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OBJECTIVE: To identify markers for late fetal death, a multicenter study was performed, based on routinely obtained data from maternal health care units. MATERIAL AND METHODS: Prospectively recorded data were obtained from maternal health care units belonging to five delivery units. In all, 233 consecutive cases of singleton pregnancy involving late fetal death (> or = 28 weeks) were identified between 1983 and 1989. As a control for each case, the next consecutive mother giving birth to a live infant at the same delivery unit was selected, the sole matching criterium being parity. RESULTS: After exclusion of pregnancies with lethal malformations or trauma, 205 cases remained for the statistical analysis. Two main subgroups were identified: mothers with placental abruption (n = 44), and pregnancies with no obvious reason for fetal death (n = 101). An increased risk for late fetal death was evident in expectant mothers > or = 40 years (10 vs 1; chi 2 = 7.6, p < 0.01), and in smokers where an association was seen to placental abruption. A significantly increased risk was also seen in women with medical treatment for essential hypertension (8 vs 1; chi 2 = 5.6, p < 0.05). On the other hand, we found no correlation between proteinuria, glucosuria, decreasing symphysis-fundal height, or changes in the Hb, on the one hand, and late fetal demise, on the other. There was no overrepresentation of post dated pregnancy (by ultrasound early in the second trimester) among the cases. Nor did post dated pregnancies (> or = 42 weeks) estimated from first day of last menstrual period (but not post dated by ultrasound) imply a higher rate of fetal death, as has been suggested in previous studies. CONCLUSION: In the present material, there was no sign of systematic error in the evaluation of data routinely obtained from the antenatal clinics and maternity units. Apart from placental abruption in smokers, a high maternal age, and medical treatment for essential hypertension, deviating data were recorded as often among controls as among cases. No correlation was evident between a post date pregnancy and fetal demise. A short symphysis-fundal height was recorded as often among controls as among cases and the even distribution of fetal birthweight in case pregnancies around the standard curve for the normal population is noteworthy.

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BACKGROUND: To evaluate the relationship between stillbirth in singleton pregnancy (> or = 28 weeks gestation) and maternal weight (weight gain) from 24 completed weeks. METHODS: All fetal deaths (n = 210) at five delivery units during seven years in southern Sweden were analysed. To each case a control mother was selected, the only matching criteria being parity and place of delivery. Regression analysis was used for comparison of body weight gain in cases and controls. RESULTS: Mothers experiencing stillbirth had a significantly lower mean body weight at 24 weeks gestation than control mothers (63.5 kg vs 67.3 kg; t = 2.4, p < 0.05). No significant difference between cases and controls was found in mean weight gain during pregnancy from 24 completed gestational weeks to delivery, even when the last three measurements before delivery for cases and controls were compared separately. CONCLUSION: There is no difference in body weight gain between mothers with stillbirth and mothers giving birth to a live infant.

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A prospective study was undertaken to evaluate the risk of uterine rupture or dehiscence after cesarean section. During the 10 years of the study, 24,644 patients were delivered of infants. Of these women, 2036 (8.3%) had previously undergone cesarean section. A trial of labor was allowed in 1008 of these patients, and 92.2% were delivered vaginally. The incidence of uterine rupture in this trial of labor group was 0.6%, compared with 0.4% in the total group. Cesarean section scar rupture caused no serious complications in either the mothers or the offspring in the trial of labor group. Uterine rupture in this group was not associated with use of oxytocin or epidural analgesia. Patients with lower-segment scar rupture had no history of puerperal pyrexia. The incidence of uterine dehiscence was 4%. In summary, the risk of uterine rupture in patients who have previously undergone cesarean section but are allowed a trial of labor is low and not associated with serious complications. Vaginal delivery is therefore considered the safest route of delivery in these patients.

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A prospective study was conducted to determine the risk of placenta previa and unexplained antepartum hemorrhage after a previous cesarean section (CS). Of a total of 24,644 patients, 81 (0.33%) had a placenta previa which demanded abdominal delivery. The risk of placenta previa was 0.25% with an unscarred uterus and 1.22% in patients with one or more previous CS (the difference was statistically significant p less than 0.001). The corresponding figures for unexplained antepartum hemorrhage were 0.40% and 3.81%, respectively (p less than 0.001). Patients presenting with a placenta previa and a scarred uterus had a 16% risk of undergoing cesarean hysterectomy because of placenta accreta and severe hemorrhage compared to 3.6% in patients with placenta previa and an unscarred uterus. In conclusion, cesarean deliveries predispose to placenta previa, placenta accreta and antepartum hemorrhage during subsequent pregnancies. This relationship has to be considered in the cost-benefit equation for decision of route of delivery.

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It is generally accepted that hypertensive cardiovascular complications can be prevented by treatment. However, during pregnancy, antihypertensive drugs might be hazardous in view of their influence on the fetus. Nevertheless, in spite of the diverging published results, even beta-blockers have been used in the pregnant patient. As our basic knowledge concerning the circulatory and fetal effects is minimal, we decided to elucidate the influence of the non-selective beta-blocker, propranolol, on the haemodynamic circumstances in hypertensive pregnant rats. Renal hypertension was induced by clamping both renal arteries 4 weeks before pregnancy. Shortly before term, cardiac output was determined with the dye-dilution technique and utero-placental blood flow was determined with the microsphere technique, both before and after propranolol injection. Mean arterial pressure and heart rate were registered continuously. The acute propranolol injection reduced mean arterial pressure by 26%. This was due mainly to a 32% decrease in cardiac output, which in turn was due to a 24% decrease in stroke volume and a 6% decrease in heart rate. Both myometrial and placental blood flow decreased significantly, by 45 and 50%, respectively. It was furthermore of interest to observe the significant increase in blood flow resistance in both myometrium and placenta. In conclusion, it can be stated that the non-selective beta-blocker propranolol, which lacks intrinsic stimulating activity, reduces mean arterial pressure mainly by a cardiac output decrease. The present results further indicate that the influence on peripheral blood flow might be caused by cardiac output changes as well as by direct effects on the uteroplacental vascular bed.

