PUERPERAL ECLAMPSIA 545 



and normal placentas, but believes that in eclampsia there is a reduced 

 capacity of the maternal blood to neutralize this poison. According 

 to Mohr and Heimann,**^ the eclamptic placenta shows a great decrease 

 in lecithin, which they ascribe to the increased autolysis, and to the 

 hydrolyzed lecithin they attribute the hemotoxic effects. On the 

 other hand Murray and Bienenfeld*''^ report the finding of an increased 

 amount of lipoids in eclamptic placenta. ^'^ 



The Fetus as a Source of Intoxication. — A reasonable view of the 

 cause of eclampsia is that it is initiated by the excessive or abnormal 

 products of metabolism thrown into the blood of the mother, both from 

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

 kidneys, leading to a further retention, or injure the liver so that 

 the normal metabolic processes of that organ (particularly oxidation) 

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

 as well 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 dehvery of the fetus, 

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

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

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

 nection is the observation of cases of eclampsia in patients with a hy- 

 datid mole and no fetus. ^^ 



The Ductless Glands in Eclampsia. — In view of the mystery surrounding 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 enlargement is usual in 

 eclampsia, and Fruhinsholz and Jeandelize*^ note the frequency of eclampsia in 

 myxedematous women. The notable 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 re- 

 s' Ibid., 1912 (46), 367. 



82 Jour. Obst. and Gyn. Brit. Empire, 1910 (18), 225: Biochem. Zeit., 1912 

 (43), 245. 



*^ The hypothesis of Mohr and Freund that oleic acid from the eclamptic 

 placenta is a hemolytic factor, is not corroborated by Polano (Zeit. Geb. u. Gyn., 

 1910 (65), 581). 



s^ See Lichtenstein, Zeit. f. Gyn., 1912 (36), 1419. 

 ^ 85 Hitschmann, Cent. f. Gyn., 1904 (28), 1089. See also Gross (Prager med. 

 Woch., 1909 (34), (365) who found records of seven cases of eclampsia with hyda- 

 tid mole, with or without a fetus. 



8« Zeit. f. Geb. u. Gyn., 1899 (40), 34. 



8- Presse M4d., 1902 (10), 1023. 



88 See Silvestri, Gaz. degli Ospcd., 1910 (31\ G89; Mitchell, Med. Record, 

 1910 (78), 906. 



