones. Active periostitis, which is important in the union of fractures, as well as in other respects, is an inflammatory hyperemia of the bone. Elephantiasis Arabum, so called, is another example of the same. Although inflammatory hypertrophy resembles active hypertrophy (see

p. 18), it is in reality totally different, and is a diseased condition which should in no wise be confounded with the above. (h) Specific Inflammation.-The term "specific inflammation" must be applied strictly to that process of inflammation caused by the lodgment of parasitic bodies. It produces various characteristic modifications in the course and appearance of the inflammation, which are due exclusively to its species morbi. The consideration of specific inflammations, i. e., tubercular, syphilitic, leprous, glanders, anthrax, etc., is, therefore, not in place here, but comes properly under the head of parasitic processes of disease, which form a separate division of special pathology. I need only say that specific inflammations embrace the most varied and interesting forms of inflammation. The diphtheritic form described above may serve as a paradigm for a large number. In this we have an external attack of cleft fungi and its consequences. This attack may also be made through the blood. The minute subdivided poison is carried by the blood throughout the whole system. As the greatest amount of friction occurs where the arteries merge into the capillaries, it is here that the vascular wall is most thoroughly inoculated with the poison, and the specific inflammation thus originated is especially prone to commence as endo- and peri-arteritis. The corpuscular infiltrate invariably produced shows peculiarities depending directly upon the action of cleft fungi. Among others, there is a certain enlargement of cells with vesicular transformation of the nuclei, epithelioid degeneration culminating in the form of giant cells. Joined to this are typical forms of cell death, fatty degeneration, cloudy swelling, coagulationnecrosis and many other phases which strongly influence the future course of the inflammation, and give it a characteristic impress.

The epiphytic parasites also produce peculiar inflammations, in which we can recognize the species morbi, each parasite being characterized by its own peculiarities of habit and life. The detailed consideration of this subject will, however, be found in the Special Part of this work.

TUMORS.

(a) GENERAL CONSIDERATIONS.

What is a tumor? Let us consider the question first at the bedside of the patient. Here we must face the difficult problem whether the "swollen something" appearing either upon or below the surface of the body is an inflammatory exudate which will disappear in various ways, leaving the part comparatively unimpaired, or whether it is a noninflammatory swelling, which, if left to itself, will continue to grow, and perhaps fatally involve the rest of the body.

It is exceedingly important to establish the differential diagnosis between inflammatory and non-inflammatory swellings. We know that inflammations generally arise from distinct external causes, and we are, therefore, inclined to call the questionable something a tumor, in the strict sense of the word, when it originates spontaneously. Inflammatory tumors usually develop rapidly, and are accompanied by hyperæmia, heat, and other painful sensations, while noninflammatory tumors develop slowly, from a minute origin, are unaccompanied by hyperemia or pain, and are at first only mechanically annoying, although their inexorable increase in size soon renders the patient restless and uneasy. From these symptoms we are able, in doubtful cases, to form a temporary diagnosis.

We have noticed before how, in inflammation, the diseased organ becomes flooded with exudate. Blood-serum, fibrin, and colorless cells rapidly take possession of a certain territory, which they relinquish, after having occupied it for a certain length of time, and disappear, leaving scarcely a trace behind them. The diseased organ is in the meantime powerfully affected; but although it may be reduced in size, changed in shape, and crippled, from the effects of the inflammation, it has of itself contributed nothing to its own destruction; it has been destroyed.

The very opposite occurs in the formation of tumors. No conspicuous participation of the blood and blood vessels is here noticed. This increase of size is not derived from without. The increase is the product of the local cells. These cells not only proliferate, but also change in character, so that when the part has lost its normal shape and color, when its size and its composition are changed, and when, finally, it

is totally destroyed, we can truly say that it has worked out its own destruction.

Investigating the nature of the local changes still further, we encounter everywhere phenomena which have their natural models in the processes of normal growth. This is especially true of the elementary histological processes. Cell- and nuclear-division conform strictly to the physiological type. In most tumors, we find that complicated form of cell division which is characterized by the division of the nuclear substance into two parts, one of which refracts light strongly, the other to a much less degree. The former forms a network which resolves itself into sections; these sections then assume the shape of an equatorial plate, and finally form the amphiaster. Occasionally the new-formed cells are larger than normal, and even attain gigantic growth, although the endeavor to retain the type of the mother cell is always apparent.

This retention of the type is still more distinct when we consider, as we shall presently, the conversion of cells into tissues, and tissues into tumors. In short, the first impression received in every stage of the process is that we have before us a caricature of the process of normal nutrition. Thus we may define a tumor to be a localized growth which has overstepped normal limits; in other words, a local perverted excess of growth.

(b) GENERAL ETIOLOGY OF TUMORS.

When I stated above that tumors, in contradistinction to inflammation, arise from influences at work within the parenchyma, I did not intend to ignore the fact that our knowledge of the causes of their origin is extremely imperfect, nor would spare any pains to investigate this mysterious subject.

I

The tendency to continuous apposition by means of assimilation is innate in living tissues. We are forced to accept this tendency, which is shown in embryonic development, and pursued until organs reach their full growth, as a preordained plan of development, apparent even in the impregnated egg, and in the local disposition of its parts. This plan of development selects, according to time and space, certain points at which more intense cell multiplication shall take place. The mechanical effect produced by one growing part upon another exerts a formative influence upon the ex