what I had been accustomed to use and recommend as made by another druggist in Edinburgh; and its taste was decidedly different. This imperfect extract proved to have been prepared from powdered root obtained from London; so that it was reasonable to conclude that the wrong root had been collected, or that it had been incorrectly dried. I believe that every druggist in good business in Edinburgh can now supply the genuine article.

As no experiments have yet been tried with other ferns, the selection of the proper species, Lastrea Filix-mas, must be considered for the present an important condition of success. Several other ferns, one common, others not so, may be readily mistaken for the true one by an uninstructed, or careless, or unconscientious collector. It is itself luckily very common. Except the Pteris aquilina, no other fern is so familiarly seen, in every dell of Scotland at least. The only other common one, and which, indeed, often grows in immediate proximity, the Athyrium Filix-Femina, is known by the frond; which, whether luxuriant in summer, or withered in winter, is easily recognised to be doubly-pinnate, and not, as in the true plant, singly-pinnate.

Peschier says the plant is efficacious chiefly between May and September, inclusive. We may trust so good an observer for the fact, that the root is efficacious in that interval. But it so happens that all my own specimens of the oleo-resin were made with fresh roots collected in February, two months at least before the young fronds begin in Scotland to peep above ground; and the preparation, which has been got in the shops of Edinburgh for almost all the cases reported to me, was prepared about the same time by one druggist. Hence I suppose the root is quite efficacious enough at any season, if it be used fresh. I know nothing of the effect of keeping the root long. Peschier thought the oleo-resin began to lose activity in a year. I have known it used of that age with complete success.

I might easily illustrate these statements, according to the rule of the day, by a long list of cases, with uniform details, tiresome by their reiteration. But they all come to the same thing as the last which was communicated to me the other day by a late pupil, Dr. J. C. Davies, of Holywell, Flintshire, in the following terms: According to your advice, I sent to Edinburgh for the male-shield-fern, and have administered it in two cases as directed by you, with the most satisfactory results."

66

In conclusion, my experience of the male-shield-fern corresponds precisely with the much more extended observation of Peschier, at Geneva, more than a quarter of a century ago. I am persuaded, therefore, that it is easy, with a few simple precautions, to obtain from a common indigenous plant a more efficacious and less disagreeable anthelmintic for the expulsion of tænia, than from either the Abyssinian kousso, the Continental pomegranate, or American turpentine. It is surprising that Peschier's observations, made on a very large scale indeed, have attracted so little attention in Britain until the late notice in the Edinburgh Monthly Journal. I ca only say this has not been for want of a strong recommendation on my own part, both in my Lectures constantly since 1833, and also in my Dispensatory,' when first published in 1842.-Monthly Journal of Med. Science, July, 1853, p. 47.

can

54. ON THE PRODUCTION OF THE FATTY CONDITION OF THE LIVER.

By DR. C. HANFIELD JONES, F.R.S., &c.

[Although a great deal has recently been written upon the subject of fatty liver, yet, we may still ask the question-What really constitutes true fatty degeneration of this organ?]

Is it to be regarded as a simple increase of the quantity of oil naturally existing in the hepatic cells, or is it a further and more important change? I am much inclined to think that the latter is the case, and that a real distinction exists between the condition of oily accumulation when there is simply an undue quantity of oil present in the parenchyma, and that of true fatty degeneration when the natural structure is more or less altered and destroyed. To illustrate this I will quote first the instance of a kitten, which had been fed for about a week on food containing

much oily matter. The liver was of a dull greyish-yellow tint, in the first stage of hepatic venous congestion. Sections viewed under the microscope were utterly opaque, and showed both the cells and intercellular substance loaded with oily molecules; the accumulation of oil was equal everywhere. The ultimate ducts were dissected out and found natural. Here all that had occurred was the addition of a quantity of oil to the hepatic parenchyma (not to the ducts), there was no degeneration of the cells. In contrast to this instance I will place the notes I made of the condition of two livers taken from the bodies of two persons who died in St. George's Hospital. In one "the liver was in a complete state of fatty degeneration; the oil drops, however, did not seem to be enclosed in distinct cells, but to lie in an indistinct granular or semi-fibrous stratum; scarce any distinct cells were to be seen." In the second, the liver being also in a state of complete fatty degeneration, I observed that the cells were, for the most part, destroyed, and that only films of granular matter remained; the number of free nuclei also seemed to be fewer than usual. In these two cases it was quite evident that the natural cell structure of the liver was, to a great extent, destroyed, that a real degeneration had taken place; and this I have repeatedly observed in most cases of fatty degeneration of the liver, occurring in persons who have died of various diseases. Whether a liver, whose cells are thus destroyed, can recover its natural condition, is a question of much interest, but one which it seems impossible to answer.

