tioned whether its action is according to the "universal law of therapy." Perhaps, however, this ought to be understood.

The foregoing is the substance of the Lancet's dealings with homœopathy in 1881. Surely Dr. Drysdale's prophecy is approaching fulfilment, that "in this country homœopathy will eventually be absorbed into general medicine."

GILES F. GOLDSBOROUGH, M. D.

MICROSCOPICAL STUDIES IN YELLOW ATROPHY OF THE

LIVER.

JOHN A. ROCKWELL M. D., NEW YORK.

[Read before Connecticut Homeopathic Medical Society, May 16, 1882.] DR. C. HEITZMANN of this city recently handed me, for examination, two pieces taken from livers of persons exhibiting distinct signs of yellow atrophy.

One of the cases was of an acute character, the person dying eight days after the first appearance of jaundice; while in the second case, two weeks before death, severe symptoms characteristic of yellow atrophy set in, though the clinical symptoms for several weeks previous had been those of interstitial hepatitis with cirrhosis.

In specimens obtained from these two cases, a difference was noticed in accordance with the clinical history. In the firstmentioned case all the evidences pointed towards a very acute destructive process in the liver, without any other complications; in the second case, the features pointed toward an acute catarrhal or interstitial hepatitis, combined with the features of yellow atrophy. In fact, some observers have claimed that both these processes are so far identical that yellow atrophy must be considered merely as a very acute interstitial hepatitis. This view, however, I cannot fully corroborate.

Sections obtained from the first case, when brought under the microscope, exhibited as the most striking feature the want of calibers throughout the portal system, the intralobular capillaries, and the hepatic veins. The second striking feature was the more or less marked reduction of the size of the lobule of the liver. The third point was a partial engorgement of the capillary blood-vessels of some lobules, combined with extravasation of blood. The fourth point was the disappearance of the lobules and the transformation of all constituent tissues of the liver into a granular mass, the so-called detritus. In addition to these points a fifth was present in the second case, comprising the phenomena of acute interstitial hepatitis.

Whereas, in normal liver tissue the portions between the lobules abound in large veins belonging to the portal system, in yellow atrophy such vessels are either wanting or, if present, considerably changed in their aspect. Portal veins which were still recognizable as such presented an irregular, seemingly jagged, bordering line surrounding an angular, as if compressed, caliber. This, instead of containing blood, held only a brown granular mass composed of shrivelled, partly disintegrated blood corpuscles. The branches, springing from such portal veins, their calibers considerably reduced, were stretched to a narrow slit, which was bounded by medullary corpuscles and, outside of these, by the so-called structureless layer, present beneath the endothelia in the normal condition. The stretching of the vessels of the portal system to such a degree that their calibers were entirely lost was observed in all places in which the disease had reached a high degree, though still in its initial stage. The former caliber was marked by the presence of endothelia, partly broken down into medullary corpuscles which were closely attached to each other, and on either side were seen a somewhat denser tract of connective tissue corresponding to the walls of the vein. The capillaries exhibited the same feature; most of them were compressed to such a degree that the endothelia of either side touched each other. Such thoroughly compressed capillaries were in communication with less compressed ones, filled apparently with detached endothelia and medullary corpuscles, evidently sprung from endothelia, and with scanty redblood corpuscles.

The interstitial tissue was everywhere augmented and composed of a large number of globular or irregular elements, such as we observe in the inflammatory process. But, while in simple acute inflammation the globular, homogeneous elements, composed of solid bioplasson, are largely prevailing, in yellow atrophy they are much less numerous, the finely granular bodies being largely in excess. Also, the constituent elements are divided into lumps of small size, showing, with high powers of the microscope, a scanty reticulum of bioplasson in clusters, which are separated from each other by narrow, light rims, though still interconnected by means of delicate, grayish filaments. In most places, the tracts of the former fibrous connective tissue could only be recognized by the rows of such split-up medullary corpuscles.

The bile ducts in the interstitial tissue were well preserved, still being lined by columnar epithelium, both in longitudinal and transverse sections. The calibers of the bile ducts were invariably compressed. Further changes of the epithelia of the bile duct consisted in the disappearance of the nucleus, and in the

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

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.

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 :

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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.