CIRRHOSIS OF THE LIVER. 



the hypogastric veins, through the hsemorrhoidal plexus ; 2. From the 

 anastomoses between the portal veins and those veins of the perito- 

 naeum which open into the diaphragmatic and oesophageal veins; 3. 

 Through newly-formed vessels in the adhesions between the liver and 

 diaphragm. Besides these ways, and other occasional abnormal com- 

 munications, by which the blood from the portal vein may elude the 

 hepatic vein and reach the vena cava, in some cases, 4, a very peculiar 

 form of collateral circulation is set up, which may be recognized, even 

 during life, by very evident symptoms. It was formerly supposed that 

 this form only occurred when the umbilical vein was incompletely 

 closed after birth, and that a fine canal remained in the ligamentum 

 teres during after-life. If considerable congestion of the liver occur 

 in such cases, this fine canal is gradually distended by the pressure of 

 the blood, and may become so pervious as to conduct the blood to the 

 anterior abdominal wall, where it empties into the ramifications of the 

 internal mammary veins. The consequent overfilling of the internal 

 mammary veins impedes the escape of blood from the cutaneous veins, 

 so that these may be excessively dilated, and surround the navel as a 

 blue cushion. The deformity thus induced, the caput Medusas^ does 

 not, however, depend on dilatation of the incompletely obliterated um- 

 bilical vein, but on dilatation of the branches of the portal vein run- 

 rung from the liver to the anterior abdominal wall, between the folds 

 of the falciform ligament, which anastomose with the roots of the epi- 

 gastric and internal mammary veins (Sappey). 



It is more difficult to explain why some of the symptoms of con- 

 gestion occur, while others are absent, than it is why none of them 

 exist. We only partly know (see above) why the spleen (which JSam- 

 berger found enlarged in fifty-eight cases out of sixty-four, and Frerichs 

 in eighteen cases out of thirty-six) remains small in some cases, and why 

 some patients have hsematemesis frequently, while others do not have 

 it throughout the disease ; and we shall not attempt to explain these 

 irregularities. 



Although, in cirrhosis of the liver, the gall-ducts are subjected to 

 the same pressure as the portal veins, there is rarely much biliary ob- 

 struction. It is true, most of the patients have a dirty-yellow color, a 

 yellow tinge of the sclerotic and dark urine ; but intense icterus is by 

 no means a frequent symptom of cirrhosis. This symptom is readily 

 explained by the physiology of the formation of bile. There is no 

 bile in the blood going to the liver, but it is prepared there from the 

 materials supplied. Hence obstruction and reabsorption of bile always 

 presuppose that at least part of the liver-cells is preserved, and acts 

 normally. In cirrhosis of the liver, on the one hand, the bile-ducts are 

 compressed, and the conditions are induced which most frequently lead 



