The cause of pregnancy-kidney is prob ably an autointoxication of the organism by a product of metabolism during preg nancy. The overloading of the organism with this virus gives rise to eclampsia. The changes which occur in the kidneys, liver, and other organs in the eelamptic are of a secondary character. Saft (Archiv f. Gyniik., vol. li, p. 2).
While the urine of healthy pregnant women has been reported as sterile, germs :nay be cultivated from it: the same organisms obtained from the urine of eclampsias. These urines are but feebly toxic when injected subcutane ously in massive doses into animals. Bar (Obstetrics, Jan., '99).
The bulk of evidence is distinctly in favor of the belief that a profound tox aunia, originating- in the bodies of the mother and fcetus, causes eclampsia. The exact agent has not been isolated. An excessive amount of serum-albumin in the urine, accompanied with kidney de bris, is a symptom of moment. The amount of urea excreted is a valuable index. A diminution in its amount in dicates a retention of toxins. Jaundice is an especially grave symptom, and, hrematogenie in origin in these eases, points to a grave toxannia. E. P. Davis (Amer. Gymec. and Obstet. Jour., July, '99).
Study of 59 cases of eclampsia in the Imperial Alaternity Iiieff. Eclampsia shown to be a primary disease of the kidneys due solely to autoinfection of the patient by the accumulation of waste-prodnets in the maternal and fcetal blood. It is essentially a disease of preg naney, not of parturition, and it always tends to interrupt gestation. Abuladse Plonats. f. Geburts. u. Gyn., Sept., '99).
Case of eclampsia complicated by a marked erythema multiforme of a bul lous character. Kaposi ascribes ery thema multiforme to: (a) Change of seasons. (b) Angioneuroses which occur principally in women. (c) Instability of the vasomotor centres. (d) Autoinfec tion: i.e., toxic substances which have entered the blood as the result of some internal disease, as chronic nephritis. The ease cited probably comes under the last division. J. D. Voorhees (Med. Record, Oct. 7, '99).
In the Boston Lying-in Hospital dur ing the last fifteen years 90 cases have occurred, although in 11 no convulsions appeared. There were 79 cases of true eelampsia in 6700 deliveries: an aver age of 11.7 to the thousand. Of these, 57, or 72.2 per cent., were primiparm, and 22, or 27.8 per cent, were multiparm. Newell (Boston Med. and Surg. Jour., Nov. 9, '99).
There is no uniform causal factor for puerperal eclampsia. Even slightly toxic products in the blood of women in child bed are sufficient to irritate the vaso motor centres, which are then in a. con dition of increased excitability. E. Herz (Wiener med. Woch., Nos. 3, 7, 8, 1900).
Case in which the rapidity of death after the fits suggested cerebral hmmor rhage. Free hmmorrhage was discovered on the surface of the convolutions of the left hemisphere and widely distributed hmmorrhages in the liver: subscapular, interlobular, and intralobular. Case in which sudden and rapidly fatal asphyxia was caused by cerebral hmmorrhage, which nearly destroyed the bulb and the floor of the fourth ventricle. Boissard (Bull. de la Soc. d'Obstet. de Paris, Feb. 15, 1900).
The etiology of puerperal eclampsia is still a mooted question. The bacteria which were supposed to be the germs causing eclampsia are found in all preg nant women. When the blood of the eelamptie patient is examined. micro organisms are rarely found, and from observations one can find no positive proof that any one germ has been iso lated which will cause eclampsia. The universal opinion at present is that eclampsia is due to a profound toxieinia, and the origin of this toxamiia is still unknown. Beattie (Jour. Amer. Med. Assoc., Aug. 24, 1901).
The toxic theory of eelampsia is now the one generally held by most obste tricians, and in this connection the fol lowing points may be mentioned: 1. That in every ease of pregnancy more or less toxremia exists, and that the blood intoxication becomes more profound toward the end of gestation. 2. That, although the eelamptie state is due to a toxannia, the toxic agent which excites the convulsions is probably not always the same; there seems to be different types of the disease. 3. Tha.t the toxins may be produced in greater abundance in some cases (twin pregnancies), and that they are generally more virulent in primiparm than in multiparm. In the primipara mechanical pressure on the renal vessels may possibly come more into play, while in the multipara a cer tain degree of immunity against the toxin may have been acquired from previous pregnancies (Allbutt). 4. That in spite of very grave toxamia no alarming symptoms will occur so long as elimination by the kidneys is suffi ciently active. Of the nature of the toxins nothing is known, and there is no clear evidence to show where they are formed.