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division of the epithelia, partly into homogeneous, shining, partly into finely granular lumps, which, by their regular arrangement in rows, reminded one of their origin from former bile ducts. At last, all differences between lumps sprung from the connective tissue and those arisen from bile ducts faded away.

The lobules of the liver were considerably reduced in size: in some places to one half, to one third, to one tenth of the former diameter. This was the result of a transformation of the liver epithelia into medullary corpuscles, as is observed in inflammation generally. The gradual changes of the epithelia, resulting in this destruction, were as follows: First, the nucleus becomes invisible, due, as revealed by high amplifications, to its splitting up into the bioplasson reticulum constructing the epithelial body. Next, the ledges of cement substance between the epithelia disappear, and a number of epithelia coalesce into granular masses containing a varying number of granules and globules of fat. In this stage the rows of the liver epithelia are still recognizable. With higher powers we recognize the granulation of epithelia to be due to the presence of their bioplasson reticulum, which is very much more marked in these diseased epithelia than it is in the normal

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Yellow atrophy of the liver. Magnified eight hundred diameters. E, confluent epithelia; V, compressed capillary blood-vessels; B, capillary vessels engorged with red blood corpuscles; L, epithelia dividing into smaller portions; S, small, irregular pieces, exhibiting a wide bioplasson reticulum, commingled with redblood corpuscles.

condition. This distinctness of the reticulum is due to an increase of the size of the meshes by means of scanty new formation of bioplasson within the epithelia. In fact, coarse granules of bioplasson, and homogeneous, shining lumps are found in the clusters of the liver epithelia exceptionally only. The next step in the destruction of the epithelia is that, within the cluster, new lines of division appear, which split up the clusters sprung from former epithelia into numerous, irregular, medullary elements, all of which are composed of rarefied bioplasson reticulum, none of which has a nucleus.

In some lobules, which were likewise decreased in size, the blood-vessels were engorged with blood corpuscles, and the interstitial tissue was crowded with red-blood corpuscles. The changes of the epithelia of such lobules were the same as before described. As the engorgement of the capillaries and the extravasation of blood in some places occupied quite extensive fields, I cannot help suggesting that what the authors have termed red atrophy of the liver, combined with yellow atrophy, is only due to an engorgement of the blood vessels and an extravasation of blood.

In the highest degrees of the disease the lobules of the liver had entirely disappeared, and, as a residue of the former liver tissue, nothing was left but an accumulation of medullary corpuscles, between which were seen small tracts composed of spindles, besides a varying number of fat globules. The most marked feature in this tissue was the absence of new formation. of living matter. In fact, only a few larger lumps, composed of a somewhat coarser reticulum of bioplasson, could be seen, while the main mass was an aggregation of small reticular lumps, indistinctly bordered by light interstices and marked by the absence of nuclei and the presence of an extremely rarefied bioplasson reticulum. The connection of the lumps and of the reticulum itself was nowhere broken, so that this remnant of the former liver tissue still deserves the name of tissue and cannot be called detritus. Where the living matter of the constituent tissues of the liver, which is so noticeably decreased in amount, has gone to, I am unable to say. Nevertheless, I am positive that the reduction of the size of the whole liver is entirely due to a loss of its living matter.

As before mentioned, in the second case which I examined, there were marked features of acute interstitial hepatitis. The interstitial tissue in some places was crowded with globular inflammatory corpuscles of a coarsely granular or homogenous appearance, several of which were enclosed in a mesh of a delicate fibrous reticulum. At the border of the lobule the stages of transition of liver epithelia into medullary or inflammatory

corpuscles, as described by C. H. Müller,* could be plainly seen. In other places, the breaking down of the liver epithelia proceeded nearly simultaneously from the epithelia of the lobule left, with the result that instead of shining, homogeneous, only finely granular, irregular, medullary corpuscles were seen. The result was materially the same as in the first case, although of much less intensity, and there was also present a more decided inflammatory new formation than in the first case. In the interstitial tissue, exhibiting marked inflammatory symptoms, there were observed in some places numerous bile ducts, while in other places these ducts were entirely absent. Whether or not these bile ducts are, in part at least, newly formed, I am unable to decide.

The results of these researches may be summed up in the following statements:

I. Yellow atrophy consists in the breaking down of all constituent elements into irregular lumps of medullary elements, accompanied by a considerable loss of living matter.

2. The disease has one feature in common with inflammation, i. e., the reduction of the constituent tissues into inflammatory elements; but the essential feature of inflammation, namely, the new formation of living matter, is absent.

2. Fatty degeneration is no characteristic sign of yellow atrophy, as in both of these cases fat was present only in a small

amount.

4. There are combinations of acute catarrhal or interstitial hepatitis with yellow atrophy, but in what causal relation to each other I have not determined.

5. Red atrophy combined with the yellow is very probably due merely to a partial engorgement of the capillaries and extravasation of blood.

6. Most of the vessels belonging to the portal system of the liver being collapsed, the conclusion is admissible that the disease is due to an impeded circulation in the larger portal vessels. The partial engorgement of the capillaries and the extravasation of blood could be explained by an impeded circulation in the hepatic artery.

