74 Quoted by Thierfelder, op. cit.

Besides these indirect evidences of portal obstruction and a contracting organ, there are direct means of ascertaining the condition of the liver. By the methods of physical diagnosis we may acquire much information. On auscultation, as our Jackson75 was the first to show, a grating or creaking like leather, or friction sound, is audible over the right hypochondrium synchronously with the respiratory movements or when produced by moving with the fingers the abdominal wall on the liver. This sound is caused by the bands of false membrane which extend between the two surfaces, and hence indicates a secondary perihepatitis.

75 The American Journal of the Medical Sciences, July, 1850.

To ascertain the dimensions of the liver—to mark out the area of hepatic dulness—with accuracy is a most necessary procedure. The period of the disease is an important element in the problem. When the new material is deposited and the congestion of the portal system first occurs, an increase in the dimensions of the organ is observed. This enlargement, of brief duration, must not be confounded with the hypertrophic sclerosis, another form of the malady. So considerable is the increase in the size of the liver that there is an evident enlargement of the right hypochondrium, and the whole abdomen seems fuller. The organ may be felt, on palpation, projecting one, two, or even three fingers' breadths below the margin of the ribs, and the left lobe extends well across the epigastrium, increasing the sense of resistance and the area of dulness in this direction. The enlarged liver, as felt below the ribs, appears firmer than is natural, is yet smooth, and the margin is sharply defined. The duration of this period of enlargement is indefinite, but it is rather brief, and is followed by the contracting and atrophic stage. It is not often, indeed, that the patient presents himself during the period of enlargement. Sometimes a perihepatitis or an unwonted tenderness in the right side compels attention during this stage, but more frequently it escapes notice. If perihepatitis occur, there will be fever, pain, and tenderness, a slight icterode hue of the skin, and possibly Jackson's76 friction sound. These symptoms, taken in conjunction with the history of the case and the obvious enlargement of the organ, will indicate the existence of the first stage of sclerosis.

76 The American Journal of the Medical Sciences, July, 1850, supra.

The contraction of the liver, or, as it may be expressed, the atrophy of the hepatic cells and the consequent shrinking of the interlobular connective tissue, goes on slowly. Several months may be occupied in an amount of atrophy distinct enough to be recognized by the narrowing of the area of hepatic dulness. Especially difficult is the recognition of the contraction when ascites has fully distended the abdomen. It may be necessary under such circumstances to postpone a decision until tapping has removed the fluid. If the organ can be felt by depressing the walls of the abdomen, more or less unevenness of surface may be detected, and the inferior margin may give the impression of hardness and sharpness of outline. At the same time, the increased dulness of the epigastric region observed during the hypertrophic stage will have gradually ceased because of the shrinking of the left lobe. The liver may be undergoing the atrophic degeneration to a marked extent and yet remain large—larger even than normal. Such a state of things may be due to conjoint amyloid or fatty degeneration of the organ, and, indeed, more or less fatty change occurs in all cases of cirrhosis. The shrinking of the liver persists until the area of dulness is not greater in area than two or three ribs.

The disturbances of function in sclerosis of the liver are not limited to the chylopoietic system. As the secreting structure of the liver is continually lessened in extent by the atrophy, symptoms result from the necessary interference in the hepatic functions. These symptoms are concerned with the liver, with the nutrition of the tissues of the body, and with the kidneys. As regards the biliary function of the liver, the quantity of bile acids and pigment is reduced below the normal in proportion to the damage done to the organ. As a rule, there is little jaundice in sclerosis, and very little bile-pigment present in the urine. Hence there must be little produced. Instead of a jaundiced hue of the skin, it has a fawn color—an earthy, sallow tint eminently characteristic of a chronic affection in which the power to produce bile is much impaired. Occasionally it happens, particularly in the early stages of cirrhosis, that a well-marked jaundice appears in the face and body, but this probably is due to a catarrh of the bile-ducts. In most cases the integument presents the earthy and sallow hue above mentioned. Graves77 appears to have been the first to interpret aright the greater significance of this appearance of the skin than the purely jaundiced tint. The glycogenic function of the liver must be impaired in the same ratio as the biliary. The nutrition of the body suffers; the skin becomes dry and harsh; the fat disappears; the temperature of the body, unless the conditions for producing fever are present, is barely up to normal, if not somewhat below; a marked degree of anæmia supervenes; and the action of the heart becomes feeble and rapid after a period of slowness. The blood is altered in quality, and hence hemorrhages—epistaxis especially—occur, petechiæ and ecchymoses appear in the skin, and stigmata are numerous about the face and nose.

77 Clinical Medicine, op. cit.

The urine in cirrhosis is high-colored because of the abundance of pigment, and in the early stages of the disease is increased in amount, although of lower specific gravity. When much effusion takes place into the peritoneal sac, the compression of the renal veins by the fluid lessens the activity of the kidneys and diminishes the urinary flow. Much discussion has taken place over the quantity of urea present in the urine in cases of cirrhosis, but it has been established that the relative quantity of urea lessens in proportion to the damage suffered by the liver.78 The urates are in excess.

78 Charcot, Leçons sur les Maladies du Foie, loc. cit., p. 252; also, Essai sur les Variations de l'Urée dans les Maladies du Foie, par F. Genevoix, Paris, 1876; Des Rapports de l'Urée avec le Foie, par A. Martin, Paris, 1877; Sur l'Urée et ces Variations dans la Cirrhose, Thèse de Paris, Audiguier; Contribution à l'Étude du Rôle du Foie dans la Product. de l'Urée, Reufflet.