PATHOLOGICAL METABOLISM IN PREGNANCY 839 



the metabolic disturbances which are due to the degeneration of the liver 

 cells with resulting failure of oxidation or deamination of the protein 

 molecule. He pointed out, however, that they could not be considered 

 identical in all respects and that eclampsia with its more striking clinical 

 symptom, the convulsion, might have an added factor to the disturbance 

 of metabolism. If there is a single causative element in eclampsia he 

 believed it to be the nephritis rather than a toxin from the fetus, placenta 

 or uterus. 



Examination of the Urine by Modern Methods 



Williams in 1905 was the first to determine the ammonia in 

 the urine and he found that in pernicious vomiting it was high, in one 

 case as high as 40 per cent of the total nitrogen. At that time he stated 

 his belief that an increase above 10 per cent was an evidence of greatly 

 disturbed metabolism and an indication to empty the uterus. In the 

 eclamptic cases the ammonia was variable but there was a marked reduc- 

 tion of the total nitrogen and the urea, with an increase of the amino- 

 acids. 



Edgar reported the nitrogen partitions in a case of early vomiting 

 toxemia that late in her pregnancy developed convulsions. 



Ewing and Wolf (6) made a most elaborate study of the divided nitro- 

 gen in all forms of pregnancy toxemias. In the pernicious vomiting cases 

 and in four cases of acute yellow atrophy they found a marked increase of 

 ammonia with a lowering of urea. In many instances they determined 

 the creatinin and uric acid nitrogen but in others these fractions together 

 with the amino-acids, purin and any other undetermined nitrogen were 

 grouped into a class termed "undetermined" or "rest" nitrogen. They 

 found this fraction high in most of the toxemic cases and came to the 

 conclusion that there was a defect in the intermediary nitrogenous 

 metabolism, resulting in a failure to split off the amino group in the syn- 

 thesis of the protein molecule. This condition they termed deficient 

 deamination. It is interesting to examine their results, especially in the 

 acute yellow atrophy cases for here we have for comparison a number 

 of instances of the relationship between urea and ammonia as noted on 

 page 837 of this article. The four cases died and extensive liver autolysis 

 and necrosis was noted in three in which autopsies were obtained. 



Excluding Case 31, where the total nitrogen excretion is not known, 

 these figures show the highest ammonia-urea relationship as 17.4 to 67.8, 

 whereas in the figures quoted by Minkowski there were those of a case of 

 Munzer's with the ratio of 17.3 per cent ammonia to 52.4 per cent urea. 



In two fatal cases of eclampsia, one revealing at autopsy early throm- 

 bosis and moderate autolysis of the liver, the figures may be considered as 



