I'uisoxs I'Roui ri:u IS jiLJtxs 563 



parently because of a profound intoxication. As evidence of intoxica- 

 tion we Imve not oidy clinical manifestations, such as delirium, iiemo- 

 ^lobinuria, and albuminuria, vomitinj>^, bloody diarrhea, etc., but, more 

 convincinoly, the anatomical lindings at autopsy, which are strikingly 

 similar to those resulting from acute intoxication with bacterial prod- 

 ucts. Uardeen found (juite constantly cloiuly swelling and focal and 

 parenchymatous degeneration in the liver and kidneys: softening and 

 enlargement of the spleen with focal degeneration in the ^Iali)ighian 

 bodies ; and particularly degenerative changes in the lymph-glands 

 and intestinal follicles resembling those observed in diphtheria, which 

 ^McCrae '••' considers due to proliferation and phagocytosis by the 

 endothelial cells of the lymphatic structures. IMarked changes are 

 usually present in the blood, consisting of fragmentation and dis- 

 tortion of the red corpuscles, hemoglobinemia, loss of water with a 

 relative increase in the number of corpuscles by from one to four 

 millions per cubic millimeter, an increase in the blood platelets, and a 

 rise in the number of leucocytes as high as 30,000 to 50,000.'^° Hem- 

 oglobinuria is also frequently present, and almost constantly gastro- 

 intestinal irritation occurs, with anatomical evidences of acute enter- 

 itis, acute gastritis, and occasionally gastric or duodenal ulcers. Ac- 

 cording to Korolenko,"^ the sympathetic nervous system is seriously 

 involved. 



It therefore seems probable that poisons are formed as a result 

 of superficial burns, which have the effect of causing hemolysis, and 

 which are also cytotoxic for parenchymatous cells and particularly 

 for nervous tissues. These hypothetical poisons seem to be eliminated 

 by the intestines and kidneys, which are injured by the poisons in 

 their passage through these organs. The attempts to explain all the 

 observed effects of burns as due to thrombosis or to embolism by al- 

 tered red corpuscles seem to have failed, for the peculiar location of 

 the lesions (e. g., duodenal ulcers, necrosis in the Malpighian bodies 

 of the spleen, etc.) does not agree with this hypothesis, and there are 

 too many evidences of the presence of some decidedly toxic substance 

 in the blood. There can be no question that the poisonous substance 

 or substances are formed in the burned area, and not in the internal 

 organs as a result of hyperpyrexia, as shown by numerous observa- 

 tions. Thus, if the burned area is removed immediately (in narco- 

 tized experimental animals), death will be prevented, whereas if the 

 burned tissue is permitted to remain for a few hours, death will 

 occur. If the burned skin is transplanted to a normal animal, this 

 animal will develop symptoms of intoxication, while the burned ani- 

 mal may be saved by the transplantation (Vogt). The poison ap- 



190.5 (180). 367. Full discussion of theories by Vopt, Zeit. exp. Path. u. Pliarm., 

 1912 (11), 191. 



69Amer. :Med.. 1901 (2), 735. 



TO Locke, Boston :\led. and Surg. Jour., 1902 (147), 480. 



71 Cent. f. Path., 1903 (10), 663. 



