T96 W. McKIM MARRIOTT 



breast milk curds there was a recurrence of all of the symptoms. Lichten- 

 stein and Lindberg, on a large series of infants, have absolutely failed 

 to confirm Meyer's results. 



In short, the theories of Finkelstein and his colleagues are based on 

 unconfirmed experimental work. Even granting the correctness of the 

 observations the theory of a sugar poisoning is insufficient to explain more 

 than a very small part of the general picture both clinical and metabolic. 



There is an idea expressed in much of the current literature that toxins 

 of one sort or another are produced in the intestinal tract during diarrhea 

 and are absorbed into the circulation. It is quite possible that such is 

 the case, but in the total absence of experimental evidence as to the na- 

 ture of the toxins or of their mode of action speculation is fruitless. 



We know that certain foods, especially easily fermentable sugars, lead 

 to diarrhea and we know that the more severe the diarrhea the greater the 

 loss of water and of mineral salts, as well as of organic food material, and 

 the more marked the clinical symptoms as a result. It would seem as 

 reasonable to assume that the loss of these substances is the cause of the 

 metabolic disturbance as to assume the presence of a hypothetical poison. 



The tremendous weight loss of these infants can only be explained by 

 a loss of water from the body. The observed concentration of the blood is 

 further evidence of water loss. The scanty secretion of urine is the direct 

 result of an increase in the colloidal osmotic pressure of the blood through 

 desiccation, for we know that when colloidal osmotic pressure exceeds 

 the arteriolar pressure in the renal vessels secretion of urine virtually 

 ceases (Starling). The concentration of the blood thus leads to an im- 

 pairment of renal function with retention of non-protein nitrogen, urea 

 and phosphates and a lowered phcnolsulphonepthalein excretion. Fail- 

 ure of the kidney to excrete acid results in acidosis whether the failure is 

 due to organic changes in the kidneys- as in nephritis or due to purely 

 functional causes as in the case of these desiccated infants. When the 

 blood volume is diminished, from any cause, a greatly decreased volume 

 flow results (Gesell(a)). A decrease in blood volume such as occurs fol- 

 lowing hemorrhage or in surgical shock leads to a compensatory constric- 

 tion of the arterioles with a piling up of corpuscles of the capillary blood 

 (Cannon, Fraser and Hooper). In the case of these infants the blood 

 being concentrated by water loss is decreased in volume and consequently 

 the flow is reduced and compensatory arteriolar constriction occurs. A 

 decreased volume flow of the blood, however brought about, leads to the 

 accumulation of acid products of metabolism in the tissues and a decreased 

 alkali reserve of the blood (Wright and Colebrook, Gesell(o.)). The acid 

 produced under such conditions is, at least in part, lactic acid (Clausen 

 (6) ). It has been shown by Araki that in conditions accompanied by vaso- 

 constriction glycosuria occurs, the so-called "asphyxial glycosuria." Fever 

 is common in conditions of desiccation of the body and is due according 





