654 LOUIS BAUMAN 



catarrhal jaundice or any influence which tends to damage the liver cells. 

 It is assumed that in this condition the parenchyma is sufficiently impaired 

 by a toxic substance to permit autodigestion by the intracellular ferments 

 (Fischler; Wells(6)). 



The changes encountered in this condition have been accurately de- 

 .termined and clearly described by Van Slyke and Stadie. These authors 

 examined the blood and urine during life and the composition of the liver 

 after death. The amino-nitrogen of the blood was found to be increased 

 to 14 to 26 mgs., that is about 2 to 3 times the normal, while the 

 urine . contained a large amount of ammonia and amino-nitrogen, but 

 was low in urea. The liver had evidently lost part of its ability to deam- 

 inize amino acids and to convert ammonia into urea. The urea accounted 

 for about 50 per cent of the total nitrogen, the ammonia for about 15 

 per cent, and the ammo-nitrogen for about 11 per cent. (The normal per- 

 centage of amino-nitrogen in the urine is 2 per cent.) Although the liver 

 was completely degenerated, urea formation still occurred. In the two 

 days before death, there was an increase in acid excretion and on the day 

 before death the plasma bicarbonate fell below the normal. This was 

 due to the production of acids; whether the aromatic and lactic acids de- 

 scribed by Roehmann were responsible for the acidosis was not ascertained. 



The Composition of the Liver in Acute Yellow Atrophy 



(Van Slyke and Stadie) 



Water 71.0 per cent 



Fat 13.5 per cent 



Total solids other than fat. 14.9 per cent 



Amino-nitrogen 0.134 per cent 



Peptide nitrogen 0.072 per cent 



Urea nitrogen 0.0043 per cent 



Ammonia nitrogen 0.034 per cent 



Creatinin nitrogen 0.0033 per cent 



Creatin nitrogen 0.0143 per cent 



The water content was considerably lower than that of the normal 

 liver, and very much less than has been found in acute yellow atrophy by 

 previous authors. The fat content was unusually high. Previous authors 

 have usually found no increase of the fat content of the liver in this 

 condition. The normal fat content of the liver is about 3 per cent. The 

 remarkably low urea and the high ammonia content is to be ascribed to 

 the diminished ability of the liver to synthesize urea from ammonia. 



The increased excretion of amino acids in acute yellow atrophy has 

 been known since the time of Frerichs (1861), who first found leucin 

 and tyrosin in the urine in this condition. Wells also found a large quan- 

 tity of free amino acids in the liver of acute yellow atrophy. 



