In this variety, therefore, the original anomaly consists in the hepatic parenchyma being gradually reduced to the capillary gall-ducts which have assumed the shape of the granulations; and in so far as this is genuine cirrhosis of the liver, it certainly bears some resemblance to the pulmonary cirrhosis described by Corrigan. The secondary metamorphosis causes a gradual atrophy of the granulations, accompanied by a predominance of the interstitial cellulo-fibrous tissue, and a uniform diminution of the entire organ.

The degree attained by the metamorphosis is proportionate to the number of obsolete granulations, or to the amount of parenchyma remaining capable of performing its functions; the organ decreases in proportion to the shrivelling and condensation of the interstitial, cellulo-fibrous tissue; and it often appears reduced to one-quarter, or even one-sixth, of its ordinary size. The condensation of the cellulo-fibrous tissue, as it gives rise to a decrease of the organ, also induces a corrugation and shrivelling of the peritoneal investment. The latter will be more or less opaque, and thickened; and, being retracted between the projecting granulations, these not unfrequently appear to have a necklike contraction. These changes in the hepatic peritoneal covering take place without any symptoms of inflammatory action.

The secondary metamorphosis chiefly affects the margin of the liver, and more particularly the left lobe. The organ very commonly appears to have been almost or entirely deprived of parenchyma, and to consist exclusively of fibro-cellular tissue, the edges more particularly being thinned off and turned back upon the body of the organ, the left lobe of which is converted into a mere appendix of fibro-cellular structure, of the size of a hen's egg or a walnut.

Not unfrequently the granulations assume, in the advanced stages, and after a long duration of the disease, a bluish or dark-green color, which particularly affects those seated at the concave surface of the liver.

This form of cirrhosis of the liver undoubtedly originates in hypercemic states, a view that is confirmed by their frequent connection with organic disease of the heart: its frequent occurrence in drunkards also points to a peculiar anomaly in the constitution of the portal blood.

/B. 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 of organization predominate in the inflammatory product. This secondary metamorphosis, from not occurring uniformly, results in a subdivision of the organ into larger or smaller scattered compartments, which present the characteristic rounded form of the granulations in the same ratio as they correspond to single hepatic lobules. Their parenchyma is frequently found in the original state of chronic inflammation, but it may be unchanged, or it may offer one of the other accidental anomalies alluded to.

It is intelligible that the diminution of size in this variety is often inconsiderable, that the organ may even be enlarged, and that the fibro-cellular tissue is accumulated in such a manner as to preponderate over the parenchymatous cellular tissue. A marked decrease of size occurs when the obliteration is extensive and the cellulo-fibrous tissue has shrunk; and as this decrease advances, the pressure exerted by the shrivelled tissue upon the parts not originally affected by the anomaly, induces an atrophy in them; they fade, and put on a rusty or dark yellow color.

Granular liver frequently presents an abnormity which appears peculiar to this variety. We allude to the presence on the condensed peritoneal investment of pseudo-membranous formations, of a cellular or cellulo-fibrous texture, which generally extend to the diaphragm in the shape of corded adhesions. They are the result of inflammatory processes, which have become extinct long before the occurrence of the secondary metamorphosis, and which appear to afford evidence of the inflammatory nature of the hepatic disease itself.

Besides these two modes of development of granular liver, the affection may also be viewed as a retrograde process, manifested in depositions or infiltrations of the hepatic parenchyma, arising from an anomalous state of the blood.

In reference to the external conformation of granular liver, we have still to advert to a variety which is characterized by the hepatic parenchyma not being reduced to granulations, but continuing in large masses, the more superficial of which are pushed out by the shrinking interstitial tissue, and being more or less contracted at their base, cause the entire organ to appear lobulated.

Granular disease of the liver is found complicated with all the essential or accidental anomalies which we have described as occurring in the paranchyma of the granulations, and these anomalies may either precede the granular disease or supervene after its development. The complications may be hypertrophy, nutmeg liver, cirrhosis, adipose and other infiltrations, acute yellow atrophy, inflammatory and other hepatic diseases. The granular disease arising from one of the essential anomalies, e. g. from inflammatory causes, is more particularly liable to combine with another essential anomaly, as, for instance, with true cirrhosis.

The complication with adipose deposit is peculiarly interesting. The latter may, -

Firstly, be the primary affection upon which the granular disease is grafted in the shape of cirrhosis. As the cirrhosis advances, the reduction of the organ generally, but more particularly of the marginal portions which have been infiltrated with fat, is impeded, and the atrophy that does take place is characterized by its affecting the margin much less than in the uncomplicated form.

Secondly; the adipose deposit may supervene upon a granular state of the liver; and if it does so before the secondary metamorphosis has advanced very far, and whilst the granulations are still very numerous, it may prevent the liver from assuming the form peculiar to the granular condition. If it occurs at a later period, it need not modify the characteristic form of the organ.

Thirdly; the cirrhotic and shrinking granulation which is cut off by dense cartilaginous interstitial tissue may degenerate into a flabby, dirty yellowish-brown fat-lobule, the degeneration apparently proceeding from the confined biliary matter.

A similar relation exists in regard to the modifications of form between the granular condition and other infiltrations of the hepatic parenchyma.

Granular liver is also very frequently coincident with the most various morbid affections of the heart, which give rise to congestion in the vena cava and in the portal system; of these, hypertrophy, dilatation, and valvular disease are the most common. Disease of the heart must be considered as an important momentum in the origin of the hepatic disease.

The symptoms resulting from the granular state of the liver bear a ratio with the degree of its development; the impermeability and obliteration of its secreting tissue induce, on the one hand, congestion in the portal system, hyperaemic states of the intestine and of the peritoneum, a blennorrhoic condition of the former, tumefaction of its membranes, and ascites; on the other, dyscrasic conditions of the blood allied to scurvy and frequently accompanied by icterus, an inclination to exudative processes, with an especial proclivity to hemorrhage, anasarca, and anaemia.

We cannot admit that the relation existing between Bright's disease of the kidneys and granular liver, though the two often coexist, has been accounted for. In one set of cases both affections would seem to have originated in common causes; in another, Bright's disease is evidently of more recent date, and has supervened upon the existing granular state of the liver; but whether in this case it is due to a separate cause, or is owing to the dyscrasia accompanying the hepatic disease, we are unable to determine.

Granular liver is invariably a chronic affection, which may often be arrested in its development for a short time, but never permanently. It terminates fatally by inducing anaemia and tabes complicated with dropsy; by disorganization of the blood, by exhausting and paralyzing exudations on the serous membranes, and especially on the peritoneum. It rarely occurs before the prime of life, but we have seen one case of it at the age of seventeen.