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the tissue of the villi, and indeed it sometimes happens that the ends of the lacteals grow wider, and swell out into a bulbous form from the great accumulations of fat, so as to be recognized even by the naked eye. Nowhere have they been so frequently witnessed in a striking form, as in cholera, and a good description of these appearances as occurring in this disease were published as far back as 1837 by Bohm. They indicate nothing more than an obstruction to the current of lymph in consequence of the disturbances in the respiration and circulation (Fig. 109, D). Since attacks of cholera are well known to occur with preponderating frequency during digestion and are attended by greatly impeded respiration, which makes itself felt throughout the whole venous system, they must of course also react upon the stream of chyle. Thus the enormous accumulation (retention) of fat in the villi is explained. This is therefore, if you will, a pathological condition, but it only depends upon a transitory obstruction, and we have every reason to suppose that, when the current again becomes free, these large drops of fat are gradually removed. But here we set foot upon other domains, where the boundaries of pathology can only be traced with great difficulty, and this is particularly the case in the liver. It has been known from of old that the liver is the organ, which is by far the most liable to fall into a state of fatty degeneration, and the knowledge of this state has long been derived from popular experiment. The history of the pates de foie gras proves this in the most agreeable manner, although M. Lereboullet of Strasburg maintains that the fatty livers of geese are physiological ones, essentially different from the pathological ones which are not eaten, but only observed. However, I must confess that I have hitherto been unable to discover the difference between physiological and pathological fatty livers; on the contrary, I believe that it is only by admitting the identity of the two that correct notions with regard to the pathological fatty liver can be obtained. We are namely acquainted with a fact which was likewise first observed by Kolliker, that in sucking animals, a few hours after digestion has taken place, a kind of fatty liver is a constant physiological occurrence. When of the same litter of animals some are made to fast, whilst the others are allowed to suck, those which have sucked, have a fatty liver a few hours afterwards, whilst the others have not. The fatty liver appears quite pale, though certainly not so white as a goose's liver. This observation led me to examine the question of the relation of the fat to the liver a little more minutely, and I certainly think we may positively conclude that there does exist a close connection between the physiological and pathological forms.

I found, namely, that a short time after the hepatic cells display this repletion with fat, a similar condition is found in the course of the biliary ducts, and that both in them and in the gall-bladder the epithelium presents the same appearances which we have witnessed in the intestinal epithelium during the absorption of fat. You only require therefore to invert the picture we just now considered (Fig. 109); instead of a villus, invested externally with epithelial cells, imagine a canal clothed on the inside with epithelium. The delicate cylindrical epithelium in the gall-bladder has the same striated border as that in the intestine (Fig. 14), and the fat is seen in the same way to penetrate into it from without, to pursue its course downwards and after a time to pass into the wall of the biliary ducts. I have watched the same process also in young sucking animals after digestion, and there it is easy to convince oneself that the fat, which for a time is contained in the hepatic cells, is manifestly excreted from them into the biliary ducts, but that in the course of these ducts the fat is reabsorbed and thus a second time returns into the circulation.


Such an intermediate interchange of matter as this, where the fat passes from the intestine into the blood, from the blood into the liver, from the liver into the bile, and thence again into the lymphatics, or into the capillaries which conduct the blood back to the hepatic veins and to the heart, presupposes of course, just as absorption in the intestines does, that the conveyance back again must take place under favourable circumstances; if any disturbing cause arises, a retention will of course ensue, and the place of the fine granules will gradually be occupied by large drops. But this is the mode of proceeding as it can really be traced in the fatty liver.

