Etiology. Pathogenesis. 533 



heart and lungs, or by pressure on the posterior vena cava, may 

 cause not only dilatation of the hepatic vessels (nutmeg liver) 

 and an atrophy of the liver cells, but also an increase in the 

 amount of connective tissue. Chronic hepatitis may also be seen 

 in cases of thrombosis of the portal vein, which may either be 

 due to the derangement of the liver parench;^aua or may be 

 the result of the cirrhosis, Avliich has some previous cause. 



Bleiehroder considers that the chronic hepatitis seen in the human subject as 

 a sequel to diseases oi" the blood originating in the portal area is produced in the 

 following manner. The blood in the portal vein has poured into it an enormous 

 number of lymphocytes from the spleen, these are deposited in the liver and lead 

 to the production of new connective tissue. This process would explain the en- 

 largement of the spleen which is suggestive of an infectious disease. The jaundice 

 is due to extensive destruction of red blood corpuscles and must therefore be con- 

 sidered as a pleioehromic icterus. The socalled Banti 's disease of the human subject, 

 the symptoms of which are anemia, enlargement of the spleen, ascites, increased 

 urobilin-content of the urine and frequently cirrhosis of the liver, is also possibly 

 brought about in this way. 



Pathogenesis. When cirrhosis of the liver is due to some 

 irritant circulating in the portal blood, the process starts in the 

 interlobular branches. There is a cellular infiltration followed 

 by the formation of connective tissue. In this way the amount 

 of connective tissue surrounding several lobules becomes in- 

 creased in amount. By the subsequent shrinking of this tissue 

 the included lobules and the branches of the portal vein ramify- 

 ing in the proliferating tissue are subjected to pressure. De- 

 generation and sometimes necrosis and destruction of the liver 

 tissue follows, partly owing to the constant pressure exerted by 

 the contracting tissue and partly owing to the olistruction of the 

 larger vessels. In the later stages the connective tissue pene- 

 trates into tlie interior of the lobules. 



Irritants in the bile ducts lead to the production of the in- 

 flammatory changes in their immediate neighborliood (cholan- 

 gioitic cirrhosis). As shown by Jiiger's extensive investigations 

 regarding cirrhosis due to flukes (q. v.), the inflammatory pro- 

 cess starts in the angle between adjacent lobules, either_ as a 

 cholangioitis or as a cellular infiltration of the connective tissue. 

 The process extends along the interlobular septa, following the 

 lymph stream, and finally attacks the peripheral parts of the 

 lobules. Localized cirrhosis appears to be caused in this way. 

 In some cases contraction of the connective tissue is delayed 

 or does not occur at all, but even in these cases there is com- 

 pression of the interlobular blood vessels. 



In Schweinsberg disease of the horse, the inflammation in- 

 volves the liver parenchyma and especially the blood vessels, 

 producing a perilobular hypertrophic cirrhosis (Mugler). Kitt 

 formerly described the disease as a chronic parenchjanatous 

 hepatitis, with secondary formation of connective tissue. 



In chronic venous congestion of the liver, the formation of 

 connective tissue commences around the hepatic and central 

 veins and then extends to the interlobular spaces. 



