In one form of cirrhosis,—the pericel lular or interstitial,—of which in man the liver of congenital syphilis affords the best example,—replacement-fibrosis is the distinguishing feature. In this the various stages of cellular atrophy can be well followed, and the little groups of cells are to be seen surrounded by del icate new tissues of a character very dif ferent from that of the dense connective bands seen in portal cirrhosis. The dif ference makes itself evidenced by the gross appearance of the organ, for this form of fibrous tissue does not contract, the surface remains smooth, and the organ is enlarged instead of being dimin ished in size. It may be urged that this enlargement is a proof of the productive character of the process, but the enlarge ment appears to be due, in the main, to a lack of pressure-atrophy of the he patic parenchyma so characteristic of portal cirrhosis, coupled with a com pensatory proliferation of the liver-cells to replace those which have been de stroyed. A proliferation or hypertrophy of this nature is occasionally well marked in the portal form, resulting in the form ation of islands of new liver-tissue and the production of a large hobnailed liver. Rarely the new growth of the paren chyma advances to an adenomatous or even cancerous condition, and we meet with a greatly-enlarged irregular cir rhotic liver with multiple neoplastic masses derived from the liver-cells.
If this process be the explanation of the hypertrophied liver of pericellular cirrhosis, then the appearances in biliary cirrhosis proper present macroscopically and microscopically so many points of approximation to what has just been de scribed, that the fibroid overgrowth here may well be largely of the nature of a replacement-fibrosis. The tendency is for recent observers to regard it as such, and to consider that biliary cirrhosis of the type which has especially been stud ied by Hanot is a cholangitis in which either the bile-capillaries within the lobule, or the cells bordering upon these, are especially affected. These liver-cells undergo gradual atrophy and replace ment by new connective tissue. Goluboff regards this form as being primarily due to the chronic, diffuse, catarrhal angi ocholitis with chronic, diffuse periangi ocholitis. Now, a catarrhal angiocholitis affecting the smallest bile-ducts affects the capillaries also, and is inevitably a process affecting the liver-cells them selves. But, while accepting these views with regard to the main characteristics of the fibroid changes of these two im portant forms of cirrhosis, it must, I think, be admitted that, save in rela tively-rare instances, the organs affected by one or other form of the disease show a mixture of both productive and replace ment changes.
There are yet otber ways in which fibroid tissues may be developed in vari ous organs \without recognizable inflam matory disturbance, and, as I have pointed out in the Middleton Goldsmith Lectures (189(3), there may be increased development of fibrous tissue of a func tional type. Such fibrosis is to be recog nized in connection with altered condi tions of the arterial, venous, and lym phatic circulation. It is difficult to say how far such_ forms manifest themselves in the liver. On the whole, the evi dence is against there being any exten sive development of new connective tis sue in the organ from such a cause; but it may well be that the indurative form of passive congestion of the organ and the growth of fibrous tissue around the interlobular branches of the hepatic vein, in cases where there is long-continued obstruction of moderate degree brought about by either heart or lung disease, are to be regarded as due to a laying down of new connective tissue around the he patic venules of non-inflammatory origin.
It is evident that, inasmuch as our definition is based upon the one condi tion of overdevelopment of fibrous tissue in the org-an, a proper classification orf the various forms of cirrhosis cannot be based primarily or adequately upon the disturbances occurring in other parts of the body as secondary results of the he patic fibrosis, but must be either etiolog ical and made dependent upon the vari ous causes leading to the development of fibrous tissue or, on the other hand, must—anatomically—be determined by the parts of the liver which are the pri mary scat of the development of the new tissue. Our knowledge of these cirrhoses is still insufficient for either the etio logical or the anatomical classification to be ideally perfect. Against the etio logical classification it may be objected that we are still uncertain as to how far the commonest form—portal cirrhosis— is due to the direct action of alcohol, how far it is due to the absorption of toxic substances from the intestinal canal sec ondary- to the gastritis and enteritis in duced by alcohol; nor again does the mere enumeration of causes help us in every case to distinguish the special type of cirrhosis which those causes induce, and so, the symptoms depending upon the form of hepatic disturbance, such a classification can be of little clinical value.
On the other hand, the anatomical classification is imperfect to the extent that, while the disease may begin by af fecting one special portion of the liver, as the process of fibrous-tissue develop ment extends, it involves many other parts, and, consequently, in well-devel oped cases cirrhosis is anatomically of a mixed type, and it is far from easy in such cases to determine how the condi tion originated. The fullest etiological classification is that given by Chauffard, and this has, at the same time, the ad vantage of being anatomical. He di vides the cirrhoses as follows:— is difficult to see how we are to make the distinction which is here made between the toxic cirrhosis and the toxi-infective. Anatomically and clinically, poisons— whether absorbed from the stomach or developed in the system itself, or again passing into the blood as a result of the growth of micro-organisms, or again given off by micro-organisms within the liver itself—may- produce similar lesions in the liver, and as a consequence bring about closely allied, if not identical, ana tomical changes in the organ with the development of like symptoms. The dis tinction thus raised by Chauffard be tween these various forms is too fine for practical use; clinically, his subdivisions are almost valueless; hence, in this ar ticle, I have divided the cirrhoses accord ing to anatomical grounds alone, and shall recognize the following forms of cirrhosis according to the origin of the process:—