Certain poisons, as antimony, arsenic, notably phosphorus, have the power to set up an irritative hyperplasia of the connective tissue of the liver. These metals accumulate in the liver in preparation for excretion. Wegner,64 in the study of the action of phosphorus on dogs, rabbits, and other animals, has induced a marked degree of sclerosis, but such results have not been observed in cases of poisoning by phosphorus in man, except in an instance reported by Küssner.
64 Virchow's Archiv, Band lv. p. 18.
Finally, a condition of the liver corresponding in all respects to cirrhosis has been induced by perihepatitis, by the organization of the exudation and its subsequent contraction, and by the extension of the morbid process from the capsule to the interlobular connective tissue (Poulin65).
65 Étude sur les Atrophies viscérales consécutives aux Inflammations chroniques du Sereuses, etc., Thèse de Paris, 1880.
PATHOLOGICAL ANATOMY.—Several forms of cirrhosis are recognized by the modern French school of pathologists. According to Sabourin,66 there is an annular, a monolobular, and a multilobular form. These differ merely in regard to the arrangement of the new connective tissue. At the outset of the disease the liver is increased in size and hyperæmic. Its consistence is also greater than normal. The outer surface is at this period smooth, but on section the islets of the parenchymatous tissue, yellowish in color, are distinctly visible between the grayish or pale-rose tint of the intervening or proliferating tissue. This reddish-gray material consists of fine connective-tissue elements containing spindle-shaped cells.67 The development of this material is such as to even exceed in quantity the proper glandular structure. The bands of newly-formed connective tissue extend between individual lobules (monolobular cirrhosis) or between groups of lobules (multilobular cirrhosis). A portion of the spindle-shaped cells form new vessels communicating with the branches of the hepatic artery.68 Coincidently with the formation of the new connective tissue ensues its contraction. The enlarged organ diminishes in size from a slight degree to one-half its original volume; especially in the left lobe is the diminution of size most marked. On the surface it exhibits a knobbed or nodular aspect (hobnail liver), and these knobs present through the capsule a yellow appearance. The granulations, so called, consist of small prominences corresponding to lobules or groups of lobules, and hence vary in size from that of a pinhead to that of a pea.69 Between these are the sharply-defined masses of connective tissue. On section the organ is found to be of firm almost cartilaginous hardness, and between the interlacing bundles of connective tissue are the small islands of parenchymatous tissue projecting above the cut surface and having a yellowish or brownish-yellow color. As the terminal branches of the portal are compressed in the process of shrinking undergone by the new connective tissue, they are destroyed. The result of this obliteration of the portal radicles is the impaired nutrition of the lobules and atrophy of the cells. Formerly it was held that the atrophy of the hepatic cells was due to the compression exercised by the contracting connective tissue, and Beale70 even maintained that the change began in the cells, the connective tissue contracting as the cells receded before them. This view has been reaffirmed by Ackermann in a paper read last year before the Congress of German Naturalists and Physicians, but without any acknowledgment, so far as I can ascertain, of Beale's long-before expressed opinions. In the discussion which followed the reading of Ackermann's paper the position of its author was supported by Aufrecht, Küssner, and others, but controverted by Rindfleisch. It has been demonstrated by Cohnheim and Litten71 that the lobule is nourished not only by the portal radicles, but by the branches of the hepatic artery, which enter, by the interlobular vein, the capillaries of the lobule, and hence the nutrition of the cells suffers in consequence of the lessened blood-supply; but it is probable also that more or less compression is exercised. When the cells are destroyed, their remains may be discerned in the mass of connective tissue as fine fat-granules or masses of pigment yellowish or brownish in color. The peculiar appearance to which the name cirrhosis is applied is due to the lobules or groups of lobules which project on section above the divided surface, and are colored yellowish by the bile-pigment, which here exists in an exaggerated quantity. The cells themselves are not normal: they are enlarged by compensatory hypertrophy, and they contain much bile-pigment and a considerable quantity of fat. The compression of the capillaries, especially their obliteration, leads to stasis of the blood and its consequences in the whole chylopoietic system.
66 Ch. Sabourin, "Du Rôle que joue le Système veineux sus-hépatique dans la topog. de la cirrhose du foie," Revue de Médecine, June, 1882.
67 Förster, Lehrbuch der pathologischen Anatomie, Jena, 1873, p. 264.
68 Cornil, "Note sur l'État anatomique des Canaux biliaires et des Vaisseaux sanguins dans la cirrhose du foie," Gaz. méd. de Paris, 1883.
69 Charcot, Leçons sur les Maladies du Foie, etc., p. 226.
70 Archives of Medicine, vol. ii. p. 82.