Congestion of the liver is a matter of small importance from the standpoint of pathology unless it be of sufficient duration to cause cyanotic atrophy and induration. However the facts that congestion of this organ occurs three times as often in the mammal as in the bird and that vascular cirrhosis has not been seen in the latter class, are interesting and noteworthy. In addition ascites of hepatic origin has not been seen in the birds. The explanation for this lies in the rich anastomosis between the intestinal area and the caudal vena cava so that the blood does not have to pass through the liver to reach the heart. This arrangement would reduce the back pressure in passive congestion and relieve the liver in the congestion due to toxic or inflammatory distention of small vessels. CIRRHOSIS. The chronic inflammations or so-called cirrhoses of the liver have been subjected to a great deal of study and many theories have been expounded as to their cause and classification. Here is not the place to discuss the academic question of nomenclature but rather to adopt an acceptable working classification and to analyze our material thereon. A cirrhosis is a chronic inflammation of the liver indicated by increased connective tissue with evidences of degeneration and attempts at regeneration on the part of the hepatic cells. Certain cases of increased connective framework fail to show the last two features and, since they must be grouped near the cirrhoses because of the prominence of connective tissue, they are called _fibroses_, _perilobular in type_. Among the instances carrying out the full stipulations are livers with evidence of a perivascular fibrosis and obstruction, to which are added degeneration and regeneration of the lobular margins; such are PORTAL CIRRHOSES in human medicine associated with passive congestion in the intestinal area, and ascites. In a second variety, fibrosis seems to succeed upon obstruction to the biliary lumina or upon peribiliary inflammation, BILIARY CIRRHOSES. The effects of this are to dam back bile with the production of varying degrees of jaundice and for the inflammation to spread into the lobules, thus distorting their internal architecture; this form is therefore unlike portal cirrhosis which alters the size and shape of lobules as a whole. Fatty change is very prominent in certain cases and it has been a custom, perhaps without warrant, to put such livers into a separate group. It may be that they represent a different chemical process. When there exists for a long time a venous stasis in the liver, necrosis is apt to occur in the cells subjected to pressure and the absence of fresh blood. This gives rise to a “nutmeg” liver upon which may succeed a definite perivenous fibrosis.