720 DISEASES OF THE LIVER. 



In the second stage the jaundice increases, the region of the liver be- 

 oomes sensitive to pressure, the patients complain of severe headache, 

 become restless, excited, and finally delirious. Occasionally the ex- 

 citement extends to the motor nerves, so that there are local or general 

 muscular twitchings. But soon, and sometimes without any previous- 

 symptoms of irritation, the patient is seized with insuperable depres- 

 sion and lassitude ; he falls into a deep sleep, from which he can at 

 first be aroused momentarily, particularly by pressure over the liver, 

 but later cannot be awakened at all. Then the previously normal or 

 even retarded pulse almost always becomes frequent. The tempera- 

 ture rises very high; tongue and gums become dry and covered 

 withsordes; the faeces and urine are evacuated involuntarily. The 

 collapse increases, the very frequent pulse becomes smaller, there is 

 copious perspiration, and, without arousing from his coma, the patient 

 usually dies the second day, more rarely the fourth or fifth day, or 

 later. We might be tempted to regard the icterus in acute yellow 

 atrophy of the liver as haematogenous, and to explain it by saying 

 that the blood-corpuscles are destroyed in the same way as the liver- 

 cells by the exciting cause of the disease. But the discoloration of 

 the contents of the intestines, although incomplete, and the jaundiced 

 appearance of the liver, as compared with the other organs, render the 

 correctness of this explanation very questionable. The intensely 

 bilious color of the liver shows that the discoloration of the contents 

 of the intestines is not due to arrested production of bile, that is, to 

 acholia. Nor can the icterus be referred to catarrh of the excretory 

 bile-ducts, of which the first symptoms of the disease remind us, for 

 neither the gall-bladder nor ducts are distended with bile. I agree 

 with Buhl and JBamberger, who refer the obstruction and reabsorption 

 of bile to a blocking up of the origin of the bile-ducts by fatty and 

 molecular detritus of the liver-cells. It is difficult to explain the 2>rain- 

 symptoms, which are the most prominent symptoms of acute yellow 

 atrophy of the liver. We have already spoken of our reasons for not 

 referring them to poisoning by the bile-acids. Barriberger also says : 

 " So much is certain, the brain-symptoms cannot be regarded as cho- 

 lasmic, for both the grade and duration of the jaundice are too slight 

 for this to be the case." Since in acute yellow atrophy the liver-cells 

 are extensively destroyed, and as in this disease abnormal products of 

 destructive assimilation have been found in the urine, there is some 

 ground for attributing the brain-symptoms in acholia to poisoning by 

 noxious substances, which are formed instead of the normal products 

 of the change of tissue. But I do not consider even this explanation 

 as proved. It is possible that the same cause may induce both the 

 degeneration of the liver and the brain troubles. The haemorrhages 