A circumstance of much interest, which seems still further to indicate the degenerative character of the fatty transformation of the human liver, is that in such livers I have almost invariably been unable to detect the existence of sugar, and this is confirmed also by the experience of my friend Mr. Blyth. This, however, was not the case with the kitten's liver, who had been fed on fatty food,—it yielded, on analysis, a full proportion of saccharine matter.

Another point which has not been much noticed is the peculiar limitation of fatty degeneration to the margins of the lobules, which is very frequent. I think the change does not consist merely in accumulation of oil in the marginal cells, but that destruction of them actually takes place. A liver affected in this way, presents the lobules most perfectly marked out by a zone of opaque matter; this varies in different cases somewhat in width, but may be said generally to occupy about one fifth or one fourth of the distance from the margin to the centre. I can give no sufficient explanation of the tendency of oil to accumulate in the marginal cells; it may, perhaps, in part depend on the circumstance that the stream of portal blood first passes through them; but this does not at all account for the converse occurrence, viz., oily accumulation in the central cells, which is sometimes very marked in the healthy livers of animals. There is commonly but little yellow matter in the cells of livers deeply affected with fatty degeneration,-sometimes, however, it is sufficiently apparent in a few here and there; the common condition of livers which present more or less of the "nutmeg" aspect, is oily accumulation or fatty degeneration of the margins, with heaping up of yellow molecules in the central cells around the intra-lobular vein.

Fatty degeneration of the liver, when complete, may occur in very different diseases; it is by no means peculiar to phthisis, as is well ascertained. Out of nineteen cases which I examined microscopically, four or five only had any connec tion with phthisis; the others occurred in diseases of various kinds, which, for the most part, but not invariably, had produced great emaciation.

Another kind of degenerative change is present in the much more rare lardaceous liver. One specimen of this kind which I examined, had the following characters: It was enlarged, bulky, of solid feel and glossy aspect, having a yellowish tint with some whitish spots, and containing very little blood. Thin sections under the microscope showed some of the lobules in a pretty natural state, the cells perhaps rather enlarged, and arranged very much in a linear manner. In other lobules there was a manifest infiltration between the cells, of an homogeneous, highly refracting substance, much resembling concrete oily matter; this was very abundant in some parts, so much so as to compress the cells and reduce them to mere bands anastomosing together, and producing the appearance of a plexus containing the homogeneous matter in its meshes. In many spots, especially in the vicinity of the deposited substance, the cells were deeply tinged with yellow matter. The refracting matter in another instance consisted of spherical, oval, or irregular shaped masses, which XXVIII.-9.

had somewhat the size and figure of the natural cells, but did not, I think, result from a transformation of these. Liquor potassæ added to thin sections under the microscope reduced the deposited matter to mere filmy fragments, and diminished considerably the refracting power; its action upon this substance and the surrounding cells, many of which contained much oil, was very different; the latter becoming more transpareut exhibited their oily contents with great distinctness; the former, though quite translucent, showed no trace of oily matter. The minute ducts in the latter specimen, as well as in the former, were of natural appearance. I have several times examined spleens from the human subject, which contained a great quantity of matter precisely similar in appearance to that which was here deposited; its seat in the spleen appears to be chiefly the Malpighian bodies whose natural cell structure it replaces, and then extending outwards, brings about an atrophy of the red pulp, which occurs to such an extent that at last mere red streaks are seen separating the translucent glistening substance, and the natural deep colour of the organ is lost. The term by which Rokitansky designates this peculiar deposit, is the "lardaceous" (speckig), and the pathological relations he assigns to it are with "constitutional disease of the vegetative system, especially with scrofulous and rickety disease, with syphilitic and mercurial cachexia," and occasionally as a sequel of intermittent fever. Dr. Budd recognises this condition as a scrofulous enlargement of the liver; this I think is so far correct, as intimating its relation to scrofulous disease, but it ought clearly to be understood that the deposit is totally different from tubercle, and is, indeed, so far as I know, sui generis.

The minute ducts in the fatty and last described condition of liver have appeared to me pretty natural; this fact renders it more easy to understand how, with so considerable alteration of the parenchyma, bile can still be secreted.

Rokitansky, describing cirrhosis, says "We are not of opinion that granular liver always takes its origin in the same fundamental affection; we are inclined to adopt two morbid states as the essential and original anomalies which give rise to granulations in the hepatic parenchyma as a secondary affection. In one case there is a morbid development of the capillary gall ducts (the so-called secreting tissue), an accumulation of the secretion, and probably also an hypertrophy of the parietes of those vessels giving rise to the nutmeg liver and to an obliteration of the capillary blood-vessels, the so-called vascular substance."