One of the most recent writers, J. Dreschfeld,† gives the following summary of the present condition of this subject, "briefly stating the main points about which authors at present disagree :

"I. As regards the icterus, many believe it to be of the hepatogenic, others believe it to be of the hematogenic kind.

*"Ueber interstitielle Leberentzündung, Sitzungsbe, der Kais. Akad. d. Wissensch., 1877.

† On the Morbid Histology of the Liver in Acute Yellow Atrophy. J. Anat. and Physiol. London, 1880, 1881, XV., 422–430.

Λ

"6 2. While all are agreed that the chief lesion in the liver, whether acute liver atrophy be considered a general disease (as most observers believe), or primarily a local disease, consists in a fatty degeneration of the liver cells, some writers (e. g., Winiwarter, Wien. Med. Jahrb. 1872) think that the first change consists in an inflammatory process in the interlobular areolar tissue, which only secondarily causes fatty degeneration of the liver cells." Again, according to Levitski and Brodowski (Virch. Arch., Vol. LXX., p. 421), there is, prior to the cell degeneration, a cell proliferation in some parts of the liver lobules, these observers having seen numerous liver cells three or four times smaller than the normal liver cells in those parts of the liver parenchyma which had not yet undergone degeneration.

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3. As to the relation of the red to the yellow atrophy, most pathologists now believe that the red atrophy is only a more advanced state of the yellow atrophy, and is found in cases which run a slow course (Zenker, Perls, etc.); while Klebs, on the other hand, believes the two to be essentially different processes. 4. The red atrophy is characterized by a more complete disintegration of the liver cells, by the presence of an interlobular embryonic tissue, and of rows of cells resembling glandular tubes, supposed by some to be proliferating biliary ducts (Cornil and Ranvier), by others to be the surviving columns of hepatic cells (Thierfelder, in Ziemmsen's Cyclopædia, Vol. IX. p. 254).

"5. Lastly, some observers (Waldeyer, Zander) have discovered bacteria in the atrophied liver. In Zander's case, however, the autopsy was not performed until fifty-eight hours after death." In 1854 and 1862,† H. Lebert gave a careful analysis of seventy-two cases, together with an abstract of the literature of acute yellow atrophy from 1660 to 1862. This subject has since been treated at length by A. Thierfelder,‡ who brings down the discussion to 1877. I have examined twenty-eight contributions, published since this last date, which, with the exception of the able paper of Dreschfeld,§ I find to consist chiefly of clinical reports of cases observed or treated, and not calling for especial mention here.

This microscopical study has been pursued in the laboratory of Dr. C. Heitzmann, to whom I am indebted for valuable suggestions.

THERE is ground for hoping that some thorough system may be adopted for the disinfection of old rags used in manufacturing paper, etc., since cases of small-pox have again lately been shown to have had their origin in this source of infection. The rags imported from Egypt and Asia Minor should be especially looked after. — Boston Medical and Surgical Journal.

* Virch. Achv. 1854, VII. 343.

Ziemmsen's Cycl. IX. 254.

† Achv. genér. de Méd. 1862, I. 431. § Loc. cit.

REVIEWS

AND

NOTICES

OF BOOKS.

ELECTRICITY IN SURGERY. By John Butler, M. D. New York: Boericke & Tafel. I 2m0. pp. III.

Dr. Butler tells us that this brochure is "intended as a practical guide for the use of the specialist and general practitioner. . . The scope of the work precludes the possibility of more than cursory allusion to clinical cases, but is based almost entirely upon the author's own personal experience.'

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The introduction treats of the subject of electricity and the progress made in the knowledge of it during the past twenty years. After some general directions in regard to electrosurgical operations, special considerations are given of some forty-two different surgical conditions, such as synovitis, hydrocele, ovarian cysts, stricture, aneurism, nævus, tumors, ulcers, ascites, hemorrhoids, fistulas, hernia, etc. Each of these subjects is replete with interesting and practical suggestions drawn from the author's experience, and which every physician can peruse with pleasure and profit. The last twenty pages are devoted to a consideration of the various kinds of instruments, and we would advise any physician who designs to purchase a battery, or who wishes to learn its uses, to first peruse this little book.

*

THE INCIDENTAL EFFECTS OF DRUGS. By Lewin, Berlin. Translated by W. J. Alexander, M. D. Wm. Wood & Co.

This is a valuable book, and ought to be found in the library of every true homoeopath. Its value, however, lies, not in its newness, for it can teach us little; nor will it enrich our armamentarium; but it is a virtual acknowledgment by the best authorities of the other school of the truth of the homoeopathic doctrine. From the introductory explanations of these anomalous drug actions upon individuals to the last section of the book, we find statements and symptoms authenticated by their most careful observers, which, though new to themselves, are to be found already presented in the "Materia Medica Pura" of Hahnemann, or the later compilation of Allen. The book seems to us important for still another fact. It leads the way towards a truer and more comprehensive observation, in that it takes more accurate note of location, character, and concomitants of drug phenomena, on which alone can rest a materia medica that will endure the changes and developments of time. While only an elementary work for the homœopath, it is the

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