JX'LAMI'SI.i 537 



of riu'tabolisni tlirown into the blood of the mother, botli from the 

 fetus and from licr own overactive tissues; these cause injury to the 

 kidneys, k^adin": to a further retention, or injure the liver so that 

 the normal metabolic processes of that organ (particularlj' oxidation) 

 cannot be carried on; or, perhaps more often, both liver and kidney 

 as Avell as other organs are injured. In this way a vicious circle 

 might be established and rapidly lead to an overwhelming of the ma- 

 ternal system with toxic products derived from both her own and the 

 fetal tissues. It must be admitted, however, that the rapid improve- 

 ment that so often follows removal of the products of conception 

 indicates strongly that the poisonous substances arise chiefly, if not 

 exclusively, in the fetus or the placenta. But, as Liepmann points 

 out, the child shows relatively little evidence of intoxication, while, 

 on the other hand, eclampsia may develop after delivery of the fetus, 

 which facts speak in favor of the place of the origin of the poison 

 being the placenta and not the fetiLs, and death of the fetus seems to 

 have no effect on the eclampsia.^' Especially important in this con- 

 nection is the observation of a case of eclampsia by Hitschmann ^^ in 

 a patient with a hydatid mole and no fetus. ^'^ 



The Ductless Glands in Eclampsia. — In view^ of the mystery sur- 

 rounding the cause and effect of the enlargement of the thyroid 

 during pregnancy, it is not strange that the suggestion has been 

 made that the enlargement is for the purpose of neutralizing the 

 excessive amounts of toxic materials in the maternal blood, and that 

 failure of this enlargement is responsible for eclampsia. In support 

 of this idea Lange ^° states that absence of the normal thyroid en- 

 largement is usual in eclampsia, and Fruhinsholz and Jeandelize ®^ 

 note the frequency of eclampsia in myxedematous women. The nota- 

 ble influence of calcium upon convulsions, and the possible deficiency 

 in calcium during pregnancy, has led to the suggestion that this 

 may be responsible for eclampsia,®- and, since the parathyroids are 

 related to calcium metabolism, that they are concerned ; *'^ but such 

 theories fail to explain the many changes other than the con\-ulsions, 

 and have not been accorded much importance. Kastle and Healy ^* 

 consider that parturient paresis of cattle, which bears some resem- 

 blance to human eclampsia, is caused by absorption of toxic substances 

 produced in the formation of the colostrum; it is cured by dilating 

 the lacteal ducts by oxygen or other means. This observation lends 



5- See Lichtenstein, Zeit. f. G^ti., 1912 (36). 1419. 

 58 Cent. f. Gyn., 1904 (28), 1*089. 



50 See also Gross (Praper mod. Woch., 1909 (.34), 36.5) who t'oinid records of 

 seven cases of eclampsia with hydatid mole, witli or without a fetus. 



60 Zeit. f. Geb. vi. Gvn.. 1899 "(40), 34. 



61 Presse Med., 1902 (10), 1023. 



62 See Silvestri, Gaz. desjli Osped., 1910 (31), 689; Mitchell, Med. Record, 

 1910 (78), 90G. 



63 Massacrlia and Sparapani, Arcli. ital. Biol.. 1907 (48), 109. 

 6* Jour. Infec. Dis., 1912 (10), 226. 



