ACUTE YELLOW ATROPHY OF THE LIVER 549 



liver changes that they are distingui.shed as echinipsia chiefly on the basis of the 

 convulsive manifestations, rather than on the ground of anatomical changes. So, 

 too, the hepatic 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 

 imderstanding of the condition described as acute yellow atrophy of 

 the liver: The "atrophy" is due entirely 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 autolj'sis 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 resulting 

 accumulation of poisonous products of incomplete metabolism. That 

 the intoxication comes in large measure from the changes in the liver, 

 even in phosphorus poisoning, is shown by the greater resistance 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 probably the 

 reason that phosphorus, bacterial poisons, snake poisons, and other 

 poisons that affect many sorts of 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 destro3''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 possible for many 

 poisons to cause this condition under certain circumstances, and there 

 seem to be certain unknown poisons (possibly of intestinal origin^) 

 that are of such a nature that thej^ cause specifically acute hepatic 

 atrophJ^ The above hypothesis seems to explain all the known facts 

 concerning this disease. That phosphorus, chloroform, and some 

 other poisons lead particularly to fatty changes may, perhaps, be due 



^ According to some investigators phosphorus augments autolysis even in vitro 

 (see Krontowski, Zeit. f. Biol., 1910 (54), 479). 



' Fischler and Bardach, Zeit. physiol. Chem., 1912 (78), 435. 



8 The mortality of cases sufhciently 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). 



« See Carbone, Riforma Med., 1902 (1), 687 and 698. 