In the second case, the original affection of the hepatic parenchyma in granular liver is proved, by the post-mortem appearance of the granulations, to consist in a slow chronic inflammation. This induces a gradual obliteration of the parts attacked, and their conversion into fibro-cellular tissue, the amount of which varies in proportion as the processes of absorption or organisation predominate in the inflammatory product. This secondary metamorphosis, from not occurring uniformly, results in a subdivision of the organ into larger and smaller scattered compartments, which present the characteristic rounded form of the granulations in the same ratio as they correspond to single hepatic lobules."

Dr. Budd, in his chapter on Cirrhosis, describes it as "the consequence of adhesive inflammation in the areolar tissue about the small twigs of the portal vein, by which serum and coagulable lymph are poured out. The serous part of the effusion gets absorbed, and the fibrine contracts and becomes converted into dense fibrous tissue, which divides the lobular substance of the liver into well-defined masses," &c.

I cannot say that I have observed any condition corresponding to the first form of cirrhosis which Rokitansky describes. A morbid development of the capillary gall ducts must mean a morbid enlargement of the hepatic cells of the lobules, and such I have never seen in this disease. Dr. Budd's description expresses the opinion ordinarily received, to which I have but little to add that can be esteemed new. I think, however, that a somewhat different view may be taken of the nature of the morbid change constituting cirrhosis, and that some of its different forms may ve more exactly traced.

in some cases, no doubt, the fibrous tissue of the Glissonian sheath is affected with what may be truly called adhesive inflammation, attended with the effusion of coagulable lymph and serum. These cases will be marked by tolerably distinct symptoms-pain in the side, vomiting, fever, perhaps jaundice, as Dr. Budd enumerates them. The portal canals are the seat of the inflammation,-chiefly, I believe, the larger, and not to any great degree the smaller, canals or the fissures. In other

instances, which I believe are more numerous, the same parts may be affected, but the nature of the change is different. The fibrous tissue of the sheaths undergoes thickening and condensation, but not as a consequence of effusion of lymph and serum in an acute attack; the process is much more of the nature of degeneration, more akin to the chronic thickenings which are so often observed in fibro-serous membranes, and which are often coincident with this condition of the liver. The result of the above changes, when they do not extend to the smallest portal canals and interlobular fissures, is, I believe, the common hob-nail condition of the liver. If the thickening and condensation proceed further, and affect the sheaths which surround and invest the lobules, then the condition is different, and corresponds very nearly with that which I described in a communication to the Pathological Society, three years ago, under the name of " nutmeg liver." This description I subjoin, but would remark, at the same time, that in several of these cases I have no doubt that there takes place also a deposition of unhealthy plasmatic fluid in the substance of the lobules, which solidifies them, and tends to increase still further the atrophy of the cells which the defective supply of blood induces. It is difficult, in examining the débris of the parts thus degenerated, to distinguish accurately, in all particulars, between what should be regarded as cause, and what as effect; but, though aware of this, I still am strongly inclined to believe that such a process as I have indicated does actually affect the lobules themselves, and that the unhealthy nutritive process, which is the essence of cirrhosis, may manifest itself chiefly in either of three situations:-1. In the larger and middling-sized portal canals, excluding only the smallest. 2. In these last, and in the fissures. 3. In the smaller canals and fissures, and in the substance of the lobules. The first form results, as said, in the common hob-nail liver; the second and third produce tough, firm, dense livers, which are sometimes termed "brawny."

If, indeed, the view should prove correct which is entertained by some eminent pathologists, that fibrine is an excrementitious or effete substance-not, as was formerly supposed, one of the highest importance to the renewal and growth of tissues-then the existence of such a diathesis and morbid state as I have just alluded to would become in a still higher degree probable. We should then recognise the fibrinous as a form of excrementitious plethora, in which a fluid material, characterised by a tendency to spontaneous coagulation, and existing in the blood probably in undue quantity, produced injurious effects, by slowly perverting the nutrition and spoiling the texture of various parts: we should perceive a connection between various phenomena which now appear isolated. The deposition of vegetations, so called, on the valves of the heart, or the deposit of fibrinous masses in the spleen or elsewhere, would then appear as instances of tumultuous and excessive formation of fibrine in the blood, which was thus cast out burriedly in these parts. The presence of fibrinous nodules beneath the capsule of the liver, or on the pulmonary pleura, would indicate a process of a similar but much more gradual nature. All the various thickenings of fibrous or fibro-serous membranes, stiffening of the valves of the heart, contraction of its orifices, shortening of its cordæ tendineæ, many of the common pleural adhesions, white pericardial patches, would be properly ranked as having their origin in a similar morbid condition of the blood. They would appear then as manifestations of a general state, and not as local affections. The common fibrous tumour of the uterus would be a particular localisation of the general diathesis. There would appear reason to consider the large, firm, dense kidney, with its adherent capsule, as another result of such morbid action. The adhesion of the capsule to the surface is evidently the result of a similar change to that which thickens the capsule of the liver, and the increased bulk and coarser condition of the epithelium of the tubes may not improbably be attributed to its having undergone a kindred change, modified, of course, by its own peculiar nature. I cannot help remarking that no term seems to me, in many cases, so exactly to describe the condition of the renal epithelium in this condition of the organ as the word stiff; comparing the morbid structure with the healthy, it gives one the idea of being as much incapacitated from undergoing its normal chemico-vital changes as a stiff and rigid aortic valve is from following its natural easy movement. Again, under the head of fibrinous disease, we should range various forms of so-called chronic pneumonia, in which, with little appearance of acute inflammation, there has taken place exudation into the cavities of the air-cells, and complete condensation of

