Interstitial Hepatitis.—Cirrhosis of the liver is in a large proportion of cases directly attributable to alcoholic excess. In this view the greater number of observers coincide. But that alcohol is not the sole cause of chronic interstitial hepatitis has been abundantly established. As long ago as 1868, Anstie34 wrote as follows: “Considering the enormous quantities of spirituous liquors which are drunk by many of the patients who apply for relief from the consequences of chronic alcoholism, it would be natural for the reader who holds the usual opinion as to the origin of cirrhosis of the liver to expect that serious symptoms produced by the latter disorder must often complicate cases of the former. The case is, however, far otherwise in my own experience. Of the immense number of patients in whom the nervous disorder has been clearly identified, I have only seen thirteen cases in which the symptoms of cirrhotic disease called for any special treatment, although a certain degree of cirrhosis was doubtless present in many of the others; and I cannot avoid the conclusion that some very powerful element over and above the influence of alcoholic excess is needed to produce the severe type of that disease.” Formad35 states as the result of his investigations as coroner's physician of the city of Philadelphia that cirrhosis of the liver is much less common in alcoholic subjects than has been generally thought. My own experience during eleven years as attending physician at the Philadelphia Hospital leads me to endorse this opinion.
34 A System of Medicine, Reynolds, vol. ii. p. 74.
35 Proceedings of the Pathological Society of Philadelphia, Dec., 1885.
The anatomical lesions of chronic interstitial hepatitis consist essentially in hyperplasia and hypertrophy of the connective tissue of the organ. The progress of the affection is insidious and gradual; some degree of enlargement, due in part to congestion and in part to interstitial exudation, is followed by gradual diminution, with retraction of the new connective tissue. When the connective-tissue new formation is excessive, and retraction fails to take place, the organ remains permanently enlarged (hypertrophic cirrhosis). During the first period the volume of the organ is increased, its consistence is more firm, and its surface is slightly granular. The second period is characterized by induration, with diminution of the volume of the organ and alteration of its form. The surface is uneven, deeply granular, and usually of a mottled yellow color. The tissue is firm, creaking under the knife. The connective tissue is enormously increased, the glandular elements being proportionately atrophied.
The contracting connective tissue exercises at the same time a compressing influence upon the hepatic cells and upon the vascular supply throughout the organ; the radicals of the portal vein and the branches of the hepatic artery are alike compressed, and in part obliterated. The same is true of the bile-ducts. The functional activity of the liver, at first diminished, is finally, to a considerable extent, arrested. In consequence of these physical alterations in the structure of the organ, the symptoms, which are at first insignificant, become progressively more grave, until at length they constitute complications of the most serious kind.
It can be no longer asserted that the interstitial hepatitis produced by alcohol presents specific characters. It nevertheless differs in many respects from that form due to valvular lesions of the heart, in which there are induration, usually augmentation in the volume of the organ, and persistent congestion. Congestion, in truth, is the chief characteristic of the latter form, in which the surface is smooth and glistening, of a deep brown or violet hue, and on section yellowish or brown—a condition which has been well described under the term cyanotic liver.
Sclerotic changes due to alcohol usually affect the organ throughout. In this respect alcoholic cirrhosis differs from that form due to syphilis in which the lesions are irregularly distributed.
The functional disturbances due to cirrhosis are, in the beginning, obscure in themselves and masked by the concomitant gastric derangement. Later, ascites constitutes the chief as well as the most constant symptom. It is rarely altogether absent. Emaciation is also a prominent symptom. No affection, not even diabetes or phthisis, produces loss of flesh so rapid, so marked, and so significant as cirrhosis of the liver in chronic alcoholism. Not only do the adipose tissues waste, but the muscles themselves undergo rapid atrophy. This fact is not surprising when we consider that the lesions of the liver give rise to grave interference with every function of that organ. In addition to the more common gastric symptoms, there is constipation, not rarely alternating, without assignable cause, with serous and sometimes bloody diarrhœa. Epigastric distress, epistaxis, and hemorrhages from other mucous surfaces are common, and are due in part to the disturbance of the general circulation, and in part to alterations in the character of the blood itself. The physical signs indicate in the early stages increase, and afterward diminution, in the volume of the liver. Enlargement of the superficial abdominal veins is a characteristic sign. Cirrhosis of the liver is a grave affection, the course of which, at first slow, afterward more rapid, almost invariably leads to a fatal termination.
Fatty Degeneration of the Liver.—Steatosis of the liver is of extremely common occurrence in the advanced stages of alcoholism. The anatomical changes consist in accumulation of fat-globules in the liver-cells. French writers distinguish two varieties of hepatic steatosis: first, that in which the cellular elements undergo no change beyond that of an accumulation of fat-globules within their substance; and second, that in which the liver-cells undergo an actual disintegration, in the course of which fat-granules are formed, and which is, as a matter of fact, a true fatty degeneration. The first of these conditions is not incompatible with the functional integrity of the organ, and is in many instances unattended by symptoms, being discovered only upon examination after death. Its occurrence is to be explained by the imperfect oxidation of waste products due to the constant presence of alcohol in the blood, and by the habitual excess of fat in the latter fluid. When fatty infiltration is of moderate amount there are no changes in the volume or the contour of the organ, and the condition is recognized only on microscopical examination. At a later stage the organ becomes enlarged, particularly in its antero-posterior diameter. The surface is now smooth and glistening, its color yellow or reddish-yellow; upon section it is anæmic, of a yellowish color, with patches of a reddish hue, and its consistence is diminished. The indentation caused by pressure of the finger persists. Under the microscope the hepatic cells are enlarged, rounded, packed with fat-globules of varying size. In some of the cells these globules coalesce and form more or less extensive drops of fat. The bile which is secreted in this condition presents in most instances the normal characteristics.
Disorders of digestion do not occur in consequence of the fatty change in the liver until the lesion has reached an advanced stage; nevertheless, they constitute the earliest symptoms of this condition. Imperfect digestion, accompanied with flatulence, distension of the belly, epigastric tenderness, with light-colored stools, and constipation alternating with diarrhœa, are common symptoms. There is no pain properly referable to the region of the liver. Whilst icterus does not occur, there is, nevertheless, a peculiar earthy pallor of the complexion and persistent greasiness of the skin—conditions, however, which are not in themselves sufficiently marked to possess, in the absence of other signs, clinical value.