836 HAROLD BAILEY 



term not one had albumin unless they also showed symptoms of intoxica- 

 tion, there was acceptance of the idea that the convulsions were due to 

 disease of the kidneys. The theory had already been promulgated that 

 in these damaged states of the kidney there was an accumulation of urea 

 in the blood and to express this condition, the term uremia was first used 

 in 1853 (Schottin). 



There were some, however, who failed to accept this explanation as 

 fully answering all the demands of the case for, as Meigs at once pointed 

 out, there are many cases of eclampsia that do not have an albuminuria 

 and, on the other hand, the true cases of Bright' s disease seldom have the 

 convulsions. In support of this statement he quoted Bright's(a) first 

 report where in 25 deaths but 2 patients had convulsions, and the later 

 report describing 35 cases with convulsions in only 3. Gourbeyre in 18 50 

 collected 164 cases of toxemia of pregnancy. Five cases had convulsions 

 but with no albumin in the urine. Of the remainder all had albumin and 

 95 developed convulsions. Meigs fell back upon the explanation, now 

 known as the Traube-Rosenstein theory, of a hyperemia of the brain as an 

 important factor in the etiology. 



The involvement of the liver in both acute yellow atrophy and eclamp- 

 sia and the connection between these diseases was first noticed by Von 

 Frerichs(/) in 1860. In 1879 Duncan called attention to the probable 

 relationship between hypermesis gravidarum and acute yellow atrophy. 

 During the next ten years, the changes in the liver were thoroughly studied 

 from an anatomical standpoint and thus the way was cleared for the 

 investigation of the disease as one involving the general metabolism. 



Pilliet(a) (6) in 1888 and in 1890 described the liver pathology in 

 eclampsia. In the latter paper he reported the autopsies of 22 cases with 

 changes in the liver in all and claimed that the degeneration in this organ 

 formed an important picture of the disease. Jiirgens not only described 

 the changes in the liver cells but also made note of the fat emboli in the 

 liver and the general blood stream. Von Klebs found emboli in the brain, 

 liver and kidneys, and finally the pathology of the disease became firmly 

 established by Schmorl's(a) monograph in 1893. In 17 cases studied he 

 found constant changes in the liver cells with hemorrhagic areas and peri- 

 portal necrotic foci. In five of the cases he found placental cell thrombosis 

 in the lungs. In a more recent study the same author found the liver de- 

 generated in 71 of 73 cases of eclampsia and all the cases showed kidney 

 involvement. 



At the time when it was recognized that the liver changes were a part 

 of the pathological picture of eclampsia, physiologists were attempting by 

 experiment to ascertain the functions of this organ and to note the varia- 

 tions in disease. In 1886 Minkowski(&) studied the nitrogenous metab- 

 olism in geese following the extirpation of their livers. In fowls the nitro- 

 gen excretion in the urine is chiefly in the form of uric acid. Liver extir- 



