540 AHSOiniAlATIES 1\ .UI:TA HOLISM 



suits. In the countries wliere phosphorus poisoning- is common (es- 

 pecialh' Austria) there has been found much difficulty in distin- 

 guishing in many cases the results of phosphorus poisoning from 

 acute yellow atrophy of the liver, and many have contended that 

 there is no real difference ; i. e., that phosphorus, as well as unknown 

 poisons, may cause acute yellow atrophy. The present trend of opin- 

 ion, however, seems to favor the view that there is a primary liver 

 atrophy which is different from that caused by phosphorus or other 

 known poisons in several essential respects.''* 



Phosphorus Poisoning. — Between phosphorus poisoning and ^"pri- 

 mary" hepatic atrophjj the following chief differences may he dis- 

 cerned: Phosphonis produces a general injurious effect upon all 

 the organs of the body, the liver merely showing the most marked 

 anatomical changes, which at first consist of a fatty metamorphosis 

 of the liver, due to migration of the body fat from the fat deposits 

 into the injured cell (Rosenfeld, Taylor) ; subsequently the liver 

 cells disintegrate, the cytoplasm being aft'ected before the nucleus, 

 and the liver may become smaller than normal, although it is usu- 

 ally enlarged because of the fat deposition. Typical acute yellow 

 atrophy is characterized by an early necrosis of a large proportion 

 of the liver-cells, the nucleus becoming unstainable while the cyto- 

 plasm is still little altered in appearance, and fatty changes play a 

 subordinate role or are absent. As Anchiitz says, the poison seems 

 to strike at the life of the cell, its nucleus, while phosphorus attacks 

 the cytoplasm. Furthermore, the poison of yellow atrophy seems to 

 be very specific, for it attacks the other organs of the body almost 

 not at all, and within the liver it affects only the hepatic cells proper, 

 while the bile-duct epithelium and the stroma cells are so little in- 

 jured that they are able to proliferate greatly, this proliferation 

 being a prominent feature. There are also clinical and chemical dif- 

 ferences that will be discussed later, but yet, on the whole, the re- 

 semblances of yellow atrophy and phospliorus poisoning are so great 

 that we have obtained much information concerning the former by 

 means of experimental studies of phosphorus poisoning. 



Delayed Chloroform Poisoning. — After chloroform narcosis, and 

 rarely after etlier, there occasionally develops a severe intoxication, 

 with clinical and anatomical findings very similar to acute yelloAV 

 atrophy and phosj)horus poisoning;"" in point of the fatty changes 

 the cases usually stand intermediate between acute yellow atro]ili,\' wnd 

 phosphorus poisoning. Tliis action of chloroform would seem, fioni 



75 See Anschiitz, Arb. a. <1. I'atli. hist. Tiiljiiiucn. 1!M>2 ( :! ) , -I'-W: raltaiif. \vy\\. 

 Deut. Path. Gesell., VMY.\ (5), !)1: liicss, ]?('rl. klin. WO.li., litOf) (42). No. 44a, 

 p. 54. 



7« Complete review and lileratvire bv Hevan ami Favill. .Tour. Amer. Med. 

 Assoc., 100,5 (45), 091; :Muskeiis. Mitt, (irenz. :\led. u. (hir., IDll (22), .lliS. Full 

 dineuKsion of clieniislry of clilorofonu necrosis liy Wells, .lour. Riol. Cheni.. 1!>()S 

 (5), 12!>. Kxpciimcnial necrosis — see \\'liip))le and Sperrv, .lohns Hopkins 

 Hosp. Bull., I'JU!) (20), 278; (Jraiuim, .lour. Ivxper Med., 1!)12 (15), '^Ol. 



