ACID IXTOMCAT/OX I\ XOXDIAnHTKJ COXDITIOyH 557 



burned, and this condition is usually aeconipanied witJL fatty changes 

 in the liver, which also depend on lack of oxidation. Throughout the 

 clinical forms of acidosis, lactic acid and fatty degeneration are 

 always associated (Ewiug). To assume, as has been generally done, 

 that the lactic acid appears in the urine when hepatic alterations are 

 marked, because of a loss of the liver tissue which should destroy it, 

 is probably not warranted. Rather, the liver conditions and the for- 

 mation of lactic acid depend upon the same cause, which is a de- 

 fective oxygen supply or interchange, either general or local. ''''"^ 



ACID INTOXICATION IN CONDITIONS OTHER THAN DIABETES «b 



Clinical Types of Acidosis. — Ewing has divided acidosis as it oc- 

 curs in man, into two main types: 1. Acidosis resembling in its 

 effects the acidosis produced by experimental injection of acids. 

 This is characterized by the excretion of the acetone bodies in large 

 amounts with a corresponding amount of ammonia in the urine, 

 and by the absence of marked and characteristic anatomical changes. 

 Diabetic acidosis and the acidosis of starvation are the clinical condi- 

 tions showing this type. 



2. Acidosis resembling that produced experimentally by extirpa- 

 tion of the liver or by the Eck fistula. Here the urine contains much 

 lactic acid and relatively little acetone bodies, the ammonia being 

 in excess of any acetone compounds, and there is also much incom- 

 pletely changed nitrogenous compounds. The clinical prototj^pes are 

 phosphorus and chloroform poisoning, the toxemias of pregnancy and 

 cyclic vomiting and acute yellow atrophy. Anatomically it is char- 

 acterized by severe hepatic degeneration, usually fatty. 



This classification is purely one of convenience, for typical and ex- 

 treme fatty liver may occur in phlorhizin diabetes with the typical 

 coma, provided the animal was fat when the experiment was begun, 

 and that the experiment was not carried on in such a way as to ex- 

 haust the fat temporarily present in the liver. It is tnie that high- 

 grade fatty livers are not usually observed in most cases of long- 

 standing diabetes, but fatty changes are severe in the acute fulmi- 

 nating types of diabetes of infancy and childhood, and here we have 

 typical acidosis. The reason that lactic acid does not occur in the 

 urine of a completely diabetic animal or man, is probably not be- 

 cause of any assumed destructive power of the comparatively nor- 

 mal liver, but because here the carbohydrate equilibrium is so dis- 

 turbed that even if lactic acid were formed it would necessarily be 

 converted into glucose and appear in the urine as such. ]\Iandel 

 and Lusk have indeed shown that even dogs poisoned with phos- 

 phorus excrete no lactic acid in the urine if, in addition, they are 



49a See Macleod and Wedd (.Tour. Biol. Clicm., 1014 (IS), 446) wlio found 

 that reducing the oxygen supply to the liver caused a marked rise in the lactic 

 acid content of the hepatic blood. 



49b See resuna^ by Frothingham, Arch. Int. Med., 1916 (IS), 717. 



