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times a day-and four times a day is better -for periods of six weeks to three months. It will, on rare occasions, produce tenderness of the gums, which I never regret, but I have never had ptyalism follow its use in the manner indicated. Of course the patient and the dose must be studiously adapted to each other. The mercuric prot-iodide is scarcely less valuable, although its effect on the alimentary tract is less certain and pronounced. As an "alterative" to the hyperplastic connective tissue of the kidney, its value is, in my judgment, undeniable. Mercuric bi-chloride and mercuric biniodide are probably quite as valuable as the milder salts recommended, but I have not used them much, preferring to employ remedies with which I am thoroughly acquainted, rather than those which are comparative strangers. Iodine uncombined-as in Lugol's solution -is a most valuable remedy when it is tolerated. Many patients cannot bear it at all, as it causes gastric irritation and general disturbance of the assimilating and eliminating organs. In clinical experience therefore it is generally necessary to seek the effect of iodine through the agency of its "haloid" combinations. Gold, as a slowlyacting but quite certain alterative or resolvent of morbid connective tissue growth, is assuredly growing in favor, among those best acquainted with its properties. Its effects seem to be quite like those of iodine, except that its action is less rapid-not, however, less sure. The chief objection at present to gold is that its compounds are not sufficiently permanent or stable for general use. The chloride of gold and sodium-the most eligible preparation-may be employed in gelatin-coated pills, which should be kept tightly corked and in the dark.

There are certain proprietary preparations of gold on the market, concerning which extravagant claims are made, but they are no more efficient than the preparation just mentioned. I have certainly seen valuable results from the prolonged use of gold in renal cirrhosis.

In nearly every case of chronic interstitial nephritis, the demand for haemogenetic agents arises sooner or later. But while anaemia is a pretty certain consequence of this disease, it varies greatly as to the time of its appearance in different cases. It is not due to loss of albumen, so much as to loss of assimilative power. Hence it does not follow that a patient needs tonics simply because he has renal cirrhosis, and hence, as I have already said, they should be administered "only when they are clearly indicated." It should also be remembered that

when the patient cannot assimilate food, neither can he assimilate iron or other haemogenics.

Iron still remains the ideal tonic in the anaemia of interstitial nephritis, having maintained its supremacy against all other remedies up to the present time. So numerous and so well known are its preparations that very little need be said about it. My personal preference is for the ferric citrate, because it seems to me to produce less gastric irritation, or rather gastric irritation in a smaller number of patients, than any other chalybeate. If a diuretic happens also to be needed, potassic citrate may be combined with the ferric citrate as in the following formula, which I have employed times without number:

B Ferri Citratis...

Potassii Citratis

Syrupi Limonis

gr. 160

.gr. 320 OZ. ii

Aquae q. s. ad......... oz. viii Sig. Take a dessertspoonful before each meal, well diluted.

Concerning such preparations as "haemoferrum" and similar vaunted blood-makers, I have no practical knowledge. Of late I have been impressed with the value of manganese as a haemogenic and also as an oxidizing agent, which is much needed in renal inadequacy. I have seen much improvement follow its use, not only in the general appearance of the patient, but also in the steady increase of red-blood globules, as proven by comparative counts. I have generally employed the binoxide in doses of 3 grains, 3 times a day. I have also employed the proprietary preparation known as "Liquor Pepto-Mangan" with good results, in spite of my aversion for the whole brood of proprietary remedies with their bizarre

names.

Diuretics are not indicated because a patient has interstitial nephritis, although they may be occasionally required, just as cholagogues are now and then required during the treatment of interstitial hepatitis. In neither instance do they "cure" or essentially modify the disease, except that they irritate and worry the diseased organ, when used injudiciously. When diuretics are indicated by scantiness of urine, or very low percentage of urea, or much deposit of waste material from the kidneys, showing that the renal tubules are filled and clogged by products of degeneration or by the appearance of symptoms of uræmic toxæmia they must be given of course. The saline diuretics are always preferable. Potassic citrate, sidoc actate, potassic acetate, potassic bitrartrate are in my estimation val

uable in about the order named. They ought always to be given largely diluted when the stomach is empty, but they ought to be suspended when they are no longer clearly indicated. Lastly the care of the heart must engage the serious attention of the physician. This branch of the subject is of sufficient importance to demand separate and detailed treatment. At present I can only give a few brief hints of a very practical nature.