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Clinical as well as experimental studies have demonstrated a 70% reduction in utero-placental blood flow in pregnancies affected by severe hypertension (13, 19). In pregnant renal hypertensive rats, propranolol administration causes a further 50% reduction in utero-placental blood flow (16). The present study on renal hypertensive rats was performed in order to explore the acute effects on central haemodynamics and utero-placental blood flow of the non-selective beta-blocker pindolol, which also has an intrinsic beta-stimulatory effect. Renal hypertension was induced by partial clamping of both renal arteries in female Wistar rats 4 weeks before pregnancy. Some 2-4 days before expected parturition, cardiac output was determined with the dye-dilution technique and blood flow to the reproductive organs with the microsphere technique, both before and after acute pindolol administration. Mean arterial pressure and heart rate were recorded continuously during the experiment. After pindolol injection, mean arterial pressure fell by 22% due to a 38% reduction in total peripheral resistance. No significant changes in cardiac output, stroke volume or heart rate were found. Placental blood flow was significantly reduced, by 30%, whereas myometrial and ovarian blood flows were reduced by only 18 and 9%, respectively. Thus, the reduction in blood supply to the reproductive organs in renal hypertensive rats after acute pindolol administration was most pronounced in the placenta. This reduction in placental flow was, however, only about half as pronounced as after propranolol, which lacks intrinsic beta-stimulatory effects. This may suggest that vasodilating beta-receptors may play an important role in the maternal placental vascular bed.

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The aim of the present study on pregnant renal hypertensive rats was to investigate the effects on central hemodynamics and uteroplacental blood flow after chronic administration of pindolol, a nonspecific beta-adrenergic receptor blocking agent with intrinsic beta-stimulatory effect. Renal hypertension was induced by partial clamping of both renal arteries four weeks before pregnancy. Pindolol was administered with the food during the entire pregnancy period. Two to four days before expected delivery mean arterial pressure, heart rate, cardiac output, (dye-dilution technique) and utero-placental blood supply (microsphere technique) were determined. The chronic pindolol treatment reduced heart rate by 25 per cent while both mean arterial pressure and cardiac output remained unchanged. However, blood flow to uterus and placentae was reduced by 43 and 64 per cent, respectively, after pindolol treatment. Clinical as well as experimental studies (15, 16) demonstrate a reduced utero-placental blood supply when pregnancies are complicated by hypertension. As pregnancies with severe hypertension are associated with an increased frequency of intrauterine growth retardation and intrauterine asphyxia the present results indicate that the combination of hypertension and long-term treatment with beta-blockers might reduce utero-placental blood flow enough as to seriously interfere with fetal oxygen supply thereby increasing the risk of intra- and extra-uterine asphyxia.

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The main purpose of this study on rats was to examine the effect of pregnancy on experimental renal hypertension and cardiac size. Renal hypertension in the rats (RHR) was induced by standardized clamping of the left renal artery early in pregnancy (SRHR) or 4 weeks before mating (ERHR). As controls served non-pregnant RHR with the duration of hypertension matched to each above mentioned group, as well as non-pregnant and pregnant normotensive rats. Only 16% of the rats with renal artery clamping early in pregnancy (SRHR) developed hypertension in contrast to 41% of similarly operated non-pregnant rats and 56% of ERHR decreased their blood pressure to normal levels during pregnancy. Concerning left ventricular heart weight there was a slight increase in left ventricular weight during normal pregnancy in spite of a significantly reduced blood pressure. In both SRHR and ERHR an increased left ventricular heart weight was noticed during pregnancy even when arterial pressure was not increased. The present results suggest an antihypertensive effect of pregnancy and the existence of "trophic" influences and/or a volume induced adaptation of the heart causing an increased myocardial mass which is associated with pregnancy and partly independent of blood pressure influences.

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An experimental study on pregnant rats was undertaken to explore whether renal hypertension interferes with uteroplacental blood supply and fetal weight. Renal hypertension was induced by standardized clamping of the left renal artery. Two days before expected delivery, blood flow to the reproductive organs was determined by microsphere technique in normal control rats, rats with short-standing renal hypertension induced early in pregnancy, and rats with established renal hypertension induced 4 weeks before pregnancy. Myometrial and placental blood supply was considerably reduced in renal hypertensive rats compared to that in normotensive pregnant rats, with the reduction in placental blood flow being as much as 68% in rats with established renal hypertension. Nevertheless, there was no reduction in fetal weights, placental weights, or number of fetuses in the litters. These findings suggest that the nutritional blood supply of the placenta normally has a considerable overcapacity, perhaps a necessary safety margin so that the fetus can manage the circulatory demands associated with delivery. If hypertension causes intrauterine growth retardation only by means of reduced placental blood flow, this reduction in flow obviously must be considerable.

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