ACITK YELLOW ATh'OI'll) <)l' Tin: Ll\ El! 541 



the studies of Evarts Graham,'"-' to be produced by the hydrochloric 

 acid formed from it in the liver. Some cases of puerperal eclampsia 

 also i)resent such profound liver changes that they are distinguished 

 as eclampsia chictiy on the basis of the convulsive manifestations, 

 rather than on the ground of anatomical changes. So, too, the hepa- 

 tic changes in certain septicemias and acute syphilis may resemble 

 those of acute yellow atrophy to a greater or less degree. 



Summary of Views on Etiology. — From a review of the literature 

 and the study of a few cases, the writer has reached the following 

 understanding of the condition described as acute yellow atrophy of 

 the liver: The "atrophy" is due entireh' to autolysis of necrotic 

 liver-cells by their own enzymes. In the most typical cases of "pri- 

 mary'' or "idiopathic"' yellow atrophy we have to do with a poison 

 having a very specific effect on the liver-cells, which destroys their 

 "life" (i. e., stops synthetic activities) without injuring their intra- 

 cellular proteolytic enzymes," and consequently autolysis occurs; as 

 the poison affects other organs but little, the necrosis and autolysis 

 continue until there is so much loss of liver function that systemic 

 poisoning results from the hepatic insufficiency and from the result- 

 ing accumulation of poisonous products of incomplete metabolism. 

 Tliat the intoxication comes in large measure from the changes in 

 the liver, even in phosphorus poisoning, is shown by the greater re- 

 sistance to phosphorus of dogs with Eck's fistulas."* The patient 

 dies from this poisoning,'^ and the liver is found at autopsy to have 

 decreased by from one-third to one-half or more in its volume. This 

 great change would not be possible if the poisons affected the heart, 

 kidneys, or brain as much as they do the liver structure, which is 

 probabl}' the reason that phosphorus, bacterial poisons, snake poisons, 

 and other poisons that destroy liver-cells do not ordinarily produce 

 the typical picture of liver atrophy. When these poisons affect the 

 liver more and the other tissues less, we approach the condition of 

 acute yellow atrophy; e. g., if the dose of phosphorus is not so great 

 as to kill the patient through injury- of other more vital organs, 

 after a few days the necrosed liver-cells undergo autolysis, and if 

 enough liver-cells have been destroj-ed, hepatic insufficiency may 

 cause death, with the finding of an anatomical condition in the liver 

 that can be properly designated as acute atrophy. Hence it is pos- 

 sible for many poisons to cause this condition under certain circum- 

 stances, and there seem to be certain unknown poisons (probably of 



76a .Jour. Exp. Med., 1015 (22), 48. 



~~ According to some investigators phosphorus augments autolysis even in vitro 

 (see Krontowski, Zeit. f. Biol."; IfllO (54) , 479) . 



T8 Fischler and Bardach. Zeit. pliysiol. Chem.. 1912 (78). 4:^5. 



79 The mortality of cases sutticiently typical to be diagnosed antemortem is 

 estimated by Rondaky (Roussky Vratch.'Oct. 28. 1900) at 97 to 98 per cent. 

 Concerning the regenerative changes in the cases which recover, see Yamasaki 

 (Zeit. f. Heilk., Path. Abt., 1903 (24), 248). 