Upon studying a fatty liver, it is generally seen that the fat is first deposited in that zone of the acini which is immediately con- FlQ-110

tiguous to the capillaries into which the branches of the portal vein break up (Fig. 110, c, c). When sections of the organ are carefully examined with the naked eye, it looks in many parts as if one had an oak-leaf with its ribs and indentations before one; the ramifications of the branches of the portal vein correspond to the ribs, the fatty zone to the substance of the leaf. The more abundant the infiltration, the broader does the fatty zone become, and there are cases in which the fat fills the whole of the acini up the central (intralobular) hepatic vein (Fig. 110, h) and every single cell is crammed full of fat. In rare cases it certainly happens, that we find just the reverse, and that the fat lies around the central vein; these are cases which are probably to be explained by

Fig. 110. The adjoining halves of two hepatic acini. p. A branch of the portal vein with branches p' p", corresponding to the interlobular veins. A, A. Transverse sections of the intralobular, or hepatic, vein. a. The pigment zone, b the amyloid zone, e the fat zone. 20 diameters.


supposing that the fat is already in process of excretion and only the last cells still retain a little of it. Only we must take care not to confound with this condition a kind of fatty, necrobiotic atrophy which occurs particularly in chronic cyanosis.1

If now we consider the process in detail, we find that the manner, in which the hepatic cells fill themselves, entirely corresponds to that, in which an epithelial cell in the intestine becomes filled with fat. At first we find fatgranules widely scattered, and indeed very small. They become more numerous, more closely aggregated, and after a time larger; at the same time the cells become larger, swell up, and larger and smaller drops of fat are found in them (Fig. 27, B, b), until, when filled to the utmost, they present the same appearance as those of adipose tissue; scarcely any membrane, and scarcely ever a nucleus is seen, nevertheless they both still continue to exist. This is the condition which is called fatty liver, in the proper sense of the word.

In it too we have what we found to be the case in adipose tissue—a persistence of the cells. There is no such thing as a fatty liver in which the cells have ceased to exist; these constituents of the organ always exist, only they are almost entirely filled with drops of fat instead of with their ordinary contents. It can scarcely be doubted but that even in this condition they still contain a certain amount of matter capable of performing its functions. For in many animals, as for example, the cod-fish from which liver-oil is obtained, the functions of the organ are still performed, FATTY LIVER. 333

1 Cyanosis (chronic) is here used to express the general venous congestion which is consequent upon chronic affections of the lungs aud heart. "Since (as the Author says in a MS. note) it has become known that cyanosis, even when produced by congenital malformation of the heart, does not arise from a commingling of arterial and venous blood, but from an obstruction to the venous circulation, it has seemed reasonable to designate every more general hyperaemia, due to such obstruction, by the same term." "Acute cyanosis," he adds, "occurs in acute affections of the lungs, as for example, in pertussis."—Tr.

however large the quantity of oil contained in the cells. In man too, even in the most advanced stage of fatty liver, we still find bile in the gall-bladder. So far therefore these conditions can in no respect be compared to the necrobiotic conditions, which are found in the course of fatty degeneration in so many other parts, and in which the elements perish. In fatty degeneration, in the ordinary sense of the word, we find, in the later stages of the affection, somewhere or other, friable, softened places, where the fat is contained in free drops—in some sort fatty abscesses. It is therefore a fact of extreme importance, and one which I consider to afford very decided indications for the correct appreciation of this form [fatty liver], that in it there is always a persistence of the histological constituents, and that, however much these constituents may become filled with foreign substances, they still continue to exist as cells. Hence it follows, that a fatty condition of the liver may be removed, that it is curable, without any particular regenerative processes being required for the cure. The only requisite is, that the causes of the retention be removed, and the hepatic cells be freed from fat. It is true we have no positive information respecting either the one or the other of these points. We are not acquainted with the states which lead to the retention of the fat, nor with the conditions under which it can again be expelled. However, now that we have got so far, it will probably also be possible to make out the remaining facts. For it is conceivable, for example, that simplythe elasticity of the histological elements is of importance; that when the cell-walls become relaxed, they may readily admit a quantity of matter, and tolerate its presence in them, whilst, if they are very elastic, a removal, an expression of their contents, may be more likely to ensue. The state of the circulation also is certainly of importance, and the frequent occurrence of fatty liver in chronic affections of the lungs and heart is certainly in no

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