In the early stage of interstitial nephritis, when progressive hypertrophy of the heart -and especially of the left ventricle-is going on; when the powerful and angry contractions of the thickened ventricle provokes resistive spasm in the far-off but already thickened arterioles of the kidney, so that there exists between these two a condition of mutual contention or defiance, the heart itself needs no medication. It is generally sufficient to diminish the alloxuric bodies to the minimum by eliminative remedies, and a few days of strict anti-nitrogenous diet. If, however, the heart-contractions become a troublesome palpitation, the patient should be placed in the recumbent

position for a few days, and a little aconite,
or some equivalent remedy should be given,
just long enough, but only long enough, to
calm and equalize the tumultuous action of
the organ.
At this stage digitalis and
other cardiac tonics ought to be avoided,
for reasons too obvious to require argu-
ment. At a later period, when the heart,
yielding to the inevitable, exhausted by the
long but unequal contest with the thick-
ened, inelastic and tortuous renal vessels,
becomes dilated and thin-walled, it will be
necessary to resort to heart tonics, whereof
the most valuable is strychnine, the next in
order is ergot, and then comes a group of
remedies headed by digitalis and supple-
mented by strophanthus, convallaria, and
adonis vernalis. In each and every case
the conservation of the heart must be com-
mitted to the judgment of the medical at-
tendant, and well is it for the patient if the
medical attendant be a man of judgment
tempered and corrected by experience.

Of course it will be understood that the foregoing remarks are in the main applicable to interstitial nephritis in the early and advancing stage only.

METRITIS.

BY BYRON ROBINSON, B. S., M. D., CHICAGO.

PROFESSOR IN THE CHICAGO POSTGRADUATE SCHOOL OF GYNECOLOGY AND ABDOMINAL SURGERY; PROFESSOR OF GYNEC-
OLOGY IN THE HARVEY MEDICAL COLLEGE AND THE ILLINOIS MEDICAL COLLEGE; GYNECOLOGIST TO THE
WOMEN'S Hospital; gynECOLOGIST TO THE WOMEN'S CHARITY HOSPITAL AND CONSULTING
GYNECOLIGIST TO THE MARY THOMPSON HOSPITAL FOR WOMEN AND CHILDREN.

Should one present the subject of endometritis it ought to be based on its histology and not on its uncertain etiology, as we know it to-day. As metritis rests chiefly on endo-metritis, we may say a few words in regard to it. The endometrum is composed of a stroma and glandular element. Hence for its inflamed condition we have for it the words endo-metritis glandularis and interstitialis. Endo-metritis fungora is simply an hypertrophy of both glands and interglandular elements. It is a diffuse hypertrophic endo-metritis. The endometrum in this variety produces the so-called uterme polypi. Endo-metritis has many varieties, as the hypertrophic, atrophic, hyperplastic. These remarks are made to introduce the subject of metritis, a subject which I have been observing in gynecologic practice for years.

It is a peculiar disease of the uterus characterized by hypertrophy, atrophy or induration. In the chronic state the uterus is hard in consistence. Its walls are rigid and

stiff. The disease may occur in a girl of 15 years, or in woman before or after the menopause. It is known as metritis, i. e., an inflammation of the uterine muscularis. I shall attempt to bring forward some views on the disease by the aid of carefully drawn microscopic illustrations. In the illustrations I have attempted to show typical specimens of a quiescent uterus or one at rest, one specimen of a uterus in the first day of menstruation, and a specimen of about ten weeks' pregnancy, and two more sections cut at right angles to the utricular glands. The specimens should be studied comparatively to observe the vast yet gradual difference occurring in the uterine mucosa.

