Comparing the morphological findings of the placentas of acidotically born babies of diabetic mothers with non-acidotically born ones, we could find an extensive correlation of macroscopically detectable changes of the placentas (diminution of placental weight, insertio velamentosa of umbilical cord, aplasia of one umbilical artery) and histological findings (severity of diabetic maturation disturbances, size of villi) with the degree of the neonatal acidosis. With the severity of acidosis, the oedematosis of the placentas increases, too. When diabetic pregnancy is complicated by the EPH gestosis, a stronger fibrosis of the chorionic villi results. The oedematosis of the stroma recedes. The oedema of the placenta is in most cases correlated with the clinical appearance of the diabetic fetopathy (cushingoid newborn). According to our findings in cases complicated by the EPH gestosis, the oedematosis of the placenta and to a minor extent the cushingoid of the newborn are to be found more seldom.

127 specimens, obtained by different methods from the myometrium and the placental bed after parturition, are investigated histologically. This material includes normal pregnancies as well as cases of maternal diabetes with and without hypertension and cases of hypertension in EPH-gestosis. The different parts of the arterial system (spiral arteries, basal arteries, radial arteries) are separately investigated. Physiologically, the pregnancy induces changes in the wall of the decidual arteries and possibly in the distal part of the radial arteries. The fibromuscular layer including the elastic fibers were destructed and replaced by fibrin and connective tissue. For this reason, in these parts of arteries it is very difficult to separate pathological from physiological changes. Maternal hypertension produces in myometrial, basal and decidual arteries (myometrial part) a thickening of the arterial wall. This thickening is caused in arteries with normal structure by hypertrophy of the media, in the spiral arteries by intimal processes (edematous reaction of the intima, deposition of foam cells) and fibrinoid necrosis of the arterial wall. The cases of maternal diabetes without hypertension are characterized by an increase of fibrin deposits in the wall of the distal part of the spiral artery. In the proximal part of the spiral artery we have found in two cases without hypertension some foam cells in the wall. Myometrial arteries show particularly thickening of the wall and narrowing of the arterial lumen, less frequently intimal swelling and groups of foam cells. In diabetes mellitus, complicated by hypertension, we could find changes in the proximal part of the spiral artery and in the basal arteries. This alterations correspond with the changes in cases of hypertension without diabetes. In the myometrial arteries the pathological processes are the same as in cases of diabetes without hypertension. A significant increase of pathological processes by the diabetes mellitus alone exists only in the myometrial arteries. Besides, in the small arterial vessels of the myometrium in diabetes occurs a proliferative angiolopathy, involving cases of White classes D and F only. We could demonstrate the so-called ‘acute atherosis’ in a small number of cases in the myometrial part of the spiral artery and in the distal part of the radial artery, too. It concerns especially cases of maternal hypertension, more seldom cases of normal pregnancy and diabetic pregnancy without hypertension.

An attempt has been made to demonstrate the feasibility of quantitating by light microscopy and histoplanimetry the pathology of placental maturation associated with maternal diabetes mellitus. The size of chorionic villi, the development of chorionic vessels, stroma edema, and the distribution of these findings were used as criteria to assess the degree of the abnormality. In addition, the size of individual villi and the distribution of these villi over areas of known size were estimated. The results of these methods coincided in 72% of 25 cases thus studied. The advantages and disadvantages of both methods were evaluated. For the correlation of placental alterations on the one hand and of maternal and fetal pathology on the other, a quantitative assessment of placental maturation appears urgently required.

From a material of 250 newborns of diabetic mothers we have selected 45 cases with a birthweight of less than 3,000 g. Among those, there were 14 doubtful and positively growth-retarded newborns. Retardation is supposed to be due to maternal diabetes, malformations of the umbilical cord and of the newborns, abuse of nicotine during pregnancy, and postmaturity and toxaemia. In the light of all our investigation results it seems likely that intrauterine somatic retardation is caused by maternal diabetes per se.

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