the tissue. Some of these cases, by the nature of the exuded material, would form a connecting link between chronic pneumonia (the fibrinous) and the recognised tubercular infiltration. The above are all instances of extra-vascular change produced by the fibrinous disease; one, however, we may refer to as originating in the interior of the vessels, and occasioning by its arrest of the circulation irremediable gangrene of the parts thus deprived of their supply of blood. I allude to the spontaneous coagulation of the blood within the vessels, of which several instances have lately been recorded, and which can be ascribed with no kind of probability to any other cause than such a state of the blood as we are now considering.

The preceding is rather a long discussion, but may be excused, I trust, from its intimate connection with the pathology of cirrhosis.

The form of cirrhosis which produces the "brawny" liver often co-exists with dilatation and hypertrophy of the heart, the former predominating more or less. The retardation of the circulation thus occasioned throws the blood back upon the large veins; and the hepatic veins in particular, with their radicles in the centre of the lobules, are in consequence much congested. I am strongly inclined to think that this congestion of the central part of the lobules has much to do with the peculiar alteration of the cells which there takes place, and which is almost exactly co-terminous with the congestion. The bile pigment is in all probability derived from the colouring matter of the blood, and it is worth noticing that this yellow matter is especially connected with those parts which are especially the seat of sanguine congestion. Hepatic venous congestion of the first degree is far the most common, and it is in the same part which this occupies, viz., in the centre of the lobules, that we find almost invariably yellow matter present in the cells.

Cirrhosis is sometimes combined with fatty transformation; a section then presents opaque inlets, the lobules gorged with fatty matter separated by wide, more transparent spaces, which are the enlarged fissures and spaces occupied by new formed fibroid tissue.

The ultimate ducts in cirrhosis are of course involved in the dense fibroid tissue, and are more or less atrophied by its pressure; their nuclei appear stunted and starved, and the structure is sometimes altogether lost, at least the ducts can no longer be discovered. Usually, however, by the aid of acetic acid they can be seen pretty readily in the widened fissures and canals.

Jaundice manifestly results from the conveyance into the blood of biliary pigment, that constituent of the bile which is certainly excrementitious and intended to be cast out with the fæcal matter. In most cases there is retention of the yellow matter in the liver, from a mechanical obstacle to its flow into the intestine, or from inaction of the excretory ducts; the retained matter, which, however, is not in excess, being absorbed into the blood instead of passing out with the secretion. In other cases it seems to be formed in excessive and unnatural quantity, as in the acute yellow atrophy of the liver, and perhaps in diseases of the heart, producing great congestion of the veins. It is extremely common to find yellow matter in the cells of the central parts of the lobules in cases of different description quite unattended with any jaundice; this is so frequently the case that it really seems probable that it results from the congestion of the intra-lobular veins and surrounding capillaries which takes place during the last hours of life. Great dilatation of the cavities of the heart, with consequent retardation of the circulation, produces most remarkable yellow engorgement of the central cells of the lobules, and this condition is, I think, not unfrequently accompanied with marked jaundice. In this case, however, I believe there is no cessation of the flow of bile into the intestine; the function of the ultimate ducts and of the exterior cells is still performed; and there seems only to be increased production of yellow pigment in the central cells. It must be borne in mind that this yellow pigment as it exists in the cells does not evidence the presence of biliary matter, of cholic acid, or its conjugates. The yellow matter can be extracted by alcohol, and gives the characteristic re-action of bile-pigment with nitric acid; but Pettenkoffer's test decides against the presence of the organic biliary acid. The deep colour of the urine in jaundice also seems to depend solely on the presence of the pigment; no trace of cholic acid is often discoverable. I conclude, therefore, that in most cases jaundice results from the absorption into the blood not of completely formed bile, but of one of the constituents only, viz., the yellow pigThis takes place, (1) when a mechanical obstacle prevents the flow of bile

ment.