Metritis is one of the most frequent diseases of women. About ten women out of fifteen who come to the clinics have a distinctly palpable metritis, over the diagnosis of which no dispute may arise. Metritis occurs in all grades, from the sensitive, acute to the stage where little sensation. remains. As an explanation of the tendency of the

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Figure 1 represents a uterus mucosa and muscularis, in the quiescent stage, in the state of rest, i. e., midway between two menstrual periods. 1, 1, the columnar nucleated ciliated, single-layered uterine epithelium; 2, a part of a utricular gland opening on the inner surface of the mucosa; 8. a whole utricular gland cut longitudinally extending from below the level of the muscularis to the internal surface of the mucosa. It is lined by a single layer of distinctly nucleated cylindric columnar (and ciliated?) epithelium. Observe how it ends in the muscularis and how the muscular trauma or contractions could induce the migration of contained pathogenic microbes into the field of the muscularis, producing inflammation and its results; 4 represents the tip end of a utricular gland far beneath the surface of the muscularis. 5, 5, 5, 5, 5, 5, show empty, resting utricular glands cut at varying angles to the longitudinal axis; 8, points to the lymphoid tissue composing the mucosa, i.e., the connective tissue cells and fibers the blood and lymph vessels; 9, 9, shows resting glands containing a little mucus; 6 shows a blood vessel in tht muscularis, and 7 points to the nucleus of the unstriped muscular cells. The two characteristic structures observed are. a, the mucosa containing utricular glands, connective tissue cells and fibers, blood and lymph vessels; 6, the muscularis containing unstriped muscular tibers and blood vessels; and c, the peculiar anatomic fact that the glands of the mucosa dip down into the muscularis. There is no submucosa in the uterus. The muscularis is not protected from the mucosa by a submucosa, and hence the easily infected utricular glands quickly carry infection into the unprotected muscularis. Other hollow viscera like most of the digestive tract are protected from infectious invasions by a layer of tissue the submucosa, which separates the glandular, the mucosa, from the muscularis. Besides the submucosa, e.g., in the stomach.allow a wide, independent movement of the mucosa and muscularis. In the uterus the mucosa and muscularis are immovably fixed on each other. Observe the solid, compact glands and tissue in the uterine mucosa and the small nucleus of the muscularis in the resting uterus.

Figure 2 represents a uterine mucosa in the first day of menstruation, which I obtained by vaginal hysterectomy from a thirty-five year old multipara. Observe the two great structures; the mucosa and the muscularis are changed like magic. The mucosa is almost doubled in thickness, the glands are elongated, sinuously dilated, with folded walls, and many contain blood and mucus. Several utricular glands (5, 5, 5) descend furthur down into the muscularis than in the resting uterus. Note the increased size of the nucleated, columnar epithelium in the menstrual uterus over the resting uterus. The interglandular substance, the lymphoid elements, connective tissue cells and fibers, the blood and lymph vessels, are all vastly increased over the resting uterus. In the menstruating uterus the muscularis the nuclei of the muscular cells, are about doub led in length and breath. With good specimens one can observe the large amount of fluid lying in the tissue and forcing the elements wide asunder. Also the ubiquitous leucocyte aids to increase the thickness of the muscularis, and especially the mucosa, in the menstruating uterus. Especial attention is directed here to the fact that the columnar, nucleated endothelium lining the mucosa and utricular glands, is no nowhere (first day of menstruation) shed, but intact everywhere, and nearly double the size of that in the resting uterus. 1, 1, represents almost complete utricular glands cut longitudinally; 3, points to the bloody debris found in this sinuously dilated menstruating gland which opens on the internal surface of the uterine mucosa and dips deep down into the muscularis; 2, points to a widely open utrieular gland with enormously developed epithelia; 4, points to the vastly increased interglandular substance, lymphoid elements, connective elements, blood and lymph vessels, all forced asunder by edema, infiltrated fluid; 5, 5, 5, 5, points to utricular glands buried beneath the museularis, and 5' can be traced from the internal surface of the uterine mucosa to a long distance below the surface of the muscularis. The blood debris in the utricular gland found deep in the uterine muscularis demonstrates that it is actively engaged in the act of menstruation

