The Journal of laboratory and clinical medicine . Iig. 3.—Same as Iig. _, but somewhat greater magnification. The parcnchyniaunis changes are well shown. 350 The Journal of Laboratory and Clinical Medicine the anasarcous fetus was one of a pair of twins. The other twin was apparent-ly normal. Delivery was not forcible, Ijut the delay caused by the delivery ofthe anasarcous infant led to the death of the healthy one. I loth were prema-ture. Schridde believed that this fetal disease was the result of a severe fetalanemia which was associated with a high grade of reparatory ane
The Journal of laboratory and clinical medicine . Iig. 3.—Same as Iig. _, but somewhat greater magnification. The parcnchyniaunis changes are well shown. 350 The Journal of Laboratory and Clinical Medicine the anasarcous fetus was one of a pair of twins. The other twin was apparent-ly normal. Delivery was not forcible, Ijut the delay caused by the delivery ofthe anasarcous infant led to the death of the healthy one. I loth were prema-ture. Schridde believed that this fetal disease was the result of a severe fetalanemia which was associated with a high grade of reparatory anemia, it was assumed, was of toxic origin. Schridde (Hd not believe it. Fig. 4.—Same as Fig. 3, but with still greater magnification. to be luetic. Fischer called attention to the similarity of the picture to thatof anemia pseudoleukaemia iiifantutn and suggested that this kakophoniouslynamed disease might be an exaggerated form, or a further development, of fetalanemia in which the criteria might be similar to, though less marked than thoseof the erythroblastosis type. One of Schriddes cases was derived from a ne-phritic mother but in this instance he believed that the fetal condition was coin-cidental and not the result of the maternal condition. This is interesting be-cause there is the tendency to lay these cases at the door of maternal disorders Fetal Erythroblastosis: fetal Bryiliroblastoinatosis 351 •• ? ?,
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