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Figure 3 represents the uterine mucosa and muscularis pregnant about ten weeks. This specimen differs from the resting uterus by hypertrophy, and from the menstruating uterus by uniform hypertrophy. In the pregnant uterus the utricular glands and blood vessels, as well as the interglandular tissue, are increased uniformly. In the minstruating uterus the utricular glands and blood vessels are not uniformly increased, but show sudden dilatation and consequent sinuous and folded walls. The glandular epithelium and the walls of the blood vessels in the menstruating uterus are much less in size than in the pregnant one. The interglandular tissue of the mucosa of the menstruating uterus is more edematous, more infiltrated with fluid than the pregnant uterus, and consequently the elements are forced wider assunder by the fluids than in the pregnant uterus. The utricular glands of the pregnant uterus do not contain blood and debris like that of the menstruating uterus. In pregnancy only mucus is found in some of the utricular glands of the uterus. The resting uterus (Figure 1) shows compact interglandular tissue and lymphoid elements. The menstruating uterus (Figure 2) shows interglandular structure, swollen, edematous lymphoid and connective elements widely separated by considerable fluids, many leucocytes, and especially sinuously dilated atricular glands with sinuous and folded walls, the glands

containing bloody debris. The nucleus of the muscles are almost doubled in size. The pregnant uterus differs by a pecullar kind of hypertrophy. Its glands are uniform and smooth, and like the resting uterus, but enormously increased; they contain mucus like those of the resting uterus. The epithelia lining the internal surface of the mucosa and utricular glands are hypertrophied with enlarged nucleus. The nucleus of the muscle cells of the pregnant uterus is three to four times the size of the resting uterus and perhaps over twice as large as those of the menstruating uterus. The utricular glands of the menstruating uterus show well their penetration of the muscularis, but the utricular glands of the pregnant uterus demonstrate vastly more than deep penetration and residence of the hypertrophied muscularis. 10, represents the vastly hypertrophied epithelia of the internal surface of the mucosa; 1 and 2, point to the epithelia of the hypertrophied utricular glands; 3, 3, 3, show empty hypertrophied utricular glands, while 3' and 3' show the same with small amount of mucus; 4 indicates hypertrophied interglandular, lymphoid connective tissue and vascular elements; 5 and 5, blood vessels; 6, hypertrophied nuclei of the muscularis; 7,8 and 2', show utricular glands, hypertrophied, well buried, deep in the recesses of the muscularis. Figures 1, 2 and 8 are carefully drawn from we l-prepared specimens.

fully prepared cuts accompanying this article, drawn from my own specimens, will explain the mechanism a thousand times better than words. The uterine wall consists of three tunics, viz.: tunica mucosa, tunica muscularis and tunica serosa.

First, the uterine mucosa, the endometrium, the tunica mucosa or propria, or the lining membrane of the uterus furnishes the clue. It is composed of tubular glands standing nearly at right angles to the uterine wall. These glands (glandulae uterinae, utricular glands) are lined by a distinctly nucleated columnar ciliated epithelium. The ground work sustaining the glands consists of a peculiar connective tissue cell and a connective tissue fiber. The mucosa is rich in this lymphoid embryoniclike tissue. It is also rich in blood vessels and abundant lymph elements. The uterine mucosa undergoes variable changes during the subject's seed-time and harvest. At the menstrual time it is often doubled in thickness, becoming about one-fifth of an inch thick. During gestation, the mucosa undergoes considerable changes, but apparently not so violent and rapid as at the monthly period. The three chief changes of the mucosa at menstruation and gestation are: 1, Elongation and sinuous dilatation of the glands; 2, Enormous distension of the blood and lymph vessels; 3, Increase of interglandular substance by multiplication of the embryonic type of connective tissue cells and fibers, the migration of red and white blood corpuscles and the infiltration of the mucosa with fluid.

The significant vascularity (blood and lymph vessels) and the predominant glandularity (lymph elements) characterize the uterine mucosa and mark it as a field rich in susceptibility to infectious invasions, and since the uterine mucosa is not only directly exposed to the external world, and especially to sexual imprudence and consequent infec

[graphic]

tion, but also to the violent congestions of menstruation and the rapid changes of gestation, it is no wonder that its delicate structure and wonderful function becomes impaired.

Now, the significant peculiarity of the uterine mucosa is, that it rests directly on, and some of its glands penetrate, the uterine muscular wall. There is no submucosa in the uterus. There is no barrier to infectious invasion from the uterine mucosa to the uterine muscularis. Infection can travel directly, by way of the utricular glands, into the muscularis. No military trocha exists between the mucosa and muscularis in the uterus to prevent general infectious invasion. No finely woven connective tissue, submucosa, forming a distinct barrier, a partially impenetrable layer to infection, is found in the uterus.

The wonderful mobility of mucosa on the muscularis, which so typically exists in the gastro-intestinal tract, does not occur in the uterus. The uterine mucosa and muscularis do not move independently of each other. They are intimately bound and connected together. In this intimate and close connection of mucosa and muscularis, perhaps is also found an explanation of further infectious invasions from muscular trauma on the utricular glands. We may call a menstruation a diminutive labor. In menstruation and gestation, the uterus is in a constant rhythm or fine small waves of contraction. Now, we observed that some of the utricular glands dipped their proximal ends a considerable distance down into the uterine muscularis. In the menstrual period the muscular waves or contractions are vigorous and active; the muscular contractions are continually traumatizing, continually disturbing the ends of the utricular glands, which lie among the contracting muscles, and hence will induce the migration of pathogenic microbes through the glandular wall into the connective tissue of the uterine muscularis, with consequent inflammatory process. Muscular trauma on contained glands holding pathogenic microbes aids to spread infection. The congestions of the uterus induces muscular contractions and this process, being often repeated, allows frequent opportunities for progressive infection.

Muscular trauma must be an admitted factor in the production of disease; it disseminates germs, especially from glands to adjacent tissue, it disturbs the blood vascular and lymph vascular system and the frequent muscular activity of the uterine muscularis on the uterine glands, which are not pro

tected by a submucosa, traumatizes them and aids to disseminate their pathogenic contents.

The first consideration in metritis is to study how metritis arises. Why does a woman have metritis, with hypertrophy or atrophy, at any time from puberty to far beyond the menopause? When a girl has her first menstruation the os dilates, the mucosa swells and becomes intensely vascular and the utricular glands dilate irregularly with sinuous and folded walls; also the muscularis is in continual waves of contraction. Intense vascularity, edema, migration of leucocytes, dilated lymphatics and highly swollen glands characterize the uterus at menstruation. In this susceptible state, a rich culture medium for germs, the uterine mucosa may become infected by microbes entering the open os from the clothing, from masturbation, from cohabitation, from the dust of the road, from the rectum, and also, it may become exacerbated from repeated menstrual processes. The resistance of her mucosa may be lowered by attacks of scarlet fever, measles, smallpox; in fact, by any acute fever. However, one of the above processes is doubtless the method by which young girls' uteri acquire metritis. Erectile tissue with congestion and decongestion alone will not explain uterine disease, because the penis passes innumerably more times through congestion and decongestion than the uterus, but does not become diseased. The element of infection must be the factor that plays the role in the glandular structure found in the muscularis-mucosa.

It may be stated that the chief forms of metritis are developed from abortion and labor. In metritis the first stage is intense congestion, venous, arterial and lymphatic. The uterus swells, considerable edema and small cell infiltration occurs in the mucosamuscularis. The serosa does not appear to suffer so much when attacked ectoperitoneally. Chronic metritis is characterized by hypertrophic thickening of connective tissue. The muscularis may be partially or completely in a state of degeneration, fatty, pressure atrophy. Some of the muscular fibers may be entirely crushed out, while others may lie in irregular bundles. Much significance rests in the blood vessels in metritis. The vessel becomes irregular, by irregular contraction of the connective tissue bundles their lumen partially obstructed. Dilatation and constriction by connective tissue characterize the uterine vessels in metritis. The vessels may become varicose. The painful menstruation in metritis rests on the fact that the uterine vessels are